Rak gruczołów łojowych
Patofizjologia i mechanizm

Rak łojowy (sebaceous carcinoma, SC) to rzadki, agresywny nowotwór skóry wywodzący się z gruczołów łojowych, stanowiący 0,2-4,6% wszystkich złośliwych nowotworów skóry, z 5-10% śmiertelnością. Etiopatogeneza obejmuje ekspozycję na promieniowanie UV, immunosupresję (np. po przeszczepach narządów, AIDS), infekcje HPV i HIV oraz tło genetyczne, zwłaszcza zespół Muira-Torre’a (MTS) – wariant zespołu Lyncha z mutacjami w genach naprawy DNA (MLH1, MSH2, MSH6, PMS2). Molekularnie wyróżnia się trzy klasy raka łojowego: związany z uszkodzeniem UV, z niestabilnością mikrosatelitarną (MSI) oraz pauci-mutacyjny, co koreluje z lokalizacją i przebiegiem klinicznym. Kluczowe szlaki sygnałowe zaangażowane w patogenezę to Wnt/β-katenina, PI3K/AKT/mTOR, Sonic Hedgehog, TGF-β oraz CASPASE-3/YAP, a także ekspresja HER2 i VEGF, co wskazuje na potencjalne cele terapii celowanej. Histopatologicznie rak łojowy wykazuje zróżnicowane wzorce wzrostu i różnicowania, z dominacją wzorca zrazikowego i obecnością komórek bazaloidalnych oraz sebocytów, a immunohistochemicznie cechuje się ekspresją EMA, BerEp4, AR, CK7, Ki-67 (mediana 35%, zakres 5-80%) i p53 (mediana 10%, zakres 0-80%), gdzie ekspresja p53 ≥10% i Ki-67 ≥25% wspierają rozpoznanie.

Patogeneza raka łojowego – zagadnienia ogólne

Rak łojowy (sebaceous carcinoma, SC) to rzadki, agresywny nowotwór skóry wywodzący się z gruczołów łojowych. Mimo że stanowi zaledwie 0,2-4,6% wszystkich złośliwych nowotworów skóry, charakteryzuje się dużą agresywnością, zdolnością do miejscowych nawrotów i przerzutów odległych, co przekłada się na wysoką śmiertelność sięgającą 5-10% przypadków.123

Dokładna patogeneza raka łojowego wciąż pozostaje nie w pełni poznana. Nowotwór ten może rozwijać się spontanicznie lub wiązać się z określonymi zespołami genetycznymi, szczególnie z zespołem Muira-Torre’a, który jest odmianą dziedzicznego niepolipowatego raka jelita grubego (zespół Lyncha).45 W patogenezie raka łojowego bierze udział szereg różnych czynników, w tym ekspozycja na promieniowanie ultrafioletowe, przeszczepy narządów, immunosupresja, zaburzenia genetyczne, zmiany w szlakach sygnałowych komórkowych oraz mechanizmy molekularne prowadzące do rozwoju guza.67

Czynniki etiologiczne w patogenezie raka łojowego

Rozwój raka łojowego wiąże się z wieloma czynnikami, które wpływają na transformację nowotworową komórek gruczołów łojowych. Do głównych czynników etiopatogenetycznych należą:

  • Ekspozycja na promieniowanie ultrafioletowe (UV) – szczególnie istotna w przypadku raków w obszarach narażonych na słońce89
  • Przeszczepy narządów – związane z 90-krotnym zwiększeniem ryzyka rozwoju raka łojowego10
  • Immunosupresja (w tym wywołana lekami takimi jak cyklosporyna oraz w przebiegu AIDS)1112
  • Wcześniejsza radioterapia okolicy głowy i szyi1314
  • Tło genetyczne – szczególnie w zespole Muira-Torre’a i innych zespołach genetycznych15
  • Infekcje HPV (ludzki wirus brodawczaka) – zwłaszcza u młodszych pacjentów1617
  • Infekcje HIV18

W niektórych przypadkach rak łojowy może również rozwijać się z wcześniej istniejących zmian, takich jak znamię łojowe (nevus sebaceus), choroba Bowena lub rogowacenie słoneczne.19 Uważa się, że za różnorodność czynników etiologicznych odpowiadają odmienne mechanizmy patogenetyczne w różnych populacjach pacjentów.20

Mechanizmy molekularne w patogenezie raka łojowego

Badania molekularne wykazały, że w patogenezie raka łojowego uczestniczy wiele ścieżek sygnałowych i zaburzeń genetycznych. Zrozumienie tych mechanizmów jest kluczowe dla opracowania nowych metod diagnostycznych i terapeutycznych.21

Mutacje i zaburzenia genetyczne

W raku łojowym zidentyfikowano różne mutacje i zaburzenia genetyczne, które odgrywają kluczową rolę w rozwoju choroby:

Badania wykazały, że raki łojowe można podzielić na trzy odrębne klasy molekularne w zależności od typu mutacji. Pierwsza grupa charakteryzuje się mutacjami związanymi z uszkodzeniami UV, druga grupa wykazuje niestabilność mikrosatelitarną (MSI), a trzecia grupa, obejmująca głównie raki oczodołowe, charakteryzuje się niskim obciążeniem mutacyjnym.2829

Zaburzenie szlaków sygnałowych

W patogenezie raka łojowego kluczową rolę odgrywają zaburzenia w następujących szlakach sygnałowych:

  1. Szlak Wnt/β-katenina – dochodzi do dysregulacji tego szlaku, co prowadzi do akumulacji β-kateniny w cytoplazmie i jej hiperaktywacji, szczególnie w rakach okolicy oczodołowej3031
  2. Szlak PI3K/AKT/mTOR – wykazuje częstą dysregulację w raku łojowym, co promuje proliferację komórek nowotworowych, przeżycie i oporność na apoptozę, przyczyniając się do progresji choroby i oporności na leczenie3233
  3. Szlak Sonic Hedgehog (SHH) – zaburzenia w tym szlaku wiążą się z nieprawidłową proliferacją w obrębie gruczołu łojowego i mogą przyczyniać się do rozwoju guza3435
  4. Szlak TGF-β – dysregulacja czynnika transformującego wzrostu beta identyfikowana w niektórych rakach łojowych3637
  5. Szlak CASPASE-3/YAP – zaangażowany w apoptozę komórek i kontrolę wzrostu guza38

Ponadto obserwuje się zmiany w ekspresji PTEN (homolog fosfatazy i tensyny) oraz czynnika jądrowego κB (NFk-B), a także inaktywację p53, co dodatkowo wspomaga proces karcinogenezy.39 Badania wykazały również podwyższoną ekspresję kinazy tyrozynowej, szczególnie HER2, co skłania do badań nad terapią celowaną.40

Mechanizmy angiogenezy w raku łojowym

Angiogeneza odgrywa ważną rolę w rozwoju i progresji raka łojowego. Badania immunohistochemiczne wykazały nadekspresję białek zaangażowanych w angiogenezę, proliferację komórek i procesy zapalne, takich jak:41

Ekspresja VEGF przez keratynocyty naskórka i komórki guza oraz jego interakcja z VEGFR-2 przyczyniają się do patogenezy raka łojowego nie tylko poprzez efekty angiogenne, ale także przez bezpośredni wpływ na komórki guza.42 Zwiększony wewnątrzguzowy stosunek małych naczyń limfatycznych do dużych naczyń limfatycznych oraz ujemna korelacja między ekspresją naskórkowego VEGF a wewnątrzguzową gęstością naczyń limfatycznych wyraźnie podkreślają hipotezę dotyczącą potencjału limfangiogenetycznego raka łojowego.43

Pochodzenie komórkowe i różnicowanie

Histologicznie rak łojowy charakteryzuje się wielorakimi wzorcami wzrostu i różnicowania, co może utrudniać diagnozę i wpływać na przebieg kliniczny choroby.4445

Typy różnicowania guza

Raki łojowe mogą wykazywać różny stopień zróżnicowania, co wpływa na ich agresywność i rokowanie:4647

  • Dobrze zróżnicowane – wykazują ułożenie zrazikowe i wakuolizację cytoplazmy komórek centralnie, zachowując cechy prawidłowych komórek łojowych
  • Średnio zróżnicowane – wykazują częściowe cechy różnicowania łojowego
  • Słabo zróżnicowane – stanowią najczęstszą postać zarówno w lokalizacji oczodołowej (38,46%) jak i pozaoczodołowej (43,75%)

W guzie obecne mogą być zarówno komórki łojowe, jak i niezróżnicowane. Obserwuje się zmienność kształtu i wielkości jąder z wysoką aktywnością mitotyczną potwierdzoną obecnością figur mitotycznych.48 Wzorce naciekania mogą być różne, ale dominuje wzorzec zrazikowy (68,75% w pozaoczodołowych i 76,92% w oczodołowych SC).49

Teorie dotyczące pochodzenia raka łojowego

Pochodzenie raka łojowego wciąż jest przedmiotem dyskusji naukowych. Istnieją różne hipotezy dotyczące komórki pochodzenia tego nowotworu:50

  1. Teoria różnicowania wielokierunkowego – gruczoły sutkowe (a podobnie inne obszary) u pacjentów z rakiem łojowym mogą wykazywać cechy gruczołów łojowych, ponieważ te gruczoły mają wspólne pochodzenie
  2. Teoria komórek progenitorowych – rak łojowy rozwija się z komórek progenitorowych zdolnych do różnicowania w kierunku gruczołów łojowych w obrębie nabłonka
  3. Teoria ektopowej lokalizacji – gruczoły łojowe są ektopowo obecne w określonych tkankach (np. w gruczole sutkowym)
  4. Teoria pluripotencjalnych komórek macierzystych – rak łojowy może pochodzić z pluripotencjalnych komórek macierzystych jednostki mieszkowo-łojowo-apokrynowej, które mogą przekształcać się w komórki mieszkowe, łojowe i apokrynowe5152

Niektóre badania sugerują, że rak łojowy może też wywodzić się z komórek przewodu łojowego lub międzymieszkowego naskórka, z określoną grupą komórek progenitorowych wykazujących ekspresję p63 i keratyny 5.53 W rzadkich przypadkach opisywano również in situ lub inwazyjny rak łojowy powstający z śródnaskórkowych zmian płaskonabłonkowych.54

Podtypy molekularne raka łojowego

Na podstawie charakterystyki genetycznej i molekularnej, raki łojowe można podzielić na trzy odrębne klasy, które wyjaśniają zarówno ich ontogenezę, jak i przebieg kliniczny:5556

Podtyp Charakterystyka molekularna Typowa lokalizacja Przebieg kliniczny
Związany z uszkodzeniem UV Mutacje związane z sygnaturą uszkodzeń UV (sygnatury 7 i 11), wysoką liczbą mutacji CCTT w dinukleotydach Głównie obszary eksponowane na słońce Bardziej agresywny, podobny do raka płaskonabłonkowego skóry
Z niestabilnością mikrosatelitarną (MSI) Inaktywacja genów naprawy niesparowanych zasad DNA, wysoki poziom niestabilności mikrosatelitarnej Częsty w zespole Muira-Torre’a Związany z innymi nowotworami wewnętrznymi
Pauci-mutacyjny Niska częstość mutacji (1,2-5,5 mutacji/Mb) Wszystkie przypadki oczodołowe i część pozaoczodołowych Wykazuje inne wzorce progresji w porównaniu z podtypami o wysokim obciążeniu mutacyjnym

Ta klasyfikacja molekularna ma istotne znaczenie kliniczne, ponieważ pomaga wyjaśnić zróżnicowane zachowanie biologiczne raków łojowych w zależności od ich pochodzenia i wpływu czynników środowiskowych.57

Rola zespołu Muira-Torre’a w patogenezie raka łojowego

Zespół Muira-Torre’a (MTS) jest istotnym czynnikiem w patogenezie części przypadków raka łojowego. Jest to autosomalnie dominujący zespół charakteryzujący się występowaniem nowotworów łojowych w połączeniu z nowotworami wewnętrznymi, szczególnie jelita grubego i układu moczowo-płciowego.5859

Podłoże genetyczne zespołu Muira-Torre’a

MTS jest wariantem dziedzicznego niepolipowatego raka jelita grubego (zespół Lyncha) i charakteryzuje się defektami w genach naprawy niesparowanych zasad DNA:6061

  • MLH1 (MutL homolog 1)
  • MSH2 (MutS homolog 2) – najczęściej dotknięty gen
  • MSH6 (MutS homolog 6)

Mutacje te prowadzą do gromadzenia się niestabilnych sekwencji mikrosatelitarnych i błędów replikacji, predysponując do rozwoju różnych nowotworów.62 W przeciwieństwie do sporadycznych raków łojowych, które zazwyczaj nie wykazują utraty genów naprawy niesparowanych zasad DNA ani niestabilności mikrosatelitarnej, raki związane z MTS charakteryzują się tymi zaburzeniami.63

Cechy charakterystyczne raków łojowych w zespole Muira-Torre’a

Raki łojowe występujące w przebiegu zespołu Muira-Torre’a wykazują pewne unikalne cechy w porównaniu z przypadkami sporadycznymi:6465

  • Często występują mnogimi zmianami
  • Są zwykle większe niż w przypadkach bez zespołu
  • Charakteryzują się mniejszą agresywnością i mniejszym prawdopodobieństwem przerzutów
  • Mogą wystąpić przed lub jednocześnie z nowotworami wewnętrznymi w około 42% przypadków

Ta obserwacja podkreśla znaczenie badań przesiewowych w kierunku nowotworów wewnętrznych u pacjentów z rakiem łojowym, szczególnie gdy istnieje podejrzenie zespołu Muira-Torre’a.66 Zalecane jest wykonywanie kolonoskopii co 3-5 lat, rozpoczynając w wieku 25-30 lat, a także coroczna mammografia i biopsja endometrium co 3-5 lat u kobiet powyżej 50 roku życia.67

Rola immunologii i zapalenia w patogenezie

Układ immunologiczny odgrywa ważną rolę w patogenezie raka łojowego, a zaburzenia immunologiczne mogą przyczyniać się do rozwoju tego nowotworu.68

Rola układu immunologicznego

Zaburzenia immunologiczne mogą sprzyjać rozwojowi raka łojowego na różne sposoby:6970

  • Selektywna utrata odpowiedzi limfocytów T przeciwko wirusom, takich jak HPV, prawdopodobnie z powodu wadliwej prezentacji antygenów wirusowych na powierzchni keratynocytów
  • Immunosupresja po przeszczepach narządów zwiększa ryzyko raka łojowego nawet 90-krotnie
  • Pacjenci z AIDS mają znacznie zwiększone ryzyko rozwoju raka łojowego

Badania wskazują, że rak łojowy może wykazywać ekspresję PD-L1 na komórkach guza i PD-1 na limfocytach naciekających guz (TILs) w 46% przypadków, co wskazuje na mechanizm ucieczki immunologicznej w obrębie aktywnego, ale stłumionego mikrośrodowiska guza.71

Rola zapalenia w patogenezie

Przewlekłe zapalenie może odgrywać istotną rolę w patogenezie raka łojowego:72

  • Przewlekłe zapalenie może powodować hiperplazję gruczołów łojowych, zaburzać różnicowanie i prowadzić do miejscowej immunosupresji, tworząc warunki sprzyjające transformacji nowotworowej
  • Zapalenie może wpływać na różnicowanie sebocytowe podczas procesów zapalnych
  • Palenie tytoniu może przyczyniać się do rozwoju raka łojowego poprzez indukowanie przewlekłego zapalenia, uszkodzenia DNA, immunosupresji i zmiany środowiska gruczołów łojowych, promując transformację nowotworową, szczególnie w połączeniu z innymi czynnikami73

Czynniki zapalne, wraz z nieprawidłowymi zmianami w komórkach łojowych i mutacjami w kluczowych genach, takich jak TP53, mogą napędzać rozwój guzów.74

Cechy histopatologiczne i wzorce naciekania

Cechy histopatologiczne raka łojowego są zróżnicowane i mają istotne znaczenie diagnostyczne i prognostyczne.75

Wzorce histologiczne

Rak łojowy może wykazywać różne wzorce wzrostu i różnicowania:7677

  • Guz jest zazwyczaj umiejscowiony w skórze właściwej z naciekaniem do tkanki podskórnej i okolicznych struktur
  • Może występować pagetodialne naciekanie naskórka
  • Komórki guza mają charakter bazaloidalny z ogniskami różnicowania łojowego
  • Sebocyty to duże komórki z wielopęcherzykową, jasną cytoplazmą
  • Główne typy komórek spotykane w raku łojowym to bazaloidalne, bazalno-płaskonabłonkowe i epidermoidalne78

W badaniu histopatologicznym guz składa się z licznych nieregularnych zrazików o różnej wielkości, składających się z sebocytów oddzielonych podścieliskiem włóknisto-naczyniowym. Komórki guza w raku łojowym są często duże i mogą wykazywać zmiany płaskonabłonkowe.79

Wzorce naciekania

Rak łojowy charakteryzuje się różnymi wzorcami naciekania, które mogą wpływać na jego zachowanie kliniczne:8081

  1. Rozprzestrzenianie się śródnabłonkowe (pagetodialne) – występuje w 44-80% przypadków, polega na naciekaniu pojedynczych komórek guza lub gniazd komórek guza do pokrywającego nabłonka
  2. Bezpośrednie rozprzestrzenianie – poprzez bezpośrednie przedłużenie w sąsiednie struktury, takie jak jama wewnątrzczaszkowa, oczodół i zatoki przynosowe
  3. Wieloogniskowa proliferacja – do tkanek śródskórnych i podskórnych
  4. Onkoforeza – hipotetyczny mechanizm, w którym komórki rakowe są złuszczane i przeszczepiane

Rozprzestrzenianie się pagetodialne jest bardziej charakterystyczne dla oczodołowego raka łojowego i może występować w do 50% nawrotowych przypadków w tej lokalizacji, podczas gdy jest znacznie rzadsze w pozaoczodołowym raku łojowym.82 Wieloogniskowy wzrost i pagetodialne rozprzestrzenianie się są związane z gorszym rokowaniem i wyższym ryzykiem nawrotu.83

Markery immunohistochemiczne

W diagnostyce raka łojowego pomocne są następujące markery immunohistochemiczne:8485

  • Antygen błonowy nabłonka (EMA) – pozytywny w sebocytach
  • BerEp4 – pozytywny w sebocytach
  • Receptor androgenowy (AR) – pozytywny w sebocytach
  • CK7 – zazwyczaj pozytywny w guzach oczodołowych
  • Specjalne barwienia, takie jak Oil Red-O, Sudan IV – pomagają w identyfikacji lipidów
  • Adipofilina – marker różnicowania łojowego86
  • Ki-67 – marker proliferacji, wykazujący wyższą ekspresję w raku łojowym w porównaniu do zmian łagodnych (mediana = 35%, zakres 5-80% vs. mediana = 5%, zakres: 0-30%)87
  • p53 – wykazuje wyższy odsetek ekspresji w raku łojowym w porównaniu do zmian łagodnych (mediana = 10%, zakres 0-80% vs. mediana = 0%, zakres: 0-5%)88

Ekspresja p53 ≥10% i ekspresja Ki-67 ≥25% są sugestywne dla diagnozy raka łojowego.89 Barwienia immunohistochemiczne zastąpiły w dużej mierze barwienia lipidowe, takie jak Oil Red-O, których czułość zmniejsza się po utrwaleniu w formalinie.90

Implikacje kliniczne mechanizmów patogenetycznych

Zrozumienie patogenezy raka łojowego ma bezpośrednie przełożenie na praktykę kliniczną, wpływając na diagnostykę, leczenie i monitorowanie pacjentów.91

Wyzwania diagnostyczne

Ze względu na swoją różnorodność i zdolność do naśladowania innych zmian, rak łojowy bywa nazywany „wielkim naśladowcą” guzów przydatkowych.92 Diagnostyka może być utrudniona z powodu:9394

  • Zróżnicowanej prezentacji klinicznej – może przypominać łagodne zmiany, takie jak jęczmień, gradówka, zapalenie spojówek
  • Różnorodnych wzorców wzrostu histopatologicznego – może naśladować raka płaskonabłonkowego, podstawnokomórkowego, chorobę Pageta czy czerniaka
  • Trudności w identyfikacji różnicowania łojowego w przypadkach słabo zróżnicowanych

Średni czas między wystąpieniem objawów a diagnozą wynosi od jednego do trzech lat, co pokazuje trudności diagnostyczne.95 Wczesne rozpoznanie ma kluczowe znaczenie dla wyników leczenia.96

Czynniki prognostyczne

Znajomość mechanizmów patogenetycznych pozwala na identyfikację czynników prognostycznych w raku łojowym:9798

  • Stopień zróżnicowania guza – słabe zróżnicowanie związane jest z gorszym rokowaniem
  • Kategoria T według AJCC – kategoria T2b lub gorsza koreluje z przerzutami do regionalnych węzłów chłonnych
  • Mutacje w genach TP53, p21, Shh i E-kadheryny – związane z inwazją, przerzutami i gorszymi wynikami klinicznymi99
  • Rozprzestrzenianie się pagetodialne i wieloogniskowy wzrost – związane z wyższym ryzykiem nawrotu100
  • Rozmiar guza powyżej 1 cm, inwazja naczyniowo-limfatyczna i zajęcie zarówno górnej, jak i dolnej powieki – wskazują na gorsze rokowanie101

Metaanaliza obejmująca 1333 pacjentów z rakiem łojowym powieki wykazała, że przerzuty występowały w 12,1% przypadków oczodołowych, nawroty w 15,9%, a śmiertelność związana z guzem wynosiła 6,2%.102

Potencjalne cele terapeutyczne

Zrozumienie mechanizmów molekularnych leżących u podstaw raka łojowego umożliwia identyfikację potencjalnych celów terapeutycznych:103104

  • Szlak PI3K/AKT/mTOR – inhibitory tego szlaku wykazały obiecujące wyniki w badaniach przedklinicznych
  • VEGFR-3 – może odgrywać krytyczną rolę w patogenezie raka łojowego i może być interesujący z terapeutycznego punktu widzenia
  • Kinazy tyrozynowe, w tym HER2 – potencjalne cele dla terapii celowanej
  • Białka związane z apoptozą, takie jak XIAP (związany z X inhibitor apoptozy) i BAG3 (Bcl-2-Associated Athanogene 3) – zaangażowane w promowanie przeżycia i proliferacji guza105

Eksperci sugerują, że nowe badania nad naturalnymi i ukierunkowanymi molekularnie metodami leczenia mogą prowadzić do opracowania nowych skutecznych strategii, uzupełniających konwencjonalne metody leczenia raka łojowego.106 Inhibitory szlaku PI3K/AKT/mTOR mogą oferować korzyści terapeutyczne pacjentom z zaawansowanym lub opornym na leczenie rakiem łojowym.107

Monitorowanie i obserwacja

Ze względu na agresywny charakter raka łojowego i możliwość nawrotów, wszyscy pacjenci wymagają ścisłego monitorowania po leczeniu:108109

  • Rak łojowy ma wysoki wskaźnik nawrotów wynoszący 11-30% po chirurgicznym usunięciu
  • U nawet 25% pacjentów nowotwór może nawrócić lub dawać przerzuty po leczeniu
  • Zalecana jest długoterminowa obserwacja pacjentów po wyleczeniu ze względu na doniesienia o późnych nawrotach

Pacjenci z zespołem Muira-Torre’a wymagają dodatkowych badań przesiewowych w kierunku nowotworów wewnętrznych, w tym regularnych kolonoskopii, mammografii i badań ginekologicznych.110 Dokładna znajomość mechanizmów patogenetycznych pozwala na lepsze zarządzanie ryzykiem i personalizację strategii monitorowania.111

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  1. 16.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Extraocular Sebaceous Carcinoma: A Report of 2 Cases | Actas Dermo-Sifiliográficas
    https://www.actasdermo.org/es-extraocular-sebaceous-carcinoma-a-report-articulo-S1578219012003113
    Sebaceous carcinoma is a rare, aggressive adnexal tumor of unknown etiology; 75% of these tumors arise in the periocular region while 25% arise at extraocular sites. This cutaneous tumor is a diagnostic sign of Muir-Torre syndrome, a disorder associated with visceral malignancies and gene abnormalities. Patients with sebaceous carcinoma should therefore be carefully evaluated; a detailed personal and family history of cancer, a thorough physical examination, additional tests where appropriate, and close monitoring will all be required. […] Sebaceous carcinoma is a rare adnexal tumor that follows an aggressive clinical course, with a risk of local recurrence and distant metastasis. Its etiology is unknown. Three-quarters of cases occur in the periocular region, although the tumor can present on any part of the body.
  • #2 Sebaceous carcinoma
    https://dermnetnz.org/topics/sebaceous-carcinoma
    Sebaceous carcinoma is a rare aggressive skin cancer arising from a sebaceous gland. […] The exact cause of sebaceous carcinoma is unclear. The following have been reported to possibly increase the risk of these tumours: […] Mutations to the tumour suppressor gene p53. […] Sebaceous carcinoma is an aggressive and potentially dangerous tumour that can lead to significant morbidity and mortality. The overall mortality rate is 510% because of inherent tumour factors, or delayed diagnosis and treatment.
  • #3 Sebaceous cell carcinoma of the scalp in a young male: A rare case report – IJPO
    https://www.ijpo.co.in/html-article/19061
    Sebaceous carcinoma is a rare locally aggressive neoplasm of the sebaceous gland, which occurs frequently in elderly males. It constitutes 0.2 to 4.6% of all the malignant cutaneous tumours and occurs commonly in the periocular area. […] The majority of sebaceous carcinomas arise from de novo mutations but those associated with Muir-Torre syndrome have a loss of mismatch repair gene expression and exhibit microsatellite instability, while those arising sporadically do not exhibit loss of mismatch repair or microsatellite instability. […] Sebaceous carcinoma usually occurs in the periocular areas, while amongst the extraocular areas, the head and neck region is more common where the sebaceous glands are most abundant. This tumour usually occurs in the sixth and seventh decade of life. […] The majority of sebaceous carcinomas arise from de novo mutations but may also develop from benign sebaceous neoplasms, though uncommon.
  • #4 Sebaceous carcinoma – UpToDate
    https://www.uptodate.com/contents/sebaceous-carcinoma/print
    Sebaceous carcinoma is a rare, malignant tumor of the sebaceous glands. […] This topic will review the pathogenesis, clinical presentation, diagnosis, and treatment of sebaceous carcinoma. […] Sebaceous carcinomas can occur sporadically or may be associated with Muir-Torre syndrome, a variant of the hereditary nonpolyposis colorectal cancer syndrome (Lynch syndrome) characterized by single or multiple sebaceous neoplasms, keratoacanthomas, and internal malignancy (particularly malignancy of the gastrointestinal or genitourinary system).
  • #5 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. Additionally, elevated expression levels of tyrosine kinase, particularly HER2, have been linked to sebaceous tumors, prompting investigations into targeted treatment. Aberrations in the Wnt/-catenin signaling pathway also strongly correlate with abnormal and malignant proliferation within the sebaceous gland.
  • #6 Sebaceous carcinoma – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/sebaceous-carcinoma/symptoms-causes/syc-20577038
    Sebaceous carcinoma is a type of cancer that begins in an oil gland in your skin. It most often affects the eyelid and may cause a lump or skin thickening. […] Sebaceous carcinoma happens when sebaceous gland cells get changes in their DNA. A cell’s DNA holds the instructions that tell the cell what to do. In healthy cells, the DNA gives instructions to grow and multiply at a set rate. The instructions tell the cells to die at a set time. In cancer cells, the DNA changes give different instructions. The changes tell the cancer cells to grow and multiply quickly. Cancer cells can keep living when healthy cells would die. This causes too many cells. The cancer cells form a growth or lump on the skin.
  • #7 Sebaceous Carcinoma: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/24087-sebaceous-carcinoma
    Sebaceous carcinoma is a rare type of skin cancer that starts in your skins oil-producing (sebaceous) glands. Its an aggressive cancer that can return after treatment. […] Sebaceous carcinoma is an aggressive skin cancer, which means it spreads quickly. […] Experts dont know why some people develop sebaceous carcinoma. Like other types of skin cancer, exposure to the suns ultraviolet (UV) rays may contribute to this cancer. It may also develop in people, especially younger people, who have had radiation therapy to the head or neck. […] People with a rare inherited disease called Muir-Torre syndrome are more likely to develop sebaceous carcinoma, as well as colorectal (colon) cancer. Muir-Torre syndrome is a form of Lynch syndrome. It causes tumors to form in your sebaceous glands. […] Sebaceous carcinoma is most likely to affect the lymph nodes. […] Sebaceous carcinoma may be aggressive. For as many as 1 in 4 people, the cancer comes back (recurs) or spreads (metastasizes) after treatment. […] Sebaceous carcinoma can be fatal if it spreads. Outcomes are worse when theres a delay in diagnosis and treatment.
  • #8 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    Sebaceous carcinoma arises from the adnexal epithelium of sebaceous glands, most commonly the Meibomian glands or glands of Zeis. […] The pathogenesis of SGc remains poorly understood. […] The majority of SGc are solitary and sporadic and believed to be associated with such factors as ultraviolet exposure, radiotherapy, and immunosuppression. […] Other SGc including those occurring outside of the head and neck region and the presentation of multiple at a time are believed to be associated with genetic defects including defects in mismatch repair genes, MuirTorre syndrome (MTS), and familial retinoblastoma. […] The observation of extraocular SGc arising from Bowen disease or actinic keratosis and the predisposition of SGc to arise in sun-exposed areas suggest a role for ultraviolet exposure or intraepidermal neoplasia in the pathogenesis of some SGc in sun-exposed areas.
  • #9 Early onset sebaceous carcinoma | Diagnostic Pathology | Full Text
    https://diagnosticpathology.biomedcentral.com/articles/10.1186/1746-1596-6-81
    A moderately well differentiated sebaceous carcinoma was established histopathologically arising from the meibomian gland of the upper eyelid. […] The G199R substitution is anticipated to alter the stability of the p53 tetrameric complex. […] The role of UV light in the etiology of sebaceous carcinoma deserves further study. […] Our findings, taken together with those of others, suggest that different environmental factors could lead to the development of sebaceous carcinoma in different patients. […] Although its etiology is largely unknown, it has been associated with Asians, Muir-Torre syndrome, Rb and p53 mutations, HIV, and HPV. […] The apparent increased rate of sebaceous carcinoma in Asians/Pacific Islanders is being challenged by recent studies indicating that the tumor is more common in Whites, and showing a distribution consistent with sunlight exposure.
  • #10 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #11 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. Additionally, elevated expression levels of tyrosine kinase, particularly HER2, have been linked to sebaceous tumors, prompting investigations into targeted treatment. Aberrations in the Wnt/-catenin signaling pathway also strongly correlate with abnormal and malignant proliferation within the sebaceous gland.
  • #12 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #13 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #14 Sebaceous Carcinoma: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/24087-sebaceous-carcinoma
    Sebaceous carcinoma is a rare type of skin cancer that starts in your skins oil-producing (sebaceous) glands. Its an aggressive cancer that can return after treatment. […] Sebaceous carcinoma is an aggressive skin cancer, which means it spreads quickly. […] Experts dont know why some people develop sebaceous carcinoma. Like other types of skin cancer, exposure to the suns ultraviolet (UV) rays may contribute to this cancer. It may also develop in people, especially younger people, who have had radiation therapy to the head or neck. […] People with a rare inherited disease called Muir-Torre syndrome are more likely to develop sebaceous carcinoma, as well as colorectal (colon) cancer. Muir-Torre syndrome is a form of Lynch syndrome. It causes tumors to form in your sebaceous glands. […] Sebaceous carcinoma is most likely to affect the lymph nodes. […] Sebaceous carcinoma may be aggressive. For as many as 1 in 4 people, the cancer comes back (recurs) or spreads (metastasizes) after treatment. […] Sebaceous carcinoma can be fatal if it spreads. Outcomes are worse when theres a delay in diagnosis and treatment.
  • #15 Extraocular Sebaceous Carcinoma: A Report of 2 Cases | Actas Dermo-Sifiliográficas
    https://www.actasdermo.org/es-extraocular-sebaceous-carcinoma-a-report-articulo-S1578219012003113
    One hypothesis is that the tumor originates in the epithelium of sebaceous glands, but recent studies suggest that it may be derived from a pluripotent cell able to differentiate into any cell line, including sebaceous cells. […] Sebaceous carcinoma has been associated with Muir-Torre syndrome, a hereditary disease of autosomal dominant transmission. Muir-Torre syndrome is characterized by the association of at least a skin tumor of sebaceous lineage (sebaceous adenoma, sebaceoma, sebaceous epithelioma, sebaceous carcinoma, or basal cell carcinoma with sebaceous differentiation), with or without a keratoacanthoma associated with 1 or more visceral neoplasms. […] Lesions associated with Muir-Torre syndrome often have unstable microsatellites, in which there is DNA repair defect after replication due to a mutation in the MutS homolog (MSH)-2, the MutL homolog (MLH)-1, and more recently and less often the MSH-6 genes.
  • #16 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    Altered expression of beta-catenin, p21, sonic hedgehog signaling (Shh), and E-cadherin have been associated with invasion, metastasis, and poor clinical outcomes. […] More recently, mutations in tumor suppressor genes including p53 and Rb have been associated with the development of sporadic SGc as well as SGc in MTS patients with intact mismatch repair and subsets of younger patients presenting with SGc harboring transcriptionally active high-risk human papillomavirus (HPV).
  • #17 Sebaceous cell carcinoma developing in epidermodysplasia verruciformis – Indian Journal of Dermatology, Venereology and Leprology
    https://ijdvl.com/sebaceous-cell-carcinoma-developing-in-epidermodysplasia-verruciformis/
    Epidermodysplasia verruciformis is a rare genodermatosis with an increased susceptibility to infection by specific strains of human papilloma virus. […] It is believed that there occurs selective loss of T-lymphocyte immune response against human papilloma virus, most likely due to the defective presentation of viral antigens on the surface of keratinocytes leading to widespread infection. […] Mutation in epidermodysplasia verruciformis genes is also proposed to cause unchecked proliferation of stem cells and transient amplifying cells infected with human papilloma virus 5 and 8. […] Over expression of p53 and human papilloma virus infection has been implicated in the pathogenesis and progression of sebaceous carcinoma thus explaining its likely occurrence in our patient.
  • #18 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #19 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    Sebaceous carcinoma arises from the adnexal epithelium of sebaceous glands, most commonly the Meibomian glands or glands of Zeis. […] The pathogenesis of SGc remains poorly understood. […] The majority of SGc are solitary and sporadic and believed to be associated with such factors as ultraviolet exposure, radiotherapy, and immunosuppression. […] Other SGc including those occurring outside of the head and neck region and the presentation of multiple at a time are believed to be associated with genetic defects including defects in mismatch repair genes, MuirTorre syndrome (MTS), and familial retinoblastoma. […] The observation of extraocular SGc arising from Bowen disease or actinic keratosis and the predisposition of SGc to arise in sun-exposed areas suggest a role for ultraviolet exposure or intraepidermal neoplasia in the pathogenesis of some SGc in sun-exposed areas.
  • #20 Early onset sebaceous carcinoma | Diagnostic Pathology | Full Text
    https://diagnosticpathology.biomedcentral.com/articles/10.1186/1746-1596-6-81
    A moderately well differentiated sebaceous carcinoma was established histopathologically arising from the meibomian gland of the upper eyelid. […] The G199R substitution is anticipated to alter the stability of the p53 tetrameric complex. […] The role of UV light in the etiology of sebaceous carcinoma deserves further study. […] Our findings, taken together with those of others, suggest that different environmental factors could lead to the development of sebaceous carcinoma in different patients. […] Although its etiology is largely unknown, it has been associated with Asians, Muir-Torre syndrome, Rb and p53 mutations, HIV, and HPV. […] The apparent increased rate of sebaceous carcinoma in Asians/Pacific Islanders is being challenged by recent studies indicating that the tumor is more common in Whites, and showing a distribution consistent with sunlight exposure.
  • #21 Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma | Nature Communications
    https://www.nature.com/articles/s41467-018-04008-y
    Sebaceous carcinomas (SeC) are cutaneous malignancies that, in rare cases, metastasize and prove fatal. Here we report whole-exome sequencing on 32 SeC, revealing distinct mutational classes that explain both cancer ontogeny and clinical course. A UV-damage signature predominates in 10/32 samples, while nine show microsatellite instability (MSI) profiles. […] Poorly differentiated ocular SeC has been reported to metastasize more frequently, often with fatal outcomes. […] Recently, Tetzlaff et al. applied targeted sequencing in ocular SeC, reporting that 52% (14 of 27) harbored somatic mutations in PI3K signaling components. […] In this study, we report that SeC fall into three distinct subtypes based on mutational genetics, and are heavily influenced by anatomic site of origin. […] These observations led us to suspect that three distinct mutational mechanisms had given rise to the tumors of our cohort.
  • #22 Early onset sebaceous carcinoma | Diagnostic Pathology | Full Text
    https://diagnosticpathology.biomedcentral.com/articles/10.1186/1746-1596-6-81
    A moderately well differentiated sebaceous carcinoma was established histopathologically arising from the meibomian gland of the upper eyelid. […] The G199R substitution is anticipated to alter the stability of the p53 tetrameric complex. […] The role of UV light in the etiology of sebaceous carcinoma deserves further study. […] Our findings, taken together with those of others, suggest that different environmental factors could lead to the development of sebaceous carcinoma in different patients. […] Although its etiology is largely unknown, it has been associated with Asians, Muir-Torre syndrome, Rb and p53 mutations, HIV, and HPV. […] The apparent increased rate of sebaceous carcinoma in Asians/Pacific Islanders is being challenged by recent studies indicating that the tumor is more common in Whites, and showing a distribution consistent with sunlight exposure.
  • #23 Early onset sebaceous carcinoma | Diagnostic Pathology | Full Text
    https://diagnosticpathology.biomedcentral.com/articles/10.1186/1746-1596-6-81
    Early recognition of sebaceous carcinoma is often challenging, requiring close collaboration between ophthalmologist and pathologist. […] The case suggests that the role of UV radiation and p53 mutations in sebaceous carcinoma deserve further study. […] Epidemiological studies suggest a role of sunlight and radiation in sebaceous carcinoma. […] Interestingly, the G199R substitution detected in our patient was due to a G:CA:T mutation at a dipyrimidine site. […] UV light is known to cause CT substitutions at dipyrimidines, or CCTT substitutions in the p53 gene. […] The diversity of mutations suggests that different mechanisms may play a role in different cases. […] Clinical data and molecular studies suggest that G199R likely interferes with p53 function. […] G199 appears to have a critical role in p53 function.
  • #24 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #25 Extraocular Sebaceous Carcinoma: A Report of 2 Cases | Actas Dermo-Sifiliográficas
    https://www.actasdermo.org/es-extraocular-sebaceous-carcinoma-a-report-articulo-S1578219012003113
    One hypothesis is that the tumor originates in the epithelium of sebaceous glands, but recent studies suggest that it may be derived from a pluripotent cell able to differentiate into any cell line, including sebaceous cells. […] Sebaceous carcinoma has been associated with Muir-Torre syndrome, a hereditary disease of autosomal dominant transmission. Muir-Torre syndrome is characterized by the association of at least a skin tumor of sebaceous lineage (sebaceous adenoma, sebaceoma, sebaceous epithelioma, sebaceous carcinoma, or basal cell carcinoma with sebaceous differentiation), with or without a keratoacanthoma associated with 1 or more visceral neoplasms. […] Lesions associated with Muir-Torre syndrome often have unstable microsatellites, in which there is DNA repair defect after replication due to a mutation in the MutS homolog (MSH)-2, the MutL homolog (MLH)-1, and more recently and less often the MSH-6 genes.
  • #26 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    Altered expression of beta-catenin, p21, sonic hedgehog signaling (Shh), and E-cadherin have been associated with invasion, metastasis, and poor clinical outcomes. […] More recently, mutations in tumor suppressor genes including p53 and Rb have been associated with the development of sporadic SGc as well as SGc in MTS patients with intact mismatch repair and subsets of younger patients presenting with SGc harboring transcriptionally active high-risk human papillomavirus (HPV).
  • #27 Sebaceous carcinoma of the intraoral origin: a literature review
    https://www.degruyter.com/document/doi/10.1515/oncologie-2024-0476/html
    SC has been linked to inherited mutations associated with Muir-Torre Syndrome, a subtype of Lynch syndrome (HNPCC), which affects DNA mismatch repair genes (MSH2, MSH6, MLH1), and causes microsatellite instability, leading to genomic errors, promoting SC development alongside other malignancies. […] Some studies further suggest that mutations in specific genes, such as Patched-1 (PTCH1) and TP53, may contribute to SC development, as these genetic changes can impair normal cell function and promote tumor formation. […] Molecular chaperones like X-linked inhibitor of apoptosis protein (XIAP) and Bcl-2-Associated Athanogene 3 (BAG3) are implicated in promoting tumor survival and proliferation. […] Studies reveal that SC may also exhibit PD-L1 expression on tumor cells and PD-1 on tumor-infiltrating lymphocytes (TILs) in 46% of cases, indicating immune evasion within an active yet suppressed tumor microenvironment. […] Current evidence does not support a direct association between UVR and the development of SC in the oral cavity. […] Despite various theories and mechanisms, the precise cause of IOSC remains uncertain due to the limited number of reported cases.
  • #28 Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma | Nature Communications
    https://www.nature.com/articles/s41467-018-04008-y
    Sebaceous carcinomas (SeC) are cutaneous malignancies that, in rare cases, metastasize and prove fatal. Here we report whole-exome sequencing on 32 SeC, revealing distinct mutational classes that explain both cancer ontogeny and clinical course. A UV-damage signature predominates in 10/32 samples, while nine show microsatellite instability (MSI) profiles. […] Poorly differentiated ocular SeC has been reported to metastasize more frequently, often with fatal outcomes. […] Recently, Tetzlaff et al. applied targeted sequencing in ocular SeC, reporting that 52% (14 of 27) harbored somatic mutations in PI3K signaling components. […] In this study, we report that SeC fall into three distinct subtypes based on mutational genetics, and are heavily influenced by anatomic site of origin. […] These observations led us to suspect that three distinct mutational mechanisms had given rise to the tumors of our cohort.
  • #29 Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma | Nature Communications
    https://www.nature.com/articles/s41467-018-04008-y
    This analysis revealed that the tumors in our study fall into three distinct classes. […] Ten different tumors were defined by mutations harboring a UV-damage signature (signatures 7 and 11) with high numbers of CCTT dinucleotide mutations induced by exposure to ultraviolet radiation. […] Interestingly, the remaining 13 of our SeC, including all nine ocular cancers, were pauci-mutational (the group described above with mutation prevalences between 1.2 and 5.5 per Mb), a phenomenon occurring much less frequently in other cancers of sun-exposed skin. […] We therefore favor an alternative model in which poorly differentiated UV-damage SeC, like cutaneous SCC, arise from a subpopulation of more superficial keratinocytes vulnerable to UV mutagenesis, either from the epidermis or superficial portion of the folliculosebaceous unit. […] In contrast, MSI SeC invariably arise through inactivation of mismatch-repair genes. […] Our data illustrates how cancers grouped by histopathologic similarity actually arise from different mutational mechanisms, likely acting on distinct cells of origin.
  • #30 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. Additionally, elevated expression levels of tyrosine kinase, particularly HER2, have been linked to sebaceous tumors, prompting investigations into targeted treatment. Aberrations in the Wnt/-catenin signaling pathway also strongly correlate with abnormal and malignant proliferation within the sebaceous gland.
  • #31 Suspected Molecular Links in Sebaceous Gland Carcinoma of the Eyelid: A scoping review
    https://www.gavinpublishers.com/article/view/suspected-molecular-links-in-sebaceous-gland-carcinoma-of-the-eyelid-a-scoping-review
    Previous studies have revealed that a defective -catenin binding site in LEF-1 leads to the accumulation of -catenin in the cytoplasm and its hyperactivation in the eyelid, caused sebaceous skin tumor generation. […] This review summarizes previous literatures based on the development of tumors in sebaceous glands. Mutations in MMR genes such as MLH1, MSH2, MSH6, PMS2, and p53 are not fully known in SGC in the Indian patients. […] Therefore, the SHH/Wnt signaling pathway could be a causative factor for tumor progression in sebaceous glands.
  • #32 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    The PI3K/AKT/mTOR pathway is commonly dysregulated in sebaceous carcinoma and may represent a potential therapeutic target. Aberrant activation of the PI3K/AKT/mTOR pathway promotes tumor cell proliferation, survival, and resistance to apoptosis, contributing to disease progression and treatment resistance. Targeting PI3K/AKT/mTOR pathway components with inhibitors has shown promise in preclinical studies and may offer therapeutic benefits to patients with advanced or refractory sebaceous carcinoma.
  • #33 Sebaceous Carcinoma | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/149613
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. […] Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. […] The PI3K/AKT/mTOR pathway is commonly dysregulated in sebaceous carcinoma and may represent a potential therapeutic target. […] Aberrant activation of the PI3K/AKT/mTOR pathway promotes tumor cell proliferation, survival, and resistance to apoptosis, contributing to disease progression and treatment resistance.
  • #34 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    Altered expression of beta-catenin, p21, sonic hedgehog signaling (Shh), and E-cadherin have been associated with invasion, metastasis, and poor clinical outcomes. […] More recently, mutations in tumor suppressor genes including p53 and Rb have been associated with the development of sporadic SGc as well as SGc in MTS patients with intact mismatch repair and subsets of younger patients presenting with SGc harboring transcriptionally active high-risk human papillomavirus (HPV).
  • #35 Suspected Molecular Links in Sebaceous Gland Carcinoma of the Eyelid: A scoping review
    https://www.gavinpublishers.com/article/view/suspected-molecular-links-in-sebaceous-gland-carcinoma-of-the-eyelid-a-scoping-review
    Dysregulation of critical signaling pathways, such as -catenin/ Wnt and hedgehog pathways, which regulate tissue differentiation, has been implicated in the development of various skin and noncutaneous tumors. […] The increasing burden of SGC on the nation and society is significant that increases the economic burden and health issues on patients, society and nation. Addressing the pathogenesis and treatment of SGC require the investigation of molecular genetic studies, including MMR genes and related signaling pathways, to improve therapeutic outcomes for patients. […] The tumorigenesis process is incomplete without considering the role of p53 genes. The transcription factor p53 is a tumor suppressor and master regulator that induces apoptosis during DNA damage. […] The activation of Wnt/-catenin and Sonic Hedgehog (SHH) signaling pathways is crucial for the normal development of embryo and adult in the vertebrates.
  • #36 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. Additionally, elevated expression levels of tyrosine kinase, particularly HER2, have been linked to sebaceous tumors, prompting investigations into targeted treatment. Aberrations in the Wnt/-catenin signaling pathway also strongly correlate with abnormal and malignant proliferation within the sebaceous gland.
  • #37 Sebaceous Carcinoma | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/149613
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. […] Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. […] The PI3K/AKT/mTOR pathway is commonly dysregulated in sebaceous carcinoma and may represent a potential therapeutic target. […] Aberrant activation of the PI3K/AKT/mTOR pathway promotes tumor cell proliferation, survival, and resistance to apoptosis, contributing to disease progression and treatment resistance.
  • #38 Suspected Molecular Links in Sebaceous Gland Carcinoma of the Eyelid: A scoping review
    https://www.gavinpublishers.com/article/view/suspected-molecular-links-in-sebaceous-gland-carcinoma-of-the-eyelid-a-scoping-review
    Objectives: This review aimed to comprehensively analyse molecular mechanisms like mismatch repair genes, cell cycle regulators, and signalling pathways including WNT, SHH, and CASPASE-3/YAP in eyelid sebaceous gland carcinoma (SGC). […] This review summarizes and concludes that mutations and dysregulation in the genes involved in MMR, WNT/-CATENIN, HEDGEHOG, and CASPASE-3/YAP signalling are crucial for SGC in the eyelid. In silico analysis provides a better understanding of the essential genes involved in the tumorigenesis of the sebaceous gland and is helpful for targeted drug therapy. […] The etiology of SGC is largely unknown, though several risk factors have been identified, including advanced age, Asian or South Asian race, female gender, Muir-Torre syndrome (MTS), colorectal carcinoma/visceral malignancies, previous irradiation of the head and neck, mutations in the Rb and p53 genes, and infections of HIV and HPV.
  • #39 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. Additionally, elevated expression levels of tyrosine kinase, particularly HER2, have been linked to sebaceous tumors, prompting investigations into targeted treatment. Aberrations in the Wnt/-catenin signaling pathway also strongly correlate with abnormal and malignant proliferation within the sebaceous gland.
  • #40 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    Sebaceous carcinoma development is linked to various factors, including ultraviolet radiation (UVR) exposure, organ transplants, and immunosuppression with medications like cyclosporine. Additionally, this malignancy is associated with genetic cancer predisposition syndromes, such as MTS-I, which is a distinct variant of hereditary nonpolyposis colorectal cancer (HNPCC), sometimes referred to as Lynch syndrome. […] The dysregulation of transforming growth factor- (TGF-), phosphatase and TENsin homolog (PTEN), and nuclear factor -B (NFk-B) and the inactivation of p53 have been identified in some sebaceous carcinomas. Additionally, elevated expression levels of tyrosine kinase, particularly HER2, have been linked to sebaceous tumors, prompting investigations into targeted treatment. Aberrations in the Wnt/-catenin signaling pathway also strongly correlate with abnormal and malignant proliferation within the sebaceous gland.
  • #41 Angiogenesis in Ocular and Extraocular Sebaceous Carcinoma | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-3342
    To shed more light on the pathogenesis of sebaceous carcinoma, we analysed the expression of proteins related to angiogenesis in 18 ocular and 22 extraocular sebaceous carcinomas using a broad panel of immunohistochemical markers. […] Immunohistochemical analyses have demonstrated that proteins involved in angiogenesis, cell proliferation and inflammation, such as epidermal growth factor receptor and vascular endothelial growth factor receptor (VEGFR), are overexpressed in SC and may play a role in its pathogenesis. […] To the best of our knowledge, this is the first study analysing the expression of proteins related to angiogenesis in ocular and extraocular SC using a broad panel of immunohistochemical markers, including D2-40 (podoplanin), vascular endothelial growth factor (VEGF), VEGFR-2 (KDR) and VEGFR-3 (FLT4). These proteins may not only contribute to the pathogenesis of SC but also act as potential therapeutic targets.
  • #42 Angiogenesis in Ocular and Extraocular Sebaceous Carcinoma | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-3342
    Our findings suggest that VEGF expression by epidermal keratinocytes and tumour cells and its interaction with VEGFR-2 seems to contribute to the pathogenesis of SC not only by its effects on angiogenesis but also by direct effects on the tumour cells. […] Our findings regarding VEGFR-3 expression indicate that this protein may play a critical role in the pathogenesis of SC and therefore might be of therapeutic interest. […] Two of our central findings, namely, an increased intratumoural ratio of small lymphatics to large lymphatics and a negative correlation between epidermal VEGF expression and the intratumoural density of lymphatics, clearly underline the hypothesis regarding the lymphangiogenetic potential of SC.
  • #43 Angiogenesis in Ocular and Extraocular Sebaceous Carcinoma | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-3342
    Our findings suggest that VEGF expression by epidermal keratinocytes and tumour cells and its interaction with VEGFR-2 seems to contribute to the pathogenesis of SC not only by its effects on angiogenesis but also by direct effects on the tumour cells. […] Our findings regarding VEGFR-3 expression indicate that this protein may play a critical role in the pathogenesis of SC and therefore might be of therapeutic interest. […] Two of our central findings, namely, an increased intratumoural ratio of small lymphatics to large lymphatics and a negative correlation between epidermal VEGF expression and the intratumoural density of lymphatics, clearly underline the hypothesis regarding the lymphangiogenetic potential of SC.
  • #44 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    The histopathology varies depending on the differentiation of the tumor. In well differentiated lesions, there is a lobular arrangement and vacuolization of the cytoplasm cells centrally. […] Cells present will include sebaceous and undifferentiated cells. There may be variation in nucleus shape and size with high mitotic activity indicated by mitotic figures. Special stains can be used to help distinguish sebaceous carcinoma: oil red-O, Sudan IV, epithelial membrane antigen, Leu-m1 immunostains. […] Sebaceous carcinoma prognosis relies on several factors, including size, location, treatment approach, and tumor stage. According to the American Joint Committee on Cancer, T category of T2b or worse correlated with regional lymph node metastasis. In a recent meta-analysis of 1333 patients with eyelid sebaceous carcinoma, metastasis was reported in 12.1% of periocular cases, recurrence occurred in 15.9%, and tumor related mortality was 6.2%.
  • #45 :: JKMS :: Journal of Korean Medical Science
    https://jkms.org/DOIx.php?id=10.3346/jkms.2017.32.8.1351
    Sebaceous carcinoma (SC) is a neoplasm derived from the adnexal epithelium of the sebaceous glands, and most studies on this neoplasm have been conducted in Caucasians. […] Most lesions were poorly differentiated (extraocular, 43.75%; ocular, 38.46%), had a lobular infiltrative growth pattern (extraocular, 68.75%; ocular, 76.92%), and were basaloid (extraocular, 56.25%; ocular, 61.54%). […] The poorly differentiated tumor type was most commonly observed in both extraocular (7/16, 43.75%) and ocular (5/13, 38.46%) SCs. […] The majority of prominent patterns of infiltrative growth were lobular in both extraocular (11/16, 68.75%) and ocular (10/13, 76.92%) SCs. […] The main cell types encountered in SC are basaloid, basosquamous, and epidermoid.
  • #46 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    The histopathology varies depending on the differentiation of the tumor. In well differentiated lesions, there is a lobular arrangement and vacuolization of the cytoplasm cells centrally. […] Cells present will include sebaceous and undifferentiated cells. There may be variation in nucleus shape and size with high mitotic activity indicated by mitotic figures. Special stains can be used to help distinguish sebaceous carcinoma: oil red-O, Sudan IV, epithelial membrane antigen, Leu-m1 immunostains. […] Sebaceous carcinoma prognosis relies on several factors, including size, location, treatment approach, and tumor stage. According to the American Joint Committee on Cancer, T category of T2b or worse correlated with regional lymph node metastasis. In a recent meta-analysis of 1333 patients with eyelid sebaceous carcinoma, metastasis was reported in 12.1% of periocular cases, recurrence occurred in 15.9%, and tumor related mortality was 6.2%.
  • #47 :: JKMS :: Journal of Korean Medical Science
    https://jkms.org/DOIx.php?id=10.3346/jkms.2017.32.8.1351
    Sebaceous carcinoma (SC) is a neoplasm derived from the adnexal epithelium of the sebaceous glands, and most studies on this neoplasm have been conducted in Caucasians. […] Most lesions were poorly differentiated (extraocular, 43.75%; ocular, 38.46%), had a lobular infiltrative growth pattern (extraocular, 68.75%; ocular, 76.92%), and were basaloid (extraocular, 56.25%; ocular, 61.54%). […] The poorly differentiated tumor type was most commonly observed in both extraocular (7/16, 43.75%) and ocular (5/13, 38.46%) SCs. […] The majority of prominent patterns of infiltrative growth were lobular in both extraocular (11/16, 68.75%) and ocular (10/13, 76.92%) SCs. […] The main cell types encountered in SC are basaloid, basosquamous, and epidermoid.
  • #48 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    The histopathology varies depending on the differentiation of the tumor. In well differentiated lesions, there is a lobular arrangement and vacuolization of the cytoplasm cells centrally. […] Cells present will include sebaceous and undifferentiated cells. There may be variation in nucleus shape and size with high mitotic activity indicated by mitotic figures. Special stains can be used to help distinguish sebaceous carcinoma: oil red-O, Sudan IV, epithelial membrane antigen, Leu-m1 immunostains. […] Sebaceous carcinoma prognosis relies on several factors, including size, location, treatment approach, and tumor stage. According to the American Joint Committee on Cancer, T category of T2b or worse correlated with regional lymph node metastasis. In a recent meta-analysis of 1333 patients with eyelid sebaceous carcinoma, metastasis was reported in 12.1% of periocular cases, recurrence occurred in 15.9%, and tumor related mortality was 6.2%.
  • #49 :: JKMS :: Journal of Korean Medical Science
    https://jkms.org/DOIx.php?id=10.3346/jkms.2017.32.8.1351
    Sebaceous carcinoma (SC) is a neoplasm derived from the adnexal epithelium of the sebaceous glands, and most studies on this neoplasm have been conducted in Caucasians. […] Most lesions were poorly differentiated (extraocular, 43.75%; ocular, 38.46%), had a lobular infiltrative growth pattern (extraocular, 68.75%; ocular, 76.92%), and were basaloid (extraocular, 56.25%; ocular, 61.54%). […] The poorly differentiated tumor type was most commonly observed in both extraocular (7/16, 43.75%) and ocular (5/13, 38.46%) SCs. […] The majority of prominent patterns of infiltrative growth were lobular in both extraocular (11/16, 68.75%) and ocular (10/13, 76.92%) SCs. […] The main cell types encountered in SC are basaloid, basosquamous, and epidermoid.
  • #50 Sebaceous carcinoma of the breast predominantly characterized by intraductal growth: a case report | Surgical Case Reports | Full Text
    https://surgicalcasereports.springeropen.com/articles/10.1186/s40792-020-0799-y
    Our present patient’s tumor originated deep within the mammary gland and was obviously separated from the adjoining skin. Further, lesions were present in the duct, which is consistent with our diagnosis of SC of the breast. […] Varga et al. […] propose hypotheses that explain the origin of SC of the breast, respectively, as follows: (a) The mammary glands of patients with breast cancer may exhibit features of sebaceous glands because these glands share the same origin. (b) SC of the breast develops from progenitor cells capable of differentiation into the sebaceous glands within the epithelium. (c) Sebaceous glands are ectopically present in the mammary gland. […] Although our findings contribute to our understanding of the pathogenesis, progression, and prognosis of SC of the breast, further studies of additional cases are required.
  • #51
    https://journals.lww.com/ijpm/fulltext/2024/67010/sebaceous_carcinoma_with_apocrine_differentiation.35.aspx
    Sebaceous carcinoma is a rare malignant tumor of adnexal origin arising from sebaceous glands. […] Apocrine differentiation in sebaceous carcinomas is rare but has been reported in the literature. […] Sebaceous carcinoma is a rare high-grade malignant adnexal neoplasm arising from sebaceous glands. […] An extensive literature search has failed to show SCs arising in BCC. […] Certain strains of human papillomavirus have been implicated in the pathogenesis of sebaceous carcinoma. […] Mutations in the p53 gene have been seen in invasive but not in situ sebaceous carcinoma. […] It is believed that pluripotent stem cells in the folliculosebaceous-apocrine unit can give rise to follicular stem cells, sebaceous stem cells, and apocrine stem cells. Therefore, SCs with apocrine differentiation can originate from pluripotent stem cells destined to become sebaceous cells or from sebaceous stem cells which also have the ability to differentiate within apocrine glands. […] Thus, SCs with apocrine change show aggressive behavior and therefore require an early diagnosis.
  • #52 Sebaceous Carcinoma (Sebaceous Gland Carcinoma, Sebaceous Cell Carcinoma, Meibomian Gland Carcinoma) – Dermatology Advisor
    https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/sebaceous-carcinoma-sebaceous-gland-carcinoma-sebaceous-cell-carcinoma-meibomian-gland-carcinoma/
    Sebaceous carcinoma (SC) has been termed the great masquerader of adnexal tumors. […] The majority of sebaceous carcinomas arise spontaneously and de novo. In the periocular region, they arise from sebaceous glands, most commonly the Meibomian glands and the glands of Zeis. Other sebaceous glands in this region include the sebaceous glands of the eyebrows (follicular), sebaceous glands of the fine hairs of the eyelids and lacrimal glands, and sebaceous glands of the caruncle. In the extracutaneous sites, sebaceous carcinomas do not appear to arise from sebaceous glands, making their origin debatable. […] A minority of sebaceous carcinomas occur in patients with Muir-Torre syndrome, providing clues that mutations in tumor suppressor genes can be causative. Muir-Torre syndrome is an autosomal dominant disease with high penetrance and variable expressivity.
  • #53 Sebaceous carcinoma in the right inguinal region with multiple metasta | CMAR
    https://www.dovepress.com/sebaceous-carcinoma-in-the-right-inguinal-region-with-multiple-metasta-peer-reviewed-fulltext-article-CMAR
    Sebaceous carcinoma (SC), a rare malignant tumor accounting for 0.7% of all skin cancers, has shown a rising incidence rate, though the cause remains unclear. The origin of SC has been reported to be either sebaceous ducts or the interfollicular epidermis, with specific findings pointing to a group of progenitor cells that express p63 and keratin 5. Additionally, there have been rare reports of in situ or invasive SC arising from squamous intraepidermal neoplasms. […] SCs have a recurrence rate ranging from 11% to 30% and are most commonly diagnosed in individuals over the age of 40, particularly during the seventh and eighth decades of life. The known risk factors for SC include advanced age, female gender, Asian race, prior radiation exposure, immunosuppression, and Muir-Torre syndrome, a variant of Lynch syndrome marked by the loss of mismatch repair genes and microsatellite instability, which increases susceptibility to other cancers, such as colorectal and genitourinary types.
  • #54 Sebaceous carcinoma in the right inguinal region with multiple metasta | CMAR
    https://www.dovepress.com/sebaceous-carcinoma-in-the-right-inguinal-region-with-multiple-metasta-peer-reviewed-fulltext-article-CMAR
    Sebaceous carcinoma (SC), a rare malignant tumor accounting for 0.7% of all skin cancers, has shown a rising incidence rate, though the cause remains unclear. The origin of SC has been reported to be either sebaceous ducts or the interfollicular epidermis, with specific findings pointing to a group of progenitor cells that express p63 and keratin 5. Additionally, there have been rare reports of in situ or invasive SC arising from squamous intraepidermal neoplasms. […] SCs have a recurrence rate ranging from 11% to 30% and are most commonly diagnosed in individuals over the age of 40, particularly during the seventh and eighth decades of life. The known risk factors for SC include advanced age, female gender, Asian race, prior radiation exposure, immunosuppression, and Muir-Torre syndrome, a variant of Lynch syndrome marked by the loss of mismatch repair genes and microsatellite instability, which increases susceptibility to other cancers, such as colorectal and genitourinary types.
  • #55 Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma | Nature Communications
    https://www.nature.com/articles/s41467-018-04008-y
    Sebaceous carcinomas (SeC) are cutaneous malignancies that, in rare cases, metastasize and prove fatal. Here we report whole-exome sequencing on 32 SeC, revealing distinct mutational classes that explain both cancer ontogeny and clinical course. A UV-damage signature predominates in 10/32 samples, while nine show microsatellite instability (MSI) profiles. […] Poorly differentiated ocular SeC has been reported to metastasize more frequently, often with fatal outcomes. […] Recently, Tetzlaff et al. applied targeted sequencing in ocular SeC, reporting that 52% (14 of 27) harbored somatic mutations in PI3K signaling components. […] In this study, we report that SeC fall into three distinct subtypes based on mutational genetics, and are heavily influenced by anatomic site of origin. […] These observations led us to suspect that three distinct mutational mechanisms had given rise to the tumors of our cohort.
  • #56 Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma | Nature Communications
    https://www.nature.com/articles/s41467-018-04008-y
    This analysis revealed that the tumors in our study fall into three distinct classes. […] Ten different tumors were defined by mutations harboring a UV-damage signature (signatures 7 and 11) with high numbers of CCTT dinucleotide mutations induced by exposure to ultraviolet radiation. […] Interestingly, the remaining 13 of our SeC, including all nine ocular cancers, were pauci-mutational (the group described above with mutation prevalences between 1.2 and 5.5 per Mb), a phenomenon occurring much less frequently in other cancers of sun-exposed skin. […] We therefore favor an alternative model in which poorly differentiated UV-damage SeC, like cutaneous SCC, arise from a subpopulation of more superficial keratinocytes vulnerable to UV mutagenesis, either from the epidermis or superficial portion of the folliculosebaceous unit. […] In contrast, MSI SeC invariably arise through inactivation of mismatch-repair genes. […] Our data illustrates how cancers grouped by histopathologic similarity actually arise from different mutational mechanisms, likely acting on distinct cells of origin.
  • #57 Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma | Nature Communications
    https://www.nature.com/articles/s41467-018-04008-y
    This analysis revealed that the tumors in our study fall into three distinct classes. […] Ten different tumors were defined by mutations harboring a UV-damage signature (signatures 7 and 11) with high numbers of CCTT dinucleotide mutations induced by exposure to ultraviolet radiation. […] Interestingly, the remaining 13 of our SeC, including all nine ocular cancers, were pauci-mutational (the group described above with mutation prevalences between 1.2 and 5.5 per Mb), a phenomenon occurring much less frequently in other cancers of sun-exposed skin. […] We therefore favor an alternative model in which poorly differentiated UV-damage SeC, like cutaneous SCC, arise from a subpopulation of more superficial keratinocytes vulnerable to UV mutagenesis, either from the epidermis or superficial portion of the folliculosebaceous unit. […] In contrast, MSI SeC invariably arise through inactivation of mismatch-repair genes. […] Our data illustrates how cancers grouped by histopathologic similarity actually arise from different mutational mechanisms, likely acting on distinct cells of origin.
  • #58 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    Sebaceous carcinoma is a rare, highly malignant, and potentially lethal tumor of the skin, which most commonly occurs in the eyelid. The neoplasm arises from sebaceous glands, such as those of the meibomian glands in the tarsus, the Zeis glands of the eyelashes, the caruncle, and the skin of the eyebrow. The lesion occurs more often in the upper eyelid, most likely due to the presence of a greater number of meibomian glands (~50 glands in upper eyelids, ~25 in lower). […] Muir-Torre Syndrome (MTS) is an important consideration when a patient is diagnosed with sebaceous carcinoma. MTS is an autosomal dominant condition of sebaceous tumors associated with gastrointestinal, endometrial, and urologic tumors (without any predisposing factors). The sebaceous tumors included in this syndrome are: sebaceous adenoma, basal cell epithelioma with sebaceous differentiation, and sebaceous carcinoma. Cohen et al. reported that 24% of 120 MTS patients had sebaceous carcinoma. The sebaceous carcinomas in MTS are less aggressive and less likely to metastasize than solitary sebaceous carcinoma.
  • #59 Sebaceous carcinoma – UpToDate
    https://www.uptodate.com/contents/sebaceous-carcinoma/print
    Sebaceous carcinoma is a rare, malignant tumor of the sebaceous glands. […] This topic will review the pathogenesis, clinical presentation, diagnosis, and treatment of sebaceous carcinoma. […] Sebaceous carcinomas can occur sporadically or may be associated with Muir-Torre syndrome, a variant of the hereditary nonpolyposis colorectal cancer syndrome (Lynch syndrome) characterized by single or multiple sebaceous neoplasms, keratoacanthomas, and internal malignancy (particularly malignancy of the gastrointestinal or genitourinary system).
  • #60 Extraocular Sebaceous Carcinoma: A Report of 2 Cases | Actas Dermo-Sifiliográficas
    https://www.actasdermo.org/es-extraocular-sebaceous-carcinoma-a-report-articulo-S1578219012003113
    One hypothesis is that the tumor originates in the epithelium of sebaceous glands, but recent studies suggest that it may be derived from a pluripotent cell able to differentiate into any cell line, including sebaceous cells. […] Sebaceous carcinoma has been associated with Muir-Torre syndrome, a hereditary disease of autosomal dominant transmission. Muir-Torre syndrome is characterized by the association of at least a skin tumor of sebaceous lineage (sebaceous adenoma, sebaceoma, sebaceous epithelioma, sebaceous carcinoma, or basal cell carcinoma with sebaceous differentiation), with or without a keratoacanthoma associated with 1 or more visceral neoplasms. […] Lesions associated with Muir-Torre syndrome often have unstable microsatellites, in which there is DNA repair defect after replication due to a mutation in the MutS homolog (MSH)-2, the MutL homolog (MLH)-1, and more recently and less often the MSH-6 genes.
  • #61 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #62 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #63 Sebaceous cell carcinoma of the scalp in a young male: A rare case report – IJPO
    https://www.ijpo.co.in/html-article/19061
    Sebaceous carcinomas associated with Muir-Torre syndrome have a loss of mismatch repair gene while those arising sporadically do not show loss of mismatch repair or any microsatellite instability. […] Risk factors for the development of sebaceous cell carcinoma are advanced age, Asian or South Asian race, previous history of irradiation, Muir-Torre syndrome, and immunosuppression following renal transplantation. […] Histopathologically, the tumour is composed of multiple irregular lobules of various sizes composed of sebocytes separated by a fibrovascular stroma. […] Tumour cells in sebaceous carcinoma are often large and may show squamoid changes. […] Immunohistochemical staining for EMA can differentiate sebaceous carcinoma from basal cell carcinoma and squamous cell carcinoma. […] Complete surgical excision is the treatment of choice while the local recurrence rates range from 9 to 36%, which tends to occur within 5 years. […] The patient developed tumour relapse after an excision biopsy which indicates the locally aggressive nature of this tumour. […] Sebaceous carcinoma is an important differential to be kept in mind while dealing with cutaneous lesions both clinically and histopathologically.
  • #64 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    Sebaceous carcinoma is a rare, highly malignant, and potentially lethal tumor of the skin, which most commonly occurs in the eyelid. The neoplasm arises from sebaceous glands, such as those of the meibomian glands in the tarsus, the Zeis glands of the eyelashes, the caruncle, and the skin of the eyebrow. The lesion occurs more often in the upper eyelid, most likely due to the presence of a greater number of meibomian glands (~50 glands in upper eyelids, ~25 in lower). […] Muir-Torre Syndrome (MTS) is an important consideration when a patient is diagnosed with sebaceous carcinoma. MTS is an autosomal dominant condition of sebaceous tumors associated with gastrointestinal, endometrial, and urologic tumors (without any predisposing factors). The sebaceous tumors included in this syndrome are: sebaceous adenoma, basal cell epithelioma with sebaceous differentiation, and sebaceous carcinoma. Cohen et al. reported that 24% of 120 MTS patients had sebaceous carcinoma. The sebaceous carcinomas in MTS are less aggressive and less likely to metastasize than solitary sebaceous carcinoma.
  • #65 Sebaceous Carcinomas of the Skin: 24 Cases and a Literature Review | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-2685
    Sebaceous carcinoma (SC) is a highly aggressive tumour arising from the sebaceous glands (1). SC may occur sporadically or be part of Muir-Torre syndrome (MTS), a rare autosomal-dominant genodermatosis characterized by sebaceous neoplasms and one or more visceral malignancies (4). Diagnosis relied on immunohistochemistry of 4 DNA mismatch repair proteins (MLH1, MSH2, MSH6, and PMS2) as a screening test and on molecular analysis in cases of strong family history of malignancy regardless of the results of immunohistochemistry. The main histological appearance of SC in this study consisted of an unencapsulated, lobular, dermally based proliferation of sebaceous and undifferentiated cells (3). Because of the variety of tumour growth and clinical presentations, diagnosis of SC can be late, as was seen in some cases in this study, with almost 15% of primary SC being diagnosed after 5 years (3).
  • #66 Sebaceous Carcinomas of the Skin: 24 Cases and a Literature Review | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-2685
    In this study, and in accordance with previous reports, our cases of SC presented before or concurrently with internal malignancy in approximately 42% of patients with MTS (12). This underlines the importance of malignancy screening in MTS and follow-up with colonoscopy every 3-5 years, starting at 25-30 years of age, yearly mammography and endometrial biopsy every 3-5 years in women over 50 years of age (14).
  • #67 Sebaceous Carcinomas of the Skin: 24 Cases and a Literature Review | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-2685
    In this study, and in accordance with previous reports, our cases of SC presented before or concurrently with internal malignancy in approximately 42% of patients with MTS (12). This underlines the importance of malignancy screening in MTS and follow-up with colonoscopy every 3-5 years, starting at 25-30 years of age, yearly mammography and endometrial biopsy every 3-5 years in women over 50 years of age (14).
  • #68 Sebaceous cell carcinoma developing in epidermodysplasia verruciformis – Indian Journal of Dermatology, Venereology and Leprology
    https://ijdvl.com/sebaceous-cell-carcinoma-developing-in-epidermodysplasia-verruciformis/
    Epidermodysplasia verruciformis is a rare genodermatosis with an increased susceptibility to infection by specific strains of human papilloma virus. […] It is believed that there occurs selective loss of T-lymphocyte immune response against human papilloma virus, most likely due to the defective presentation of viral antigens on the surface of keratinocytes leading to widespread infection. […] Mutation in epidermodysplasia verruciformis genes is also proposed to cause unchecked proliferation of stem cells and transient amplifying cells infected with human papilloma virus 5 and 8. […] Over expression of p53 and human papilloma virus infection has been implicated in the pathogenesis and progression of sebaceous carcinoma thus explaining its likely occurrence in our patient.
  • #69 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    While there are markedly increased rates of cutaneous neoplasms in solid organ transplant recipients, there is evidence to suggest that solid organ transplantation may increase the risk of SGc up to 90 times. […] Others have observed a significantly increased risk of SGc in patients with AIDS, suggesting some role for immunosuppression. […] Reports have also shown the onset of SGc within the field of irradiation for patients undergoing radiotherapy for retinoblastoma, eczema, or cosmetic epilation. […] There are cases reported of SGc arising from nevus sebaceus. […] MTS results from defects in DNA mismatch repair genes, MLH1, MSH2, and MSH6, leading to a buildup of unstable microsatellite sequences and replication errors predisposing to various malignancies. […] Besides mutations in mismatch repair genes, Wnt/beta-catenin signaling is known to be altered and play a significant role in the development of sebaceous tumors.
  • #70 Sebaceous cell carcinoma developing in epidermodysplasia verruciformis – Indian Journal of Dermatology, Venereology and Leprology
    https://ijdvl.com/sebaceous-cell-carcinoma-developing-in-epidermodysplasia-verruciformis/
    Epidermodysplasia verruciformis is a rare genodermatosis with an increased susceptibility to infection by specific strains of human papilloma virus. […] It is believed that there occurs selective loss of T-lymphocyte immune response against human papilloma virus, most likely due to the defective presentation of viral antigens on the surface of keratinocytes leading to widespread infection. […] Mutation in epidermodysplasia verruciformis genes is also proposed to cause unchecked proliferation of stem cells and transient amplifying cells infected with human papilloma virus 5 and 8. […] Over expression of p53 and human papilloma virus infection has been implicated in the pathogenesis and progression of sebaceous carcinoma thus explaining its likely occurrence in our patient.
  • #71 Sebaceous carcinoma of the intraoral origin: a literature review
    https://www.degruyter.com/document/doi/10.1515/oncologie-2024-0476/html
    SC has been linked to inherited mutations associated with Muir-Torre Syndrome, a subtype of Lynch syndrome (HNPCC), which affects DNA mismatch repair genes (MSH2, MSH6, MLH1), and causes microsatellite instability, leading to genomic errors, promoting SC development alongside other malignancies. […] Some studies further suggest that mutations in specific genes, such as Patched-1 (PTCH1) and TP53, may contribute to SC development, as these genetic changes can impair normal cell function and promote tumor formation. […] Molecular chaperones like X-linked inhibitor of apoptosis protein (XIAP) and Bcl-2-Associated Athanogene 3 (BAG3) are implicated in promoting tumor survival and proliferation. […] Studies reveal that SC may also exhibit PD-L1 expression on tumor cells and PD-1 on tumor-infiltrating lymphocytes (TILs) in 46% of cases, indicating immune evasion within an active yet suppressed tumor microenvironment. […] Current evidence does not support a direct association between UVR and the development of SC in the oral cavity. […] Despite various theories and mechanisms, the precise cause of IOSC remains uncertain due to the limited number of reported cases.
  • #72 Sebaceous carcinoma of the intraoral origin: a literature review
    https://www.degruyter.com/document/doi/10.1515/oncologie-2024-0476/html
    Additionally, factors such as subcutaneous injections and sebaceous differentiation during inflammation seem to contribute to a specific anatomical predisposition for SC in the eyelids. […] Persistent inflammation can cause sebaceous gland hyperplasia, disrupted differentiation, and local immune suppression, creating conditions conducive to malignant transformation. […] Abnormal changes in sebaceous cells, coupled with mutations in critical genes like tumor suppressor-53 (TP53), can drive the development of tumors. […] Although these theories are touched upon in the literature, the exact pathogenesis of SC still remains unclear, with possible contributions from other factors. Environmental and genetic influences may also play essential roles in the development of ocular and extra-ocular SC.
  • #73 Sebaceous carcinoma of the intraoral origin: a literature review
    https://www.degruyter.com/document/doi/10.1515/oncologie-2024-0476/html
    Sebaceous carcinoma (SC) is an aggressive cancer arising from sebaceous glands, rarely occurring in the oral cavity (IOSC). […] The cause remains unclear, but Fordyce granules, sebaceous structures in oral mucosa, may play a role in malignancy. […] While Fordyce granules are considered the most likely risk factor or potential precancerous condition for SC, other pathogenic mechanisms may also be considered as other risk factors. Smoking may contribute to IOSC by inducing chronic inflammation, DNA damage, immune suppression, and altering sebaceous gland environments, promoting malignant transformation, especially when combined with other factors. […] It has been also suggested that some extra-ocular SCs might originate from intraepidermal pluripotent neoplastic cells. […] These malignant cells can act as precursors or coexist with invasive SC, contributing to local recurrence and tumor progression.
  • #74 Sebaceous carcinoma of the intraoral origin: a literature review
    https://www.degruyter.com/document/doi/10.1515/oncologie-2024-0476/html
    Additionally, factors such as subcutaneous injections and sebaceous differentiation during inflammation seem to contribute to a specific anatomical predisposition for SC in the eyelids. […] Persistent inflammation can cause sebaceous gland hyperplasia, disrupted differentiation, and local immune suppression, creating conditions conducive to malignant transformation. […] Abnormal changes in sebaceous cells, coupled with mutations in critical genes like tumor suppressor-53 (TP53), can drive the development of tumors. […] Although these theories are touched upon in the literature, the exact pathogenesis of SC still remains unclear, with possible contributions from other factors. Environmental and genetic influences may also play essential roles in the development of ocular and extra-ocular SC.
  • #75 Sebaceous carcinoma pathology
    https://dermnetnz.org/topics/sebaceous-carcinoma-pathology
    Sebaceous carcinoma arises from ocular adnexa or sebaceous glands of the skin. The clinical course seems to range from indolent to highly aggressive depending on the grade of the tumour and the anatomic site (ocular tumours are thought to be more aggressive). […] In sebaceous carcinoma, the tumour is generally dermally based with invasion into subcutis and native structures. Pagetoid invasion of the overlying epidermis may be seen. The tumour cells are basaloid with foci of sebocytic differentiation. Sebocytes are large cells with a multivacuolated clear cytoplasm. […] Sebocytes are positive with EMA, BerEp4, and Androgen receptor (AR). Ocular tumors usually express CK7.
  • #76 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    The histopathology varies depending on the differentiation of the tumor. In well differentiated lesions, there is a lobular arrangement and vacuolization of the cytoplasm cells centrally. […] Cells present will include sebaceous and undifferentiated cells. There may be variation in nucleus shape and size with high mitotic activity indicated by mitotic figures. Special stains can be used to help distinguish sebaceous carcinoma: oil red-O, Sudan IV, epithelial membrane antigen, Leu-m1 immunostains. […] Sebaceous carcinoma prognosis relies on several factors, including size, location, treatment approach, and tumor stage. According to the American Joint Committee on Cancer, T category of T2b or worse correlated with regional lymph node metastasis. In a recent meta-analysis of 1333 patients with eyelid sebaceous carcinoma, metastasis was reported in 12.1% of periocular cases, recurrence occurred in 15.9%, and tumor related mortality was 6.2%.
  • #77 Sebaceous carcinoma pathology
    https://dermnetnz.org/topics/sebaceous-carcinoma-pathology
    Sebaceous carcinoma arises from ocular adnexa or sebaceous glands of the skin. The clinical course seems to range from indolent to highly aggressive depending on the grade of the tumour and the anatomic site (ocular tumours are thought to be more aggressive). […] In sebaceous carcinoma, the tumour is generally dermally based with invasion into subcutis and native structures. Pagetoid invasion of the overlying epidermis may be seen. The tumour cells are basaloid with foci of sebocytic differentiation. Sebocytes are large cells with a multivacuolated clear cytoplasm. […] Sebocytes are positive with EMA, BerEp4, and Androgen receptor (AR). Ocular tumors usually express CK7.
  • #78 :: JKMS :: Journal of Korean Medical Science
    https://jkms.org/DOIx.php?id=10.3346/jkms.2017.32.8.1351
    Sebaceous carcinoma (SC) is a neoplasm derived from the adnexal epithelium of the sebaceous glands, and most studies on this neoplasm have been conducted in Caucasians. […] Most lesions were poorly differentiated (extraocular, 43.75%; ocular, 38.46%), had a lobular infiltrative growth pattern (extraocular, 68.75%; ocular, 76.92%), and were basaloid (extraocular, 56.25%; ocular, 61.54%). […] The poorly differentiated tumor type was most commonly observed in both extraocular (7/16, 43.75%) and ocular (5/13, 38.46%) SCs. […] The majority of prominent patterns of infiltrative growth were lobular in both extraocular (11/16, 68.75%) and ocular (10/13, 76.92%) SCs. […] The main cell types encountered in SC are basaloid, basosquamous, and epidermoid.
  • #79 Sebaceous cell carcinoma of the scalp in a young male: A rare case report – IJPO
    https://www.ijpo.co.in/html-article/19061
    Sebaceous carcinomas associated with Muir-Torre syndrome have a loss of mismatch repair gene while those arising sporadically do not show loss of mismatch repair or any microsatellite instability. […] Risk factors for the development of sebaceous cell carcinoma are advanced age, Asian or South Asian race, previous history of irradiation, Muir-Torre syndrome, and immunosuppression following renal transplantation. […] Histopathologically, the tumour is composed of multiple irregular lobules of various sizes composed of sebocytes separated by a fibrovascular stroma. […] Tumour cells in sebaceous carcinoma are often large and may show squamoid changes. […] Immunohistochemical staining for EMA can differentiate sebaceous carcinoma from basal cell carcinoma and squamous cell carcinoma. […] Complete surgical excision is the treatment of choice while the local recurrence rates range from 9 to 36%, which tends to occur within 5 years. […] The patient developed tumour relapse after an excision biopsy which indicates the locally aggressive nature of this tumour. […] Sebaceous carcinoma is an important differential to be kept in mind while dealing with cutaneous lesions both clinically and histopathologically.
  • #80 EyeRounds.org: Sebaceous Cell Carcinoma: A Masquerade Syndrome
    http://eyerounds.org/cases/62-Sebaceous-Cell-Carcinoma-Eyelid-Masquerade-Syndrome.htm
    A characteristic feature of sebaceous cell carcinoma is the way it infiltrates. Intraepithelial spread or pagetoid spread is reported in 44-80% of cases. Pagetoid spread is the infiltration of single tumor cells or nests of tumor cells into the overlying epithelium. When this infiltration becomes confluent it is called Bowenoid change. Sebaceous cell carcinoma may also spread through direct extension into adjacent structures such as the intracranial cavity, orbit and paranasal sinuses. These are not considered metastases since there is no lymphatic drainage from the eyelids to these structures. However, the eyelids do have lymphatic drainage to the intraparotid, preauricular and submandibular lymph nodes, which are all potential sites for regional metastases (30%). Distant metastases are possible, but rare and the involved organs include liver, lung, brain and bone.
  • #81 Sebaceous Carcinoma (Sebaceous Gland Carcinoma, Sebaceous Cell Carcinoma, Meibomian Gland Carcinoma) – Dermatology Advisor
    https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/sebaceous-carcinoma-sebaceous-gland-carcinoma-sebaceous-cell-carcinoma-meibomian-gland-carcinoma/
    MSH-1 and MLH-2 are genes important for the repair of DNA mismatch. Germline mutations in these genes lead to microsatellite instability in DNA and in the process lead to inactivation of tumor suppressor genes. […] The invasion of sebaceous carcinoma is believed to occur by direct extension into subdermal and/or epithelial tissues (epitheliotropism), multifocal proliferation into intradermal and subcutaneous tissues, and by oncophoresis whereby cancer cells are hypothetically shed and transplanted. […] There can also be direct intraepidermal extension by pagetoid spread. Up to 50% of recurrent periocular sebaceous carcinomas may involve pagetoid spread and 100% in exenterated specimens. Pagetoid spread is reported to be much less common in extraocular sebaceous carcinoma.
  • #82 Sebaceous Carcinoma (Sebaceous Gland Carcinoma, Sebaceous Cell Carcinoma, Meibomian Gland Carcinoma) – Dermatology Advisor
    https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/sebaceous-carcinoma-sebaceous-gland-carcinoma-sebaceous-cell-carcinoma-meibomian-gland-carcinoma/
    MSH-1 and MLH-2 are genes important for the repair of DNA mismatch. Germline mutations in these genes lead to microsatellite instability in DNA and in the process lead to inactivation of tumor suppressor genes. […] The invasion of sebaceous carcinoma is believed to occur by direct extension into subdermal and/or epithelial tissues (epitheliotropism), multifocal proliferation into intradermal and subcutaneous tissues, and by oncophoresis whereby cancer cells are hypothetically shed and transplanted. […] There can also be direct intraepidermal extension by pagetoid spread. Up to 50% of recurrent periocular sebaceous carcinomas may involve pagetoid spread and 100% in exenterated specimens. Pagetoid spread is reported to be much less common in extraocular sebaceous carcinoma.
  • #83 Sebaceous carcinoma in the right inguinal region with multiple metasta | CMAR
    https://www.dovepress.com/sebaceous-carcinoma-in-the-right-inguinal-region-with-multiple-metasta-peer-reviewed-fulltext-article-CMAR
    Based on the location of SC, it can be divided into ocular SC and extra-ocular SC. Ocular SC is mostly observed in the periorbital area, accounting for approximately 75% of all SC cases. The remaining 25% of SC cases are extraocular, with approximately 70% located in the head and neck region, and 13% occurring on the back or trunk, but capable of arising wherever sebaceous glands are found. Both ocular and extra-ocular SC have high recurrence rates and are associated with regional nodal metastasis. […] SC is histologically marked by noncontiguous multicentric growth patterns and pagetoid spread, where cells proliferate randomly in the epithelium or other tissues. This multicentric growth pattern, a poor prognosis marker, is distinctive of ocular SC. Pagetoid spread also mainly characterizes ocular SC and is rarely observed in extra-ocular SC. Metastases primarily affect lymph nodes but have also been reported in the lungs, brain, liver, small intestine, and urinary tract. The 5-year survival rate for metastatic SC ranges from 50% to 68%, compared to 75-78% for localized/regional disease. Poor prognostic indicators include tumors larger than 1 cm, poor differentiation, lympho-vascular invasion, and involvement of both upper and lower eyelids.
  • #84 Sebaceous carcinoma pathology
    https://dermnetnz.org/topics/sebaceous-carcinoma-pathology
    Sebaceous carcinoma arises from ocular adnexa or sebaceous glands of the skin. The clinical course seems to range from indolent to highly aggressive depending on the grade of the tumour and the anatomic site (ocular tumours are thought to be more aggressive). […] In sebaceous carcinoma, the tumour is generally dermally based with invasion into subcutis and native structures. Pagetoid invasion of the overlying epidermis may be seen. The tumour cells are basaloid with foci of sebocytic differentiation. Sebocytes are large cells with a multivacuolated clear cytoplasm. […] Sebocytes are positive with EMA, BerEp4, and Androgen receptor (AR). Ocular tumors usually express CK7.
  • #85 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    The histopathology varies depending on the differentiation of the tumor. In well differentiated lesions, there is a lobular arrangement and vacuolization of the cytoplasm cells centrally. […] Cells present will include sebaceous and undifferentiated cells. There may be variation in nucleus shape and size with high mitotic activity indicated by mitotic figures. Special stains can be used to help distinguish sebaceous carcinoma: oil red-O, Sudan IV, epithelial membrane antigen, Leu-m1 immunostains. […] Sebaceous carcinoma prognosis relies on several factors, including size, location, treatment approach, and tumor stage. According to the American Joint Committee on Cancer, T category of T2b or worse correlated with regional lymph node metastasis. In a recent meta-analysis of 1333 patients with eyelid sebaceous carcinoma, metastasis was reported in 12.1% of periocular cases, recurrence occurred in 15.9%, and tumor related mortality was 6.2%.
  • #86 Sebaceous carcinoma of the breast: a case report | Surgical Case Reports | Full Text
    https://surgicalcasereports.springeropen.com/articles/10.1186/s40792-017-0312-4
    Sebaceous carcinoma is a malignant epithelial tumor derived from or mimicking the sebaceous glands. […] The tumor revealed solid growth of small, round uniform cells with clear cytoplasm, partially intermingled with vacuolated cells indicative of sebaceous differentiation. […] The tumor cells contained abundant Sudan Black B-positive lipid droplets in the cytoplasm, and they were immunohistochemically positive for adipophilin. […] Pathological diagnosis of sebaceous carcinoma of the breast is considered to be difficult when sebaceous differentiation is morphologically obscure. […] In addition, the tumor cells were negative for the neuroendocrine markers such as synaptophysin and chromogranin A. […] According to the World Health Organization histological classification of tumors of the breast, the definition of the sebaceous carcinoma of the breast is that a primary breast carcinoma of the skin adnexal type with sebaceous differentiation at least 50% of cells and there should be no evidence of derivation from cutaneous adnexal sebaceous glands.
  • #87 Role of p53 and ki-67 in sebaceous neoplasms
    http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S2524-177X2020000400147
    Sebaceous carcinoma showed a higher percentage of p53 expression compared to benign lesions (median = 10%, range 0-80% vs. median = 0%, range: 0-5%, p = 0.001), and the latter more frequently expressed p53 10% (100% vs. 30%, p 0.0001). […] As for Ki-67 expression, sebaceous carcinoma displayed a higher Ki-67 expression percentage compared to benign lesions (median = 35%, range 5-80% vs. median = 5%, range: 0-30%, p 0.0001). […] A p53 expression 10% and a Ki-67 expression 25% are suggestive for the diagnosis of sebaceous carcinoma.
  • #88 Role of p53 and ki-67 in sebaceous neoplasms
    http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S2524-177X2020000400147
    Sebaceous carcinoma showed a higher percentage of p53 expression compared to benign lesions (median = 10%, range 0-80% vs. median = 0%, range: 0-5%, p = 0.001), and the latter more frequently expressed p53 10% (100% vs. 30%, p 0.0001). […] As for Ki-67 expression, sebaceous carcinoma displayed a higher Ki-67 expression percentage compared to benign lesions (median = 35%, range 5-80% vs. median = 5%, range: 0-30%, p 0.0001). […] A p53 expression 10% and a Ki-67 expression 25% are suggestive for the diagnosis of sebaceous carcinoma.
  • #89 Role of p53 and ki-67 in sebaceous neoplasms
    http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S2524-177X2020000400147
    Sebaceous carcinoma showed a higher percentage of p53 expression compared to benign lesions (median = 10%, range 0-80% vs. median = 0%, range: 0-5%, p = 0.001), and the latter more frequently expressed p53 10% (100% vs. 30%, p 0.0001). […] As for Ki-67 expression, sebaceous carcinoma displayed a higher Ki-67 expression percentage compared to benign lesions (median = 35%, range 5-80% vs. median = 5%, range: 0-30%, p 0.0001). […] A p53 expression 10% and a Ki-67 expression 25% are suggestive for the diagnosis of sebaceous carcinoma.
  • #90 Aggressive sebaceous carcinoma of the scalp: a case report and literature review – Li – Translational Cancer Research
    https://tcr.amegroups.org/article/view/54815/html
    Imaging inspection appears to be crucial for aggressive SC of the scalp. CT may reveal skull destruction, and MRI can delineate intracranial soft tissue involvement by tumor. […] Immunohistochemistry has largely replaced lipid stains such as oil red O, of which the sensitivity decreases after formalin fixation, in the diagnosis of SC. […] The role of radiation therapy and systemic chemotherapy after surgery is not clear in the extraocular SC, which are only suggested for patients who are poor surgical candidates or those with recurrent or metastatic disease. […] Early precise diagnosis and improved radical treatment remain an essential step against aggressive cutaneous malignancy.
  • #91 Sebaceous Carcinoma: A Rare Extraocular Presentation of the Cheek – European Medical Journal
    https://www.emjreviews.com/dermatology/article/sebaceous-carcinoma-a-rare-extraocular-presentation-of-the-cheek/
    The diagnosis of sebaceous carcinoma is established via incisional or partial-thickness biopsy. The morphological hallmark of sebaceous differentiation is the detection of sebaceous cells and demonstration of fat in vacuolated tumour cells. Common positive immunohistochemical markers include CK, EMA, CAM 5.2, and Anti-BCA-225 antibody. […] Sebaceous carcinomas are known to have a significant association with MuirTorre syndrome, a subset of hereditary nonpolyposis colorectal carcinoma. The primary internal malignancies associated with this syndrome are genitourinary and colorectal cancer as seen in this patient. […] Wide excision with clear margins is the treatment of choice for well-differentiated sebaceous carcinoma. In poorly differentiated lesions, wide excision, adjuvant radiotherapy, and regular follow-up of the skin and lymph nodes are advised. Although not the mainstay treatment, limited data of Mohs micrographic surgery has been reported to have lower recurrence rates as compared to wide excision.
  • #92 Sebaceous Carcinoma (Sebaceous Gland Carcinoma, Sebaceous Cell Carcinoma, Meibomian Gland Carcinoma) – Dermatology Advisor
    https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/sebaceous-carcinoma-sebaceous-gland-carcinoma-sebaceous-cell-carcinoma-meibomian-gland-carcinoma/
    Sebaceous carcinoma (SC) has been termed the great masquerader of adnexal tumors. […] The majority of sebaceous carcinomas arise spontaneously and de novo. In the periocular region, they arise from sebaceous glands, most commonly the Meibomian glands and the glands of Zeis. Other sebaceous glands in this region include the sebaceous glands of the eyebrows (follicular), sebaceous glands of the fine hairs of the eyelids and lacrimal glands, and sebaceous glands of the caruncle. In the extracutaneous sites, sebaceous carcinomas do not appear to arise from sebaceous glands, making their origin debatable. […] A minority of sebaceous carcinomas occur in patients with Muir-Torre syndrome, providing clues that mutations in tumor suppressor genes can be causative. Muir-Torre syndrome is an autosomal dominant disease with high penetrance and variable expressivity.
  • #93 EyeRounds.org: Sebaceous Cell Carcinoma: A Masquerade Syndrome
    http://eyerounds.org/cases/62-Sebaceous-Cell-Carcinoma-Eyelid-Masquerade-Syndrome.htm
    Sebaceous Cell Carcinoma can arise from any of these types of sebaceous glands. However, classically it arises from the Meibomian glands of tarsal plate and from the upper eyelids, which accounts for approximately 2/3 of cases. Less commonly, it is found in the Glands of Zeiss and the lower eyelids. It is rare to find the lesion in the caruncle or eyebrow and very rare to find it in the lacrimal gland, which accounts for only a handful of poorly differentiated cases. […] Although sebaceous cell carcinoma is one of the most malignant lesions of the eyelids, it may be difficult to diagnose. This is demonstrated by the fact that the average intervening time between presentation and diagnosis ranges from one to three years. The reason for this difficulty in diagnosis is due to its varied presentation both clinically and histopathologically. It tends to masquerade as more common benign conditions, mimicking other tumors as well as inflammatory conditions. Consequently sebaceous cell carcinoma is known to masquerade other conditions. So it is important to include sebaceous gland carcinoma in the differential diagnosis of most eyelid masses and recurrent inflammatory conditions.
  • #94 Sebaceous Carcinoma: A Rare Extraocular Presentation of the Cheek – European Medical Journal
    https://www.emjreviews.com/dermatology/article/sebaceous-carcinoma-a-rare-extraocular-presentation-of-the-cheek/
    Sebaceous carcinoma is a rare malignant cutaneous tumour that mainly arises in areas abundant in sebaceous glands. Derived from adnexal epithelium of the dermis, this tumour may arise in periocular or extraocular sites. The periocular variant constitutes approximately 75% of sebaceous neoplasms. Extraocular sebaceous carcinoma represents 25% of the sebaceous tumours and has been reported to present more commonly on the head and neck followed by the trunk, salivary glands, genitalia, breast, ear canal, and intraoral activity. […] The typical clinical presentation of sebaceous carcinoma is a painless localised papular or nodular subcutaneous growth. These lesions grow insidiously within the surface epithelium and can appear yellow in colour, attributable to the lipid accumulation. It can also present as pedunculated lesions, an irregular mass, or diffusely thickened skin. The varying appearance allows sebaceous carcinoma to mimic other benign tumours or inflammatory conditions. This is the primary reason for delay in proper diagnosis, inappropriate management, and increased morbidity and mortality.
  • #95 EyeRounds.org: Sebaceous Cell Carcinoma: A Masquerade Syndrome
    http://eyerounds.org/cases/62-Sebaceous-Cell-Carcinoma-Eyelid-Masquerade-Syndrome.htm
    Sebaceous Cell Carcinoma can arise from any of these types of sebaceous glands. However, classically it arises from the Meibomian glands of tarsal plate and from the upper eyelids, which accounts for approximately 2/3 of cases. Less commonly, it is found in the Glands of Zeiss and the lower eyelids. It is rare to find the lesion in the caruncle or eyebrow and very rare to find it in the lacrimal gland, which accounts for only a handful of poorly differentiated cases. […] Although sebaceous cell carcinoma is one of the most malignant lesions of the eyelids, it may be difficult to diagnose. This is demonstrated by the fact that the average intervening time between presentation and diagnosis ranges from one to three years. The reason for this difficulty in diagnosis is due to its varied presentation both clinically and histopathologically. It tends to masquerade as more common benign conditions, mimicking other tumors as well as inflammatory conditions. Consequently sebaceous cell carcinoma is known to masquerade other conditions. So it is important to include sebaceous gland carcinoma in the differential diagnosis of most eyelid masses and recurrent inflammatory conditions.
  • #96 Case Report: Sebaceous carcinoma of the eyelid | F1000Research
    https://f1000research.com/articles/12-1563
    The treatment of choice for sebaceous carcinoma is surgery, with complete excision verified by negative margins. […] Sebaceous carcinoma of the eyelid is a rare entity, but might be difficult to diagnose because of its ability to masquerade as the periocular lesions. However, accurate and prompt diagnosis is crucial for planning further management of the disease and prevention of any complications such as loss of vision, metastasis to other organs etc, therefore tissue diagnosis is the gold standard method and it can be aided by a panel of immunohistochemistry stains.
  • #97 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    The histopathology varies depending on the differentiation of the tumor. In well differentiated lesions, there is a lobular arrangement and vacuolization of the cytoplasm cells centrally. […] Cells present will include sebaceous and undifferentiated cells. There may be variation in nucleus shape and size with high mitotic activity indicated by mitotic figures. Special stains can be used to help distinguish sebaceous carcinoma: oil red-O, Sudan IV, epithelial membrane antigen, Leu-m1 immunostains. […] Sebaceous carcinoma prognosis relies on several factors, including size, location, treatment approach, and tumor stage. According to the American Joint Committee on Cancer, T category of T2b or worse correlated with regional lymph node metastasis. In a recent meta-analysis of 1333 patients with eyelid sebaceous carcinoma, metastasis was reported in 12.1% of periocular cases, recurrence occurred in 15.9%, and tumor related mortality was 6.2%.
  • #98 Sebaceous Carcinoma: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/24087-sebaceous-carcinoma
    Sebaceous carcinoma is a rare type of skin cancer that starts in your skins oil-producing (sebaceous) glands. Its an aggressive cancer that can return after treatment. […] Sebaceous carcinoma is an aggressive skin cancer, which means it spreads quickly. […] Experts dont know why some people develop sebaceous carcinoma. Like other types of skin cancer, exposure to the suns ultraviolet (UV) rays may contribute to this cancer. It may also develop in people, especially younger people, who have had radiation therapy to the head or neck. […] People with a rare inherited disease called Muir-Torre syndrome are more likely to develop sebaceous carcinoma, as well as colorectal (colon) cancer. Muir-Torre syndrome is a form of Lynch syndrome. It causes tumors to form in your sebaceous glands. […] Sebaceous carcinoma is most likely to affect the lymph nodes. […] Sebaceous carcinoma may be aggressive. For as many as 1 in 4 people, the cancer comes back (recurs) or spreads (metastasizes) after treatment. […] Sebaceous carcinoma can be fatal if it spreads. Outcomes are worse when theres a delay in diagnosis and treatment.
  • #99 Sebaceous carcinoma – Wikipedia
    https://en.wikipedia.org/wiki/Sebaceous_carcinoma
    Altered expression of beta-catenin, p21, sonic hedgehog signaling (Shh), and E-cadherin have been associated with invasion, metastasis, and poor clinical outcomes. […] More recently, mutations in tumor suppressor genes including p53 and Rb have been associated with the development of sporadic SGc as well as SGc in MTS patients with intact mismatch repair and subsets of younger patients presenting with SGc harboring transcriptionally active high-risk human papillomavirus (HPV).
  • #100 Sebaceous Carcinoma (Sebaceous Gland Carcinoma, Sebaceous Cell Carcinoma, Meibomian Gland Carcinoma) – Dermatology Advisor
    https://www.dermatologyadvisor.com/home/decision-support-in-medicine/dermatology/sebaceous-carcinoma-sebaceous-gland-carcinoma-sebaceous-cell-carcinoma-meibomian-gland-carcinoma/
    MSH-1 and MLH-2 are genes important for the repair of DNA mismatch. Germline mutations in these genes lead to microsatellite instability in DNA and in the process lead to inactivation of tumor suppressor genes. […] The invasion of sebaceous carcinoma is believed to occur by direct extension into subdermal and/or epithelial tissues (epitheliotropism), multifocal proliferation into intradermal and subcutaneous tissues, and by oncophoresis whereby cancer cells are hypothetically shed and transplanted. […] There can also be direct intraepidermal extension by pagetoid spread. Up to 50% of recurrent periocular sebaceous carcinomas may involve pagetoid spread and 100% in exenterated specimens. Pagetoid spread is reported to be much less common in extraocular sebaceous carcinoma.
  • #101 Sebaceous carcinoma in the right inguinal region with multiple metasta | CMAR
    https://www.dovepress.com/sebaceous-carcinoma-in-the-right-inguinal-region-with-multiple-metasta-peer-reviewed-fulltext-article-CMAR
    Based on the location of SC, it can be divided into ocular SC and extra-ocular SC. Ocular SC is mostly observed in the periorbital area, accounting for approximately 75% of all SC cases. The remaining 25% of SC cases are extraocular, with approximately 70% located in the head and neck region, and 13% occurring on the back or trunk, but capable of arising wherever sebaceous glands are found. Both ocular and extra-ocular SC have high recurrence rates and are associated with regional nodal metastasis. […] SC is histologically marked by noncontiguous multicentric growth patterns and pagetoid spread, where cells proliferate randomly in the epithelium or other tissues. This multicentric growth pattern, a poor prognosis marker, is distinctive of ocular SC. Pagetoid spread also mainly characterizes ocular SC and is rarely observed in extra-ocular SC. Metastases primarily affect lymph nodes but have also been reported in the lungs, brain, liver, small intestine, and urinary tract. The 5-year survival rate for metastatic SC ranges from 50% to 68%, compared to 75-78% for localized/regional disease. Poor prognostic indicators include tumors larger than 1 cm, poor differentiation, lympho-vascular invasion, and involvement of both upper and lower eyelids.
  • #102 Sebaceous Carcinoma – EyeWiki
    https://eyewiki.org/Sebaceous_Carcinoma
    The histopathology varies depending on the differentiation of the tumor. In well differentiated lesions, there is a lobular arrangement and vacuolization of the cytoplasm cells centrally. […] Cells present will include sebaceous and undifferentiated cells. There may be variation in nucleus shape and size with high mitotic activity indicated by mitotic figures. Special stains can be used to help distinguish sebaceous carcinoma: oil red-O, Sudan IV, epithelial membrane antigen, Leu-m1 immunostains. […] Sebaceous carcinoma prognosis relies on several factors, including size, location, treatment approach, and tumor stage. According to the American Joint Committee on Cancer, T category of T2b or worse correlated with regional lymph node metastasis. In a recent meta-analysis of 1333 patients with eyelid sebaceous carcinoma, metastasis was reported in 12.1% of periocular cases, recurrence occurred in 15.9%, and tumor related mortality was 6.2%.
  • #103 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    The PI3K/AKT/mTOR pathway is commonly dysregulated in sebaceous carcinoma and may represent a potential therapeutic target. Aberrant activation of the PI3K/AKT/mTOR pathway promotes tumor cell proliferation, survival, and resistance to apoptosis, contributing to disease progression and treatment resistance. Targeting PI3K/AKT/mTOR pathway components with inhibitors has shown promise in preclinical studies and may offer therapeutic benefits to patients with advanced or refractory sebaceous carcinoma.
  • #104 Angiogenesis in Ocular and Extraocular Sebaceous Carcinoma | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-3342
    Our findings suggest that VEGF expression by epidermal keratinocytes and tumour cells and its interaction with VEGFR-2 seems to contribute to the pathogenesis of SC not only by its effects on angiogenesis but also by direct effects on the tumour cells. […] Our findings regarding VEGFR-3 expression indicate that this protein may play a critical role in the pathogenesis of SC and therefore might be of therapeutic interest. […] Two of our central findings, namely, an increased intratumoural ratio of small lymphatics to large lymphatics and a negative correlation between epidermal VEGF expression and the intratumoural density of lymphatics, clearly underline the hypothesis regarding the lymphangiogenetic potential of SC.
  • #105 Sebaceous carcinoma of the intraoral origin: a literature review
    https://www.degruyter.com/document/doi/10.1515/oncologie-2024-0476/html
    SC has been linked to inherited mutations associated with Muir-Torre Syndrome, a subtype of Lynch syndrome (HNPCC), which affects DNA mismatch repair genes (MSH2, MSH6, MLH1), and causes microsatellite instability, leading to genomic errors, promoting SC development alongside other malignancies. […] Some studies further suggest that mutations in specific genes, such as Patched-1 (PTCH1) and TP53, may contribute to SC development, as these genetic changes can impair normal cell function and promote tumor formation. […] Molecular chaperones like X-linked inhibitor of apoptosis protein (XIAP) and Bcl-2-Associated Athanogene 3 (BAG3) are implicated in promoting tumor survival and proliferation. […] Studies reveal that SC may also exhibit PD-L1 expression on tumor cells and PD-1 on tumor-infiltrating lymphocytes (TILs) in 46% of cases, indicating immune evasion within an active yet suppressed tumor microenvironment. […] Current evidence does not support a direct association between UVR and the development of SC in the oral cavity. […] Despite various theories and mechanisms, the precise cause of IOSC remains uncertain due to the limited number of reported cases.
  • #106 Sebaceous gland carcinoma of ocular region in India: A brief literature review for disease management – Latin American Journal of Ophthalmology
    https://latinamericanjo.com/sebaceous-gland-carcinoma-of-ocular-region-in-india-a-brief-literature-review-for-disease-management/
    Sebaceous carcinoma (SGC) is slow growing, but the most aggressive and lethal eyelid malignancy. A previously published article illustrates the molecular genetic framework stating the drivers of sebaceous carcinoma. […] Thus, new insight into the natural and molecular-oriented treatment modalities may lead to the development of new effective strategies, along with the conventional method. […] SGC has some major risk factors which include patients age, prior exposure to UV, systemic association, and patients infected with HIV and Muir-Torre syndrome. […] Several studies have investigated the genetic alteration driving the sebaceous carcinoma of the eyelid. Sebaceous carcinoma is considered as a marker for the Muir-Torre syndrome, an autosomal dominant condition often associated with germline mutation of mismatch repair (MMR) genes MLH1, PMS2, MSH6, and MSH2.
  • #107 Sebaceous Carcinoma – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK610689/
    The PI3K/AKT/mTOR pathway is commonly dysregulated in sebaceous carcinoma and may represent a potential therapeutic target. Aberrant activation of the PI3K/AKT/mTOR pathway promotes tumor cell proliferation, survival, and resistance to apoptosis, contributing to disease progression and treatment resistance. Targeting PI3K/AKT/mTOR pathway components with inhibitors has shown promise in preclinical studies and may offer therapeutic benefits to patients with advanced or refractory sebaceous carcinoma.
  • #108 Sebaceous Carcinoma: A Rare Extraocular Presentation of the Cheek – European Medical Journal
    https://www.emjreviews.com/dermatology/article/sebaceous-carcinoma-a-rare-extraocular-presentation-of-the-cheek/
    It is important to be aware of sebaceous carcinomas risk for recurrence and distant metastasis: more common in the ocular type as compared to the extraocular. Long-term follow up is recommended for patients after resolution of the cancer because of reports of late relapses. […] Exhibiting a variable presentation of histopathological and clinical presentations, this cancer is often misdiagnosed, delaying proper patient prognosis and care. Increasing awareness of this disease can help expand the differential diagnoses in patients who present with relevant features and prompt an early diagnostic and management plan.
  • #109 Sebaceous Carcinoma: Symptoms, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/24087-sebaceous-carcinoma
    Sebaceous carcinoma is a rare type of skin cancer that starts in your skins oil-producing (sebaceous) glands. Its an aggressive cancer that can return after treatment. […] Sebaceous carcinoma is an aggressive skin cancer, which means it spreads quickly. […] Experts dont know why some people develop sebaceous carcinoma. Like other types of skin cancer, exposure to the suns ultraviolet (UV) rays may contribute to this cancer. It may also develop in people, especially younger people, who have had radiation therapy to the head or neck. […] People with a rare inherited disease called Muir-Torre syndrome are more likely to develop sebaceous carcinoma, as well as colorectal (colon) cancer. Muir-Torre syndrome is a form of Lynch syndrome. It causes tumors to form in your sebaceous glands. […] Sebaceous carcinoma is most likely to affect the lymph nodes. […] Sebaceous carcinoma may be aggressive. For as many as 1 in 4 people, the cancer comes back (recurs) or spreads (metastasizes) after treatment. […] Sebaceous carcinoma can be fatal if it spreads. Outcomes are worse when theres a delay in diagnosis and treatment.
  • #110 Sebaceous Carcinomas of the Skin: 24 Cases and a Literature Review | HTML | Acta Dermato-Venereologica
    https://www.medicaljournals.se/acta/content/html/10.2340/00015555-2685
    In this study, and in accordance with previous reports, our cases of SC presented before or concurrently with internal malignancy in approximately 42% of patients with MTS (12). This underlines the importance of malignancy screening in MTS and follow-up with colonoscopy every 3-5 years, starting at 25-30 years of age, yearly mammography and endometrial biopsy every 3-5 years in women over 50 years of age (14).
  • #111 Sebaceous Carcinoma: A Rare Extraocular Presentation of the Cheek – European Medical Journal
    https://www.emjreviews.com/dermatology/article/sebaceous-carcinoma-a-rare-extraocular-presentation-of-the-cheek/
    It is important to be aware of sebaceous carcinomas risk for recurrence and distant metastasis: more common in the ocular type as compared to the extraocular. Long-term follow up is recommended for patients after resolution of the cancer because of reports of late relapses. […] Exhibiting a variable presentation of histopathological and clinical presentations, this cancer is often misdiagnosed, delaying proper patient prognosis and care. Increasing awareness of this disease can help expand the differential diagnoses in patients who present with relevant features and prompt an early diagnostic and management plan.