Guzy
Patofizjologia i mechanizm

Guzy, zarówno nowotworowe, jak i nienowotworowe, powstają w wyniku złożonych mechanizmów patogenetycznych, w tym mutacji genetycznych, procesów zapalnych oraz urazów mechanicznych. Przykładowo, lipoma wykazuje nieprawidłowości genetyczne w około 66% przypadków, z genem HMGA2 na chromosomie 12q14.3 odgrywającym kluczową rolę. Procesy zapalne, takie jak ziarniniak ropotwórczy czy rumień guzowaty, manifestują się przez specyficzne reakcje immunologiczne i histologiczne, np. promieniste ziarniniaki Mieschera w tkance tłuszczowej. W kontekście guzów piersi, hormony takie jak estrogen i progesteron zwiększają ryzyko proliferacji łagodnych zmian do 74%, a mutacje genów BRCA1, BRCA2 i TP53 klasyfikowane są jako wysokiego ryzyka rozwoju raka. W przypadku choroby guzowatej skóry (LSD) u bydła, wirus z rodziny Poxviridae wywołuje zmiany skórne o średnicy 1-7 cm, z okresem inkubacji 7-28 dni i objawami gorączki do 41,5°C. Guzy tkanek miękkich, w tym mięsaki, wykazują heterogenność histologiczną i często agresywne zachowanie miejscowe, z tendencją do nawrotów i przerzutów, co wymaga kompleksowego leczenia chirurgicznego i radioterapii.

  1. Patogeneza guzów
    1. Mechanizmy genetyczne w rozwoju guzów
    2. Mechanizmy zapalne i immunologiczne
    3. Mechanizmy związane z urazem
  2. Patofizjologia różnych typów guzów
    1. Guzy reaktywne dziąseł
    2. Guzy typu torbieli i gangliony
    3. Guzy piersi i mechanizmy hormonalne
    4. Guzy zakaźne i mechanizmy rozwoju
  3. Mechanizmy powstawania guzów nowotworowych
    1. Mutacje genetyczne w nowotworach
    2. Miękotkankowe guzy nowotworowe
    3. Przerzuty i inwazja nowotworowa
  4. Czynniki wpływające na rozwój guzów
    1. Czynniki genetyczne i dziedziczne
    2. Czynniki środowiskowe i ekspozycja na karcynogeny
    3. Czynniki zapalne i immunologiczne
    4. Czynniki hormonalne
  5. Patofizjologia guzów w kontekście różnych chorób
    1. Artretyczne guzki reumatoidalne
    2. Guzki w gruczole piersiowym
    3. Hidradenitis suppurativa i guzki podskórne
    4. Guzowata choroba skóry u bydła
  6. Guzy a choroby węzłów chłonnych i układu limfatycznego
  7. Guzy w praktyce klinicznej
    1. Diagnostyka guzów
    2. Podejście do leczenia guzów
    3. Kolejne rozdziały

Patogeneza guzów

Guzy, określane również jako zmiany guzowate, są powszechnym objawem klinicznym charakteryzującym się obecnością różnego rodzaju guzowatych zmian w tkankach ciała. Patogeneza guzów jest złożona i zależy od ich etiologii, przy czym mechanizmy rozwoju tych zmian różnią się znacząco w zależności od ich typu.12

Mechanizmy genetyczne w rozwoju guzów

Znacząca liczba guzów rozwija się na skutek zmian genetycznych. W przypadku lipoma (tłuszczaka), około dwóch trzecich tych zmian wykazuje nieprawidłowości genetyczne. W podgrupie tłuszczaków gen HMGA2 (zlokalizowany na chromosomie 12q14.3) odgrywa istotną rolę w patogenezie guza.1 W przypadku guzów nowotworowych, zarówno łagodnych jak i złośliwych, zmiany w DNA prowadzą do przekształcenia prawidłowych genów w onkogeny, które tracą zdolność do hamowania wzrostu, co skutkuje niekontrolowanym wzrostem komórek.1

Mutacje genetyczne mogą także prowadzić do rozwoju guzów nienowotworowych. Na przykład fasciitis nodularis (włóknienie guzkowe) pojawia się, gdy dochodzi do genetycznej rearanżacji skutkującej fuzją genów MYH9 i USP6.1 Z kolei w przypadku obciążenia rodzinnego lipomatozą, rzadkiej choroby charakteryzującej się występowaniem wielu tłuszczaków, stwierdza się dziedziczenie wadliwego genu.12

Mechanizmy zapalne i immunologiczne

Wiele guzów rozwija się w odpowiedzi na procesy zapalne. Przykładem jest naczyniowy nabytek (ziarniniak ropotwórczy), będący reaktywną zmianą naczyniową, która powstaje najczęściej na dziąsłach w wyniku urazu lub przewlekłego podrażnienia.1 Ziarniniak ropotwórczy rozwija się głównie u kobiet i charakteryzuje się niszczącym zapaleniem naczyń.2

Guzy w wyniku reakcji ziarniniakowej stanowią szczególny rodzaj odpowiedzi immunologicznej. Ziarniniaki tworzą się, gdy komórki układu odpornościowego zlepiają się i tworzą małe grudki w miejscu infekcji lub zapalenia. Jest to sposób, w jaki organizm izoluje zakażenia bakteryjne, wirusowe lub grzybicze, aby zapobiec ich rozprzestrzenianiu (ziarniniaki serowaciejące) lub izoluje substancje drażniące czy ciała obce (ziarniniaki nieserowaciejące).1

W przypadku rumienia guzowatego, wykazującego histologicznie cechy zapalenia przegród w tkance tłuszczowej podskórnej (panniculitis), dochodzi do infiltracji neutrofilowej i eozynofilowej wokół naczyń włosowatych oraz pogrubienia przegród w tkance tłuszczowej. Charakterystycznym markerem diagnostycznym dla tej choroby jest tworzenie się skupisk makrofagów wokół naczyń krwionośnych lub przegród międzypłatowych, znanych jako promieniste ziarniniaki Mieschera.1

Mechanizmy związane z urazem

Uraz mechaniczny jest istotnym czynnikiem w patogenezie niektórych guzów. W przypadku tłuszczaków, jeden z proponowanych mechanizmów działania sugeruje, że rozwijają się one po urazie danego obszaru. Przypuszcza się jednak, że dotyczy to tylko urazów, które skutkują martwicą komórek tłuszczowych i następnie miejscowym stanem zapalnym, co inicjuje formowanie się tłuszczaka.12

Martwica tłuszczowa (fat necrosis) jest procesem powolnym, zachodzącym etapowo po uszkodzeniu tkanki tłuszczowej. Komórki tkanki tłuszczowej zaczynają obumierać, co powoduje zmiany w teksturze lub wyglądzie skóry w tym obszarze. Martwica tłuszczowa może dotyczyć każdego, kto doznał urazu tkanki tłuszczowej, ale najczęściej występuje w tkance piersiowej, a także może pojawić się w innych tłustych obszarach, takich jak brzuch, pośladki i uda w wyniku zabiegów medycznych lub kosmetycznych.1

Patofizjologia różnych typów guzów

Guzy reaktywne dziąseł

Zmiany guzowate dziąseł są jednymi z najczęstszych zmian spotykanych u pacjentów, z czego zdecydowana większość to reaktywne rozrosty związane z szeregiem przewlekłych bodźców drażniących.1 Histologicznie wykazują one hiperplastyczny i zwykle skeratynizowany nabłonek pokrywający guzkową tkankę łączną włóknistą.2

Stopień kolagenizacji i unaczynienia trzonu zmiany zależy od jej dojrzałości i obecności lub braku stanu zapalnego. Składnik fibroblastyczny jest zwykle łagodny i w większości przypadków składa się z drobnych komórek wrzecionowatych, przy czym większość zmian jest stosunkowo ubogokomórkowa. W niektórych przypadkach fibroblasty mogą być duże i gwiaździste w morfologii, a czasami wielojądrzaste, choć cytologicznie łagodne.1

Do jednej trzeciej takich zmian na dziąsłach zawiera beleczki kości metaplastycznej, szczególnie te na wargowej dziąsłach szczęki, które są lub były owrzodzone. Takie zmiany są określane jako obwodowy włókniak kostniący (peripheral ossifying fibroma).23 Histologicznie składnik mineralizujący składa się z beleczek lub kropelkowych zwapnień przypominających kość splotowatą lub cement w tle aktywnego podścieliska komórkowego.1

Guzy typu torbieli i gangliony

Torbiele (cysty) to okrągłe zmiany zbudowane z torebki wypełnionej keratyną (materiału strukturalnego tworzącego zewnętrzną warstwę skóry), łojem (olejem ze skóry), płynem lub materiałem ropnym. Niektóre torbiele tworzą się, gdy mieszki włosowe, przewody potowe lub gruczoły śluzowe zostają zablokowane, a płyn gromadzi się za blokadą.12

Gangliony są szczególnym rodzajem torbieli związanych ze stawami lub pochewkami ścięgnistymi. Choć nie ma ustalonej definitywnej etiologii, dominująca od 1893 roku teoria sugeruje, że ganglion jest degeneracją śluzowatej tkanki łącznej, szczególnie kolagenu.1 Gangliony powstają jako wypuklenia błony maziowej; jako podrażnienie tkanki stawowej, tworzące nową formację; lub, według najbardziej powszechnej i akceptowanej teorii, jako degeneracja tkanki łącznej i tworzenie się przestrzeni torbielowatej.2

Sugeruje się również, że degeneracja tkanki łącznej jest spowodowana podrażnieniem lub przewlekłym uszkodzeniem, powodującym, że komórki mezenchymalne lub fibroblasty produkują mucynę. Chociaż torbiele ganglionu mogą być jednokomórkowe, najczęściej są wielokomorowe, z przegrodami wykonanymi z tkanki łącznej oddzielającymi płaty lub jamy.3

Guzy piersi i mechanizmy hormonalne

Rozwój piersi jest pod wpływem różnych hormonów, takich jak estrogen, progesteron, prolaktyna i estradiol. Patofizjologia guzów piersi zależy od podtypów histologicznych. Wyniki histologiczne guzów piersi różnią się od siebie, co prowadzi do diagnozy. Uważa się, że guzy piersi są wynikiem zdarzeń hormonalnych i mutacji genetycznych.1

Estrogen i progesteron mogą zwiększać ryzyko łagodnej choroby proliferacyjnej do 74%, a łagodne zmiany piersi u kobiet po menopauzie, które otrzymują estrogen z progesteronem lub bez przez ponad 8 lat, wzrastają 1,7-krotnie. Mutacje genów są klasyfikowane na 3 kategorie na podstawie ryzyka raka: BRCA1, BRCA2, TP53 uważane za mutacje wysokiego ryzyka, homozygotyczna ataksja-telangiektazja, mutacja somatyczna w CHEK2, BRIP1, PALB2 jako mutacje umiarkowanego ryzyka, a mutacje genów niskiego ryzyka nie zostały jeszcze określone.2

Zmiany włóknisto-torbielowate prowadzą do rozwoju wypełnionych płynem okrągłych lub owalnych woreczków, zwanych torbielami. Torbiele mogą powodować, że piersi stają się wrażliwe, grudkowate lub włókniste. Dokładna przyczyna zmian włóknisto-torbielowatych nie jest znana, ale eksperci podejrzewają, że hormony reprodukcyjne, zwłaszcza estrogen, odgrywają rolę.1

Guzy zakaźne i mechanizmy rozwoju

Choroba guzowata skóry (Lumpy Skin Disease, LSD) jest przykładem choroby zakaźnej powodującej charakterystyczne zmiany guzowate. Jest wywoływana przez wirus choroby guzowatej skóry (LSDV), należący do rodziny Poxviridae. Zakażenie LSDV inicjuje kaskadę zdarzeń, w tym replikację wirusa, wiremię, gorączkę, lokalizację skórną i tworzenie guzków.1

Badania eksperymentalne po wstrzyknięciu śródskórnym wirusa określiły konkretne ramy czasowe dla różnych wyników: między 4 a 7 dniem po zakażeniu (DPI) pojawiły się guzki lub blaszki o średnicy 1-3 cm w miejscu inokulacji; między 6 a 18 DPI wystąpiło rozsiewanie wirusa drogą ustną i donosową, wraz z wiremią; między 7 a 19 DPI rozwinęła się regionalna limfadenopatia i uogólnione guzki skórne; a 42 dni po wystąpieniu gorączki wirus został wykryty w nasieniu.2

Replikacja wirusa w makrofagach, komórkach śródbłonka, perycytach i fibroblastach powoduje zapalenie naczyń i limfangitis. Ze względu na niedobór odporności humoralnej, krowy karmiące, nowonarodzone cielęta i zwierzęta o niedowadze są bardziej podatne na infekcje naturalne, podczas gdy zwierzęta, które przeżyją po ekspozycji na wirus, rozwijają dożywotnią odporność.3

Mechanizmy powstawania guzów nowotworowych

Guzy nowotworowe powstają, gdy normalny proces podziału komórkowego ulega zaburzeniu, a komórki anormalne lub uszkodzone rosną i mnożą się, gdy nie powinny. Te komórki mogą tworzyć guzy, które są grudkami tkanki. Guzy mogą być nowotworowe lub nienowotworowe (łagodne).1

Mutacje genetyczne w nowotworach

Rak jest spowodowany zmianami w DNA. Większość zmian DNA powodujących raka występuje w odcinkach DNA zwanych genami. Te zmiany są również nazywane zmianami genetycznymi. Zmiana DNA może powodować, że geny zaangażowane w normalny wzrost komórek stają się onkogenami. W przeciwieństwie do normalnych genów, onkogeny nie mogą być wyłączone, dlatego powodują niekontrolowany wzrost komórek.2

W normalnych komórkach geny supresorowe nowotworów zapobiegają rakowi, spowalniając lub zatrzymując wzrost komórek. Zmiany DNA inaktywujące geny supresorowe nowotworów mogą prowadzić do niekontrolowanego wzrostu komórek i raka.3

Miękotkankowe guzy nowotworowe

Guzy tkanek miękkich stanowią dużą i heterogeniczną grupę nowotworów. Dane histomorfologiczne, immunohistochemiczne i eksperymentalne sugerują, że większość, jeśli nie wszystkie mięsaki, powstają z prymitywnych, wielopotencjalnych komórek mezenchymalnych, które w trakcie transformacji nowotworowej różnicują się wzdłuż jednej lub więcej linii.1

Choć większość guzów tkanek miękkich różnych typów histogenetycznych jest klasyfikowana jako łagodne lub złośliwe, wiele z nich ma charakter pośredni, co zwykle oznacza agresywne zachowanie miejscowe z niską do umiarkowanej skłonnością do przerzutów.2

Generalnie, guzy tkanek miękkich rosną dośrodkowo, choć niektóre guzy łagodne (np. zmiany włókniste) mogą rosnąć wzdłużnie wzdłuż płaszczyzn tkanek. Gdy guz osiąga anatomiczne granice przedziału, jest bardziej prawdopodobne, że narusza granice przedziałowe.1

Obwodowa część guza uciska otaczającą, normalną tkankę miękką ze względu na dośrodkowy wzrost rozprężający. Cienka warstwa tkanki zwana strefą reaktywną otacza strefę kompresji, szczególnie w guzach wyższego stopnia.2 Niektóre niezwykle agresywne zmiany o naciekającym wzorcu wzrostu, takie jak dziecięcy mięsak prążkowany, mogą nie respektować anatomicznych granic przedziałowych i często naciekają płaszczyzny powięziowe.3

Przerzuty i inwazja nowotworowa

Mięsaki tkanek miękkich mają tendencję do nawrotów miejscowych. Pseudotorebka zapewnia chirurgom mniej lub bardziej oczywistą płaszczyznę rozcięcia; jednak takie wycięcie może pozostawić mikroskopowy lub okazjonalnie makroskopowy guz. Dodanie pooperacyjnej radioterapii zmniejsza ryzyko nawrotu związanego z marginalnym wycięciem.1

Wzorzec nawrotu jest zasadniczo przewidywalny, a większość guzów przeznaczonych do nawrotu robi to w ciągu pierwszych 2-3 lat. Uzupełniająca radioterapia wyraźnie minimalizuje nawroty miejscowe, ale jej zdolność do zwiększenia ogólnych szans na przeżycie, choć prawdopodobna, nie jest pewna.2

Wielu pacjentów z mięsakami tkanek miękkich wysokiego stopnia, a także kilku z typem niskiego stopnia, postępuje do choroby przerzutowej, nawet po osiągnięciu odpowiedniej kontroli miejscowej guza pierwotnego. Chociaż większość pacjentów nie ma klinicznie oczywistych przerzutów w momencie prezentacji, mogą mieć ukryte mikrometastazy, które ostatecznie manifestują się klinicznie.3

Komórki rakowe mogą oderwać się od oryginalnego guza i przemieszczać się przez krew lub układ limfatyczny do odległych miejsc w ciele, gdzie wychodzą z naczyń, aby tworzyć dodatkowe guzy. Jest to nazywane przerzutem.4

Czynniki wpływające na rozwój guzów

Czynniki genetyczne i dziedziczne

Istnieją solidne dowody sugerujące, że pewne zaburzenia genetyczne i mutacje genów są czynnikami predysponującymi do niektórych łagodnych i złośliwych guzów tkanek miękkich.1 W wielu przypadkach dziedziczone są wadliwe geny, które mogą zwiększać ryzyko rozwoju guzów. Przykładowo, rzadkie schorzenie znane jako rodzinna lipomatoza wielokrotna jest dziedziczone jako cecha autosomalnie dominująca.12

W przypadku guzów sutka u mężczyzn, ginekomastia stanowi najczęstszą nieprawidłowość, będąc jednoczesną proliferacją przewodów i podścieliska bez enkapsulacji, więc musi zlewać się z otaczającą tkanką tłuszczową. Nie ma proliferacji zrazików, jak to jest u kobiet. Z tego względu nie będzie obserwować się guzów, które zaczynają się w zrazikach, na przykład gruczolaków laktacyjnych, gruczolaków włóknistych, guzów liściowych, a także inwazyjne raki zrazikowe są niezwykle rzadkie.1

Czynniki środowiskowe i ekspozycja na karcynogeny

Zgłaszano związek między ekspozycją na różne karcynogeny a zwiększoną częstością występowania guzów tkanek miękkich.2 Mechanizm patogenetyczny polega na pojawieniu się indukowanych promieniowaniem mutacji genetycznych, które sprzyjają transformacji nowotworowej.3

Klasycznym przykładem guza tkanek miękkich wywołanego infekcją jest mięsak Kaposiego wynikający z ludzkiego herpeswirusa typu 8 u pacjentów z wirusem ludzkiego niedoboru odporności (HIV).4

Czynniki zapalne i immunologiczne

Przewlekłe stany zapalne mogą prowadzić do rozwoju różnych typów guzów. W przypadku guzkowatego zapalenia naczyń (nodular vasculitis), dokładna przyczyna jest nieznana, ale rozproszone zapalenie naczyń krwionośnych i limfatycznych w głębokiej skórze właściwej i tkance podskórnej wydaje się być związane ze spowolnionym krążeniem.1

Spowolnienie przepływu w głębokich naczyniach może również sprzyjać osadzaniu się bakterii z krwiobiegu, w tym prątków gruźlicy, a u niektórych pacjentów guzkowate zapalenie naczyń jest objawem gruźlicy, kiedy to może być nazywane rumień stwardniały lub choroba Bazina.2

Biopsja skóry guzków ujawnia panniculitis, z różnymi stopniami zapalenia naczyń krwionośnych i limfatycznych w głębokiej skórze właściwej i tkance podskórnej. Bolesne grudki są zazwyczaj spowodowane formą panniculitis i/lub zapalenia naczyń.3

Czynniki hormonalne

Wiadomo, że guzy piersi są wynikiem zdarzeń hormonalnych: Częstość występowania łagodnych zmian piersi u kobiet po menopauzie, które otrzymują estrogen z lub bez progesteronu przez ponad 8 lat, wzrasta 1,7-krotnie. Estrogen i progesteron zwiększają częstość łagodnej proliferacyjnej choroby piersi do 74%. Leki antyestrogenowe, takie jak tamoksyfen, zmniejszają częstość występowania zmian piersi, takich jak adenoza, torbiele, hiperplazja, rozszerzenie przewodów do 28%.1

Chociaż receptory estrogenowe (ER) i receptory progesteronowe (PR) przypisywane są słabemu rokowaniu, mogą one przewidywać odpowiedź pacjentów na terapię endokrynologiczną. Ocena obecności ER i PR jest wymagana w inwazyjnych rakach piersi. Wynik ER-dodatni występuje w 70% raków piersi, a wynik PR-dodatni występuje w 60% raków piersi.2

HER2/neu jest proto-onkogenem, który uczestniczy w szlakach regulacyjnych piersi, takich jak proliferacja, ruchliwość komórek i inwazja. W 10% do 34% raków piersi zgłaszana jest nadekspresja i amplifikacja HER2. W 90% przypadków można zaobserwować nadekspresję, amplifikację i ekspresję białka błony powierzchniowej HER2/neu.3

Patofizjologia guzów w kontekście różnych chorób

Artretyczne guzki reumatoidalne

Chociaż dokładny proces nie jest znany, istnieje kilka hipotez dotyczących powstawania guzków reumatoidalnych. Zaobserwowano, że guzki reumatoidalne często tworzą się nad miejscami wyprostowanymi i obszarami narażonymi na urazy. Uraz powoduje gromadzenie się cząstek zapalnych i prowadzi do wtórnej odpowiedzi zapalnej, która ostatecznie powoduje uwolnienie fibryny i martwicę.1

Inna hipoteza sugeruje, że zapalenie naczyń krwionośnych aktywuje składniki dopełniacza, co prowadzi do osadzania się czynników reumatoidalnych i fibryny. Guzek reumatoidalny jest najczęstszą skórną manifestacją reumatoidalnego zapalenia stawów. Reumatoidalne zapalenie stawów obejmuje przewlekłe zapalenie błon maziowych, co prowadzi do degradacji chrząstki stawowej i kości przykostnej.2

Zapalenie jest wywoływane przez komórki T, komórki B i monocyty, gdy komórki śródbłonka są aktywowane. Neowaskularyzacja, wzrost nowych naczyń krwionośnych, służy jako dodatkowy marker reumatoidalnego zapalenia stawów. Hiperplastyczna warstwa wyściełająca maziówkę może być spowodowana ekspansją fibroblastów maziówki i komórek makrofagów. Ta ekspansja błony maziowej, czasami określana jako „łuszczka”, może prowadzić do erozji kostnych i degradacji chrząstki w miejscu połączenia chrząstki i kości w kości okołostawowej.3

Guzki w gruczole piersiowym

Jak każda kobieta wie, wczesnym testem na raka piersi jest wyczuwanie guzków. To, czego lekarz lub sama pacjentka faktycznie szuka, kiedy to robi, to jeden z pierwszych oznak rozwoju guza: niezwykłe usztywnienie tkanki.1

W zdrowych komórkach piersi wykazano, że właściwości adhezyjne integryn prowadzą komórki do zmniejszenia siły, którą stosują do swojego środowiska, jeśli tkanka jest sztywniejsza niż normalnie.2 Jednak komórki rakowe w piersi wykazują inny typ integryny o różnych właściwościach adhezyjnych. Ta inna integryna prowadzi komórki do stosowania większych sił, gdy sztywność tkanki wzrasta, tworząc mechanizm sprzężenia zwrotnego, który może ostatecznie prowadzić do twardych guzków charakterystycznych dla guzów piersi.3

Te badania są pierwszym w historii opisem molekularnego mechanizmu odczuwania sztywności przez komórki, który wykazano w zdrowych i niezdrowych ludzkich komórkach piersi. Oznacza to, że zmiany mechaniczne wywołane zmienioną ekspresją integryny mogą być kluczowym aspektem stojącym za początkiem kilku chorób. Jeśli tak, to miałoby to ogromny potencjał dla możliwych terapii mających na celu zapobieganie złośliwym zmianom w sztywności tkanki.12

Hidradenitis suppurativa i guzki podskórne

Hidradenitis suppurativa, znana również jako trądzik odwrócony, to przewlekła choroba skóry charakteryzująca się nawracającymi przypominającymi wrzody guzkami (guzami) pod skórą. Stan ten prawdopodobnie wynika z kombinacji czynników genetycznych i środowiskowych.1

Początkowo badacze uważali, że zaburzenie było spowodowane blokadą (okluzją) wyspecjalizowanych gruczołów potowych zwanych gruczołami apokrynowymi. Jednak niedawne badania wykazały, że stan ten faktycznie zaczyna się od blokady mieszków włosowych w obszarach ciała, które zawierają również wysoką koncentrację gruczołów apokrynowych (takich jak pachy i pachwiny).2

Czynniki genetyczne wyraźnie odgrywają rolę w powodowaniu hidradenitis suppurativa. Niektóre przypadki okazały się wynikiem wariantów (znanych również jako mutacje) w genie NCSTN, PSEN1 lub PSENEN. Chociaż niewiele wiadomo o mechanizmie, nieprawidłowa sygnalizacja Notch wydaje się sprzyjać rozwojowi guzków i prowadzić do zapalenia skóry.3

Hidradenitis suppurativa rozwija się, gdy mieszki włosowe zostają zablokowane, ale przyczyna tej blokady nie jest znana. Eksperci uważają, że może to być związane z hormonami, predyspozycją genetyczną, paleniem papierosów lub nadwagą. Stan ten występuje najczęściej u osób rasy czarnej, prawdopodobnie ze względu na czynniki genetyczne.1

Guzowata choroba skóry u bydła

Zakażenie LSDV inicjuje kaskadę zdarzeń, w tym replikację wirusa, wiremię, gorączkę, lokalizację skórną i tworzenie guzków. Replikacja wirusa w makrofagach, komórkach śródbłonka, perycytach i fibroblastach powoduje zapalenie naczyń i limfangitis.1

Zakażenia LSDV wykazują różnorodną gamę manifestacji klinicznych, w tym zarówno tymczasowe, jak i przewlekłe zakażenia podkliniczne, a w ciężkich przypadkach śmierć. Okres inkubacji wirusa po udanej transmisji do gospodarza waha się od 7 do 28 dni.1

LSD początkowo manifestuje się gorączką (40°C do 41,5°C), depresją, zmniejszonym apetytem i zmniejszoną aktywnością fizyczną. W ciągu 5–7 dni pojawiają się liczne dobrze zdefiniowane zmiany skórne (guzki), o średnicy od 2 do 7 cm. Te zmiany, charakteryzujące się papulami i guzkami o płaskich wierzchołkach, wpływają na skórę właściwą i naskórek, okazjonalnie rozszerzając się do hypodermy i rzadko do przyległych mięśni prążkowanych.2

LSDV może utrzymywać się w różnych rezerwuarach, w tym w zmianach skórnych, krwi, strupach, wydzielinach ustnych i donosowych, nasieniu, a czasem w skórze zwierzęcia bez wyraźnych objawów. Jest szeroko rozpowszechniony w kilku tkankach, z bolesnymi guzkami początkowo pojawiającymi się w pobliżu głowy, ust, nosa i oczu, a następnie rozprzestrzeniającymi się do okolicy szyjnej, kończyn, krocza, gruczołu sutkowego i narządów rozrodczych.3

Podczas początkowych faz zakażenia wirusowego, te guzki wykazują wewnętrzne zabarwienie szaro-białe i mogą wydzielać surowicę. Około 14 dni po zakażeniu, guzki mogą rozwinąć centralny rdzeń materiału martwiczego znany jako „sit-fast”. Te martwicze rdzenie zapewniają okazję do wtórnej infekcji bakteryjnej.4

Gdy wrzody tworzą się w zakażonych guzkach, LSDV może inwadować różne płyny ustrojowe, takie jak ślina, wydzieliny donosowe i oczne oraz wydzielina pochwowa. W konsekwencji zakażone bydło często wykazuje znaczne wyniszczenie i kruchość, prowadzące do przedłużonych strat w produktywności i potencjalnych uszkodzeń skóry.5

Guzy a choroby węzłów chłonnych i układu limfatycznego

Ropne zapalenie węzłów chłonnych (Caseous Lymphadenitis) u owiec i kóz jest przykładem zaburzenia, które powoduje tworzenie guzków w węzłach chłonnych. Jest ono powodowane przez C. pseudotuberculosis, który jest gram-dodatnim, fakultatywnym, wewnątrzkomórkowym kokobacylem.1

Wszystkie szczepy produkują egzotoksynę, zwaną fosfolipazą D, która wzmacnia dyseminację bakterii przez uszkadzanie komórek śródbłonka i zwiększanie przepuszczalności naczyń. C. pseudotuberculosis ma drugi czynnik wirulencji, którym jest zewnętrzna powłoka lipidowa, która zapewnia ochronę przed enzymami hydrolitycznymi w fagocytach gospodarza.2

Bakterie replikują się w fagocytach, które następnie pękają i uwalniają bakterie. Trwający proces replikacji bakterii, a następnie przyciągania i następnej śmierci komórek zapalnych, tworzy charakterystyczne ropnie związane z CL.3

Aby ustanowić infekcję, C. pseudotuberculosis musi penetrować skórę lub błony śluzowe. Najczęstszym miejscem wejścia jest skóra po urazie, który może wynikać z strzyżenia, tagowania, obcinania ogona, kastracji lub innych zagrożeń środowiskowych.1

Po wejściu do organizmu bakterie przemieszczają się do węzłów chłonnych poprzez regionalny układ limfatyczny. Wewnętrznie bakterie ustanawiają infekcję nie tylko w węzłach chłonnych, ale także we wnętrznościach. Okres inkubacji waha się od 1 do 3 miesięcy, kulminując w rozwoju otoczkowanych ropni.2

Guzy w praktyce klinicznej

Diagnostyka guzów

Biopsja to usunięcie tkanki w celu zbadania jej pod kątem choroby. Próbki tkanek mogą być pobierane z dowolnej części ciała. Biopsje są wykonywane na kilka różnych sposobów. Niektóre biopsje obejmują usunięcie małej ilości tkanki igłą, podczas gdy inne obejmują chirurgiczne usunięcie całego guzka lub węzła, który budzi podejrzenia.1

Biopsja może być konieczna, gdy badania obrazowe nie mogą jasno zdefiniować nieprawidłowości. Biopsje są często używane do diagnozowania raka, ale mogą pomóc zidentyfikować inne stany, takie jak infekcje oraz zaburzenia zapalne i autoimmunologiczne.2

W niektórych przypadkach ilość tkanki uzyskanej z biopsji igłowej może być niewystarczająca i biopsja może musieć być powtórzona. Rzadko mniej inwazyjne procedury biopsji piersi mogą nie być w stanie wykryć niektórych zmiany lub określić zakres obecnej choroby. Jakiekolwiek procedury kierowane obrazem nie będą mogły być wykorzystane, chyba że obszar nieprawidłowości można zobaczyć.1

Podejście do leczenia guzów

Podejście do leczenia guzów zależy od ich typu i podstawowej przyczyny. Zarządzanie niektórymi guzami (szczególnie niektóre miejsca i wyniki kliniczne) może być użytecznie omówione z konsultantami. Typowym przykładem jest limfadenopatia w szyi. Łagodna patologia może prezentować się w alarmujący sposób z twardymi, ustalonymi i szybko rosnącymi guzkami, które sugerują złośliwość. Pilne skierowanie do dalszego badania jest potrzebne, aby postawić diagnozę i, miejmy nadzieję, złagodzić niepokój.1

Zmiana złośliwa jest bardzo rzadka (podejrzewaj, jeśli jest szybki wzrost, lub jeśli utwardzanie lub unaczynienie występuje). Podejrzenie będzie wzbudzone ogólnie rzecz biorąc przez szybki wzrost i twardą konsystencję tych guzów.2

W przypadku guzków reumatoidalnych, terapie modyfikujące chorobę i terapie biologiczne, w szczególności rytuksymab, wydają się zmniejszać częstość występowania tworzenia guzków. Jeśli mikroguzki rozwijają się podczas przyjmowania metotreksatu, to dodanie hydroksychlorochiny i innych leków modyfikujących chorobę, w tym prednizolonu, może zmniejszyć ich rozmiar. Czasami wstrzyknięcie sterydu do lub tuż pod guzek może zmniejszyć ich rozmiar.1

Jeśli torbiel nie powoduje żadnego bólu, zazwyczaj zalecane leczenie to po prostu monitorowanie, ponieważ torbiele często znikają samoistnie bez dalszej interwencji. Jeśli torbiel powoduje ból lub poważnie ogranicza zakres ruchu, istnieją dwie główne interwencje, które można wykonać: Aspiracja +/- wstrzyknięcie sterydu, chociaż wiąże się to z infekcją i wyższym wskaźnikiem nawrotów; Wycięcie torbieli, usunięcie torebki torbieli wraz z częścią związanej pochewki ścięgna (nawrót jest mniejszy niż w przypadku aspiracji, ale nadal możliwy).1

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 17.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Lipoma Pathology – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK482343/
    Lipomas are defined as a common subcutaneous tumor composed of adipose (fat) cells, often encapsulated by a thin layer of fibrous tissue. […] While the etiology of lipomas is unclear, some studies have shown a genetic link, whereby about two-thirds of lipomas demonstrate genetic abnormalities. […] A possible mechanism of action of lipoma development is post-trauma to the respective area. It has also been theorized that this is true only for traumas that result in necrosis of adipose/fat cells and subsequent local inflammation. These are what are responsible for triggering the lipoma formation. […] A genetic link has been demonstrated that cites that about two-thirds of lipomas exhibit genetic abnormalities. In a subgroup of lipomas, the HMGA2 gene (located on 12q14.3) was involved in tumor pathogenesis.
  • #1 What Is Cancer? – NCI
    https://www.cancer.gov/about-cancer/understanding/what-is-cancer
    Cancer is a disease in which some of the bodys cells grow uncontrollably and spread to other parts of the body. […] Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldnt. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous or not cancerous (benign). […] Cancer is caused by changes to DNA. Most cancer-causing DNA changes occur in sections of DNA called genes. These changes are also called genetic changes. […] A DNA change can cause genes involved in normal cell growth to become oncogenes. Unlike normal genes, oncogenes cannot be turned off, so they cause uncontrolled cell growth. […] In normal cells, tumor suppressor genes prevent cancer by slowing or stopping cell growth. DNA changes that inactivate tumor suppressor genes can lead to uncontrolled cell growth and cancer. […] Cancer cells can break away from the original tumor and travel through the blood or lymph system to distant locations in the body, where they exit the vessels to form additional tumors. This is called metastasis.
  • #1 Nodular Fasciitis: Pathology, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/23510-nodular-fasciitis
    Fasciitis occurs when a genetic rearrangement results in a gene fusion of MYH9 and _USP6 _genes. This genetic mutation only happens in the cells that are part of the nodular fasciitis tumor. […] Nodular fasciitis is completely benign. The tumor may go away over time or after surgery to remove it. Its extremely unlikely to come back. This mass doesnt develop into cancer or increase your cancer risk.
  • #1 Lipoma Benign Lump | Other Conditions | Cancer Research UK
    https://www.cancerresearchuk.org/about-cancer/other-conditions/lipoma
    A lipoma is a non cancerous (benign) lump that forms due to an overgrowth of fat cells. […] Lipomas are not cancer. Cancerous tumours of the fat cells are called liposarcomas. […] We dont know what causes them, but some people develop them because of an inherited faulty gene. This condition is known as familial multiple lipomatosis and is not common. […] Rarely, doctors cant tell for certain whether the lump is a lipoma or not. Lipomas can be confused with malignant (cancerous) tumours, called liposarcomas. […] Your doctor may feel it is best to remove it or take a biopsy so that they can be certain it is a lipoma. […] Lipomas dont usually need removing. But in some cases, your doctor, or you, might want your lipoma removed. […] The removed lipoma should then be sent to the laboratory to be looked at under the microscope.
  • #1 Lumps and Bumps of the Gingiva: A Pathological Miscellany
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6404662/
    Histologically, the mineralizing component consists of trabeculae or drop-like calcifications resembling woven bone or cementum in a background of active cellular stroma. […] The recurrence rate of such lesions is higher than for other forms of fibrous epulis. […] The vascular epulis (syn. pyogenic granuloma) is a reactive vascular lesion, which, in the mouth, is most common on the gingiva. […] These lesions develop as a result of trauma or recurrent irritation, most commonly in females. […] The clinical differential diagnosis includes peripheral giant cell granuloma, as both lesions tend to be vascular in nature. […] The characteristic feature is of a destructive vasculitis. […] Affected vessels show inflammatory cells throughout the wall and these may be associated with vessel obliteration creating areas of necrosis.
  • #1 Granuloma – types, diagnosis and treatment | healthdirect
    https://www.healthdirect.gov.au/granulomas
    A granuloma is a tiny cluster of white blood cells and other tissue. […] They form as a reaction to infections, inflammation, irritants or foreign objects. Granulomas arent cancerous. […] Granulomas form when immune cells clump together and create tiny nodules at the site of the infection or inflammation. […] A granuloma is the body’s way of containing a bacterial, viral or fungal infection, to keep it from spreading (also called a caseating granuloma); isolating irritants or foreign objects (also called a non-caseating granuloma). […] Granulomas can be part of conditions such as: sarcoidosis a non-infectious disease that can cause multiple granulomas in the lungs and other parts of the body; chronic granulomatous disease an inherited immunodeficiency condition that starts in childhood and leads to recurring bacterial and fungal infections; Crohn’s disease and inflammatory bowel disease; rheumatoid arthritis. […] Although granulomas may appear cancerous, they are not they are benign.
  • #1 Painful red lumps on the shins
    https://www.racgp.org.au/afp/2014/september/painful-red-lumps-on-the-shins
    Erythema nodosum is a hypersensitive inflammatory response of subcutaneous fatty tissues to certain antigenic triggers. Classified as septal panniculitis, erythema nodosum is one of the commonest forms of panniculitis. Histologically, there are multiple areas of neutrophilic and eosinophilic infiltration around the blood capillaries and thickening of the septa in the adipose tissues. The formation of macrophage clusters around blood vessels or interlobular septa, known as Mieschers radial granuloma, is a diagnostic marker for erythema nodosum. The exact pathogenesis of erythema nodosum is still unknown. The original hypothesis of circulating immune complexes proposed in the 1970s was refuted in the 1980s. Other theories include mediation via leucocyte activation and reactive oxygen intermediates; increased TNF-production (in sarcoidosis-associated erythema nodosum) and hypersensitivity to oestrogens and progesterone (in pregnancy-induced erythema nodosum). There are numerous triggers for erythema nodosum, although 55% of cases are idiopathic.
  • #1 Fat Necrosis: What It Is, Causes & Treatment
    https://my.clevelandclinic.org/health/diseases/24187-fat-necrosis
    Fat necrosis occurs in your adipose tissue (fat tissue) when its been injured in some way. […] Fat necrosis is a slow, delayed process with several stages. […] As adipose tissue cells begin to die, you may notice changes in the texture or appearance of your skin in the area. […] Fat necrosis can affect anyone who sustains an injury to their fatty tissue. […] Fat necrosis most commonly affects breast tissue, and its more likely the more breast tissue you have. […] Fat necrosis can also occur in other fatty areas such as your abdomen, buttocks and thighs as a result of medical or cosmetic procedures. […] Fat necrosis occurs when injury to your adipose tissue causes cells to die. […] Fat necrosis may cause some procedures, such as breast reconstruction, to fail entirely. […] Fat necrosis can be especially stressful for people who are being treated for cancer, who may have come successfully through radiation and surgery only to find themselves returning to the hospital with complications from those treatments. […] Fat necrosis can usually be diagnosed with radiology, but there are two possible difficulties. […] Fat necrosis isn’t harmful and usually resolves on its own. […] Fat necrosis isn’t harmful, but oil cysts under your skin can resemble cancerous tumors.
  • #1 Lumps and Bumps of the Gingiva: A Pathological Miscellany
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6404662/
    Lesions of the gingivae are amongst the commonest lesions seen in patients and the vast majority are reactive hyperplasias, related to a number of chronic irritant stimuli. […] The purpose of this paper is to discuss the clinical and histological differential diagnoses when presented with a lump on the gingivae, including the approach to diagnosis and diagnostic pitfalls. […] The majority of these lesions are reactive (with varied appearance), but other developmental and neoplastic conditions can also present in the gingiva, giving rise to areas of clinical and histological uncertainty in diagnosis. […] The descriptions below will cover the most salient features of a range of different pathologies of the gingival tissues. […] Histology shows hyperplastic and usually keratinized epithelium overlying nodular fibrous connective tissue.
  • #1 Lumps and Bumps of the Gingiva: A Pathological Miscellany
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6404662/
    The extent of collagenisation and vascularity of the body of the lesion will depend on its maturity and the presence or absence of inflammation. […] The fibroblast component is bland and in most cases comprises fine spindle shaped cells, with most lesions relatively paucicellular. […] However, in some cases, the fibroblasts may be large and stellate in morphology, and occasionally multinucleated, albeit cytologically bland. […] Up to a third of such lesions on the gingiva contain trabeculae of metaplastic bone, particularly those on the maxillary labial gingiva, and which are or have been ulcerated. […] Such lesions are termed peripheral ossifying fibroma. […] The use of this terminology varies geographically, as does the viewpoint that this represents a separate diagnostic entity.
  • #1 Common lumps and bumps on and under the skin: what are they? – Dermatology Research Centre – University of Queensland
    https://dermatology-research.centre.uq.edu.au/blog/2022/04/common-lumps-and-bumps-and-under-skin-what-are-they
    Moles, or naevi, are the most common skin lesions. They are formed by a cluster of melanocytes, the skins pigment-producing cells. […] Moles themselves are harmless, but around 25% of melanomas arise in an existing mole. Many more look like moles in their early stages. […] Having many moles is the strongest predictor of a high melanoma risk, so people with many moles are often advised to have regular skin checks with a dermatologist. […] Seborrhoeic keratoses, sometimes inelegantly called senile warts or barnacles, are another common benign skin lesion. […] If many itchy seborrhoeic keratoses erupt suddenly, it is occasionally a sign of an internal cancer. Very rarely, basal or squamous cell carcinomas arise within a pre-existing seborrhoeic keratosis. […] A cyst is a round lesion made of a capsule filled with keratin (the structural material that makes up the outer layer of our skin), sebum (the oil from our skin), fluid or pus-like material.
  • #1 Ganglion Cyst: Practice Essentials, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/1243454-overview
    Although no definitive etiology has been established, the theory that the ganglion is the degeneration of the mucoid connective tissue, specifically collagen, has dominated since 1893, when Ledderhose described it as such. […] The etiology of the ganglion cyst has been described as an outpouching of synovium; as an irritation of articular tissue, creating a new formation; and, the most common and accepted theory, as a degeneration of connective tissue and cystic space formation. It has also been suggested that degeneration of the connective tissue is caused by an irritation or chronic damage causing the mesenchymal cells or fibroblasts to produce mucin. […] Although ganglion cysts can be unilobulated, they are most often multilobulated, with septa made from connective tissue separating the lobes or cavities. Thornburg pointed out that because there is no epithelial lining of the cyst wall, a ganglion cyst is not a true cyst; because of this histologic observation, the theories of synovial herniation or synovial tumor formation are not supported and may be disputed.
  • #1 Breast lumps pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Breast_lumps_pathophysiology
    Breast development is influenced by different hormones such as estrogen, progesterone, prolactin, and estradiol. The pathophysiology of breast lumps depends on the histological subtypes. Histological findings of breast lumps are different from each other which lead to diagnosis. It is thought that breast lumps are the result of hormonal events and genetic mutations. Estrogen and progesterone may increase risk of benign proliferative disease to 74% and benign breast lesion in post-menopausal women receiving estrogen with or without progesteron for more than 8 years raise by 1.7 fold. Gene mutations are classified into 3 categories based on cancer risk such as BRCA1, BRCA2, TP53 considered as high risk mutations, Homozygous ataxia-telangiectasia, somatic mutation in CHEK2, BRIP1, PALB2 moderate risk mutations, and low risk genes mutation are not determined yet.
  • #1 Fibrocystic breasts – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/fibrocystic-breasts/symptoms-causes/syc-20350438
    Fibrocystic breast changes lead to the development of fluid-filled round or oval sacs, called cysts. The cysts can make breasts feel tender, lumpy or ropy. They feel distinct from other breast tissue. […] The exact cause of fibrocystic breast changes isn’t known, but experts suspect that reproductive hormones especially estrogen play a role. […] Fluctuating hormone levels during the menstrual cycle can cause breast discomfort and areas of lumpy breast tissue that feel tender, sore and swollen. Fibrocystic breast changes tend to be more bothersome before your menstrual period and ease up after your period begins. […] When examined under a microscope, fibrocystic breast tissue includes distinct components such as: fluid-filled round or oval sacs (cysts), a prominence of scar-like fibrous tissue (fibrosis), overgrowth of cells (hyperplasia) lining the milk ducts or milk-producing tissues (lobules) of the breast, enlarged breast lobules (adenosis).
  • #1 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infection initiates a cascade of events including viral replication, viremia, fever, cutaneous localization, and nodule formation. Experimental studies following intradermal viral injection outlined specific timelines for various outcomes: between 4 and 7 days post-infection (DPI), nodules or plaques of 1 to 3 cm appeared at the inoculation site; between 6 and 18 DPI, viral shedding occurred through oral and nasal routes, along with viremia; between 7 and 19 DPI, regional lymphadenopathy and generalized skin nodules developed; and 42 days after fever onset, the virus was detected in semen. Virus replication within macrophages, endothelial cells, pericytes, and fibroblasts resulted in vasculitis and lymphangitis. Due to humoral immune deficiency, lactating cows, newborn calves, and underweight animals are more susceptible to natural infections, while animals that survive after virus exposure develop lifelong immunity. Maternal antibodies provide passive immunity to calves, which can help protect them from infection during the first few months of life. However, once a calf is infected with LSDV, these maternal antibodies can still play a role in modulating the disease’s severity. While they do not prevent the infection itself, maternal antibodies may help reduce the intensity of clinical symptoms and support the calf’s immune response in combating the virus. This protective effect is particularly important in young animals, as their immune systems are still developing. Thus, while maternal antibodies do not prevent infection, they can mitigate the impact of the disease in already infected calves. Infected animals with LSDV typically recover completely, and there are no documented carriers of the virus. Understanding the evolution and clinical manifestations of LSDV includes tracing the progression from the initial signs to subsequent symptoms.
  • #1 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Soft-tissue tumors constitute a large and heterogeneous group of neoplasms. […] However, histomorphologic, immunohistochemical, and experimental data suggest that most, if not all, sarcomas arise from primitive, multipotential mesenchymal cells, which in the course of neoplastic transformation differentiate along one or more lines. […] Although most soft-tissue tumors of various histogenetic types are classified as either benign or malignant, many are of an intermediate nature, which typically implies aggressive local behavior with a low-to-moderate propensity for metastasis. […] Current achievements in the field of soft-tissue tumors are the result of advances in molecular biology, oncogenetics, imaging techniques, immunochemistry, diagnosis by fine-needle aspiration (FNA), surgical reconstruction, radiation therapy, and tissue banking.
  • #1 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Future advances in molecular oncology may further improve diagnostic, prognostic, and treatment protocols for patients with soft-tissue sarcomas. […] Generally, soft-tissue tumors grow centripetally, though some benign tumors (eg, fibrous lesions) may grow longitudinally along tissue planes. […] Once the tumor reaches the anatomic limits of the compartment, the tumor is more likely to breach compartmental boundaries. […] The peripheral portion of the tumor compresses surrounding, normal soft tissue because of centripetal expansile growth. […] A thin layer of tissue called the reactive zone surrounds the compression zone, especially in higher-grade tumors. […] Some extremely aggressive lesions with infiltrative growth patterns, such as childhood rhabdomyosarcoma, may not respect anatomic compartmental boundaries and frequently will invade fascial planes.
  • #1 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Soft-tissue sarcomas have a propensity for local recurrence. […] The pseudocapsule provides surgeons with a more or less obvious plane of dissection; however, such an excision can leave behind microscopic or occasionally gross tumor. […] The addition of postoperative radiation therapy decreases the risk of recurrence associated with a marginal resection. […] The pattern of recurrence generally is predictable, and most tumors destined to recur do so within the first 2-3 years. […] Adjuvant radiation therapy clearly minimizes local recurrence, but its ability to increase overall chances of survival, though likely, is not certain. […] Many patients with high-grade soft-tissue sarcomas, as well as a few with the low-grade type, progress to metastatic disease, even after adequate local control of the primary tumor has been achieved.
  • #1 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Although most patients do not have clinically evident metastases at the time of presentation, they may have occult micrometastases that eventually manifest clinically. […] Good evidence exists suggesting that certain genetic disorders and gene mutations are predisposing factors for some benign and malignant soft-tissue tumors. […] The pathogenetic mechanism is the emergence of radiation-induced genetic mutations that encourage neoplastic transformation. […] An association between exposure to various carcinogens and an increased incidence of soft-tissue tumors has been reported. […] A classic example of an infection-induced soft-tissue tumor is Kaposi sarcoma resulting from human herpesvirus type 8 in patients with human immunodeficiency virus (HIV). […] The relation between trauma and soft-tissue tumors appears to be coincidental.
  • #1 Lipoma: Causes, symptoms, and treatment
    https://www.medicalnewstoday.com/articles/322551
    A lipoma is a lump under the skin that occurs due to an overgrowth of fat cells. […] Experts do not fully understand what causes a lipoma. […] Some people inherit a faulty gene from their parents that can cause one or more lipomas. This is rare and is known as familial multiple lipomatosis. […] Researchers associate lipomas with some medical conditions, including Gardners syndrome, Cowden syndrome, Madelungs disease, and adiposis dolorosa. […] Some lipomas may also result from an injury that involves a substantial impact on the area. […] Lipomas are benign masses of fat cells. […] Lipomas are not the same as liposarcomas. Liposarcomas are a cancerous mass of fat cells. Lipomas cannot turn into liposarcomas, but the two types of tumors can look very similar. […] Fatty tumors can be benign or cancerous. However, most experts agree that lipomas do not usually become cancerous.
  • #1 The Radiology Assistant : Pathology of the Male Breast
    https://radiologyassistant.nl/breast/male-breast/pathology-of-the-male-breast
    Gynecomastia is the most common abnormality in the male breast. Clinically, it presents as a soft mobile tender subareolar mass. Every word in this sentence is critical: soft – mobile – tender – subareolar. So it has to be soft and mobile. It is tender in the acute phase, but not in the chronic phase. Gynecomastia must be subareolar! Any mass that is not subareolar is not gynecomastia. […] Gynecomastia is simultaneous proliferation of ducts and stroma without encapsulation, so it must blend into the surrounding fat tissue. There is no proliferation of lobuli, like there is in women. So you will not see tumors that start in the lobuli, for example lactating adenomas, fibroadenomas, phyllodes tumors, and also invasive lobular carcinomas are extremely rare. […] By definition gynecomastia is 2 cm or more of subareolar tissue in a non obese male. It is a common 'normal’ finding, that is seen in 55% of men at autopsy. The peak incidence is 60 – 69 years. It is significant if it is new or symptomatic. In elderly males gynecomastia makes up 65% of all breast lesions. 25% is carcinoma and 10% are other lesions.
  • #1 Nodular vasculitis
    https://dermnetnz.org/topics/nodular-vasculitis
    Nodular vasculitis refers to a group of poorly defined conditions causing nodules on the legs in which inflamed blood vessels (vasculitis) are found on biopsy. […] The exact cause of nodular vasculitis is unknown but the patchy inflammation in the blood vessels and lymphatics in the deep dermis and subcutaneous fat appears to relate to a slowed circulation. […] Slowing of the flow in the deep vessels can also encourage deposition of bacteria from the bloodstream, including tubercle bacilli, and in some patients, nodular vasculitis is a sign of tuberculosis, when it may be called erythema induratum or Bazin disease. […] Skin biopsy of the nodules reveals panniculitis, with varying degrees of inflammation of the blood vessels and lymphatics in the deep dermis and subcutaneous tissue. […] Painful lumps are usually due to a form of panniculitis and/or vasculitis.
  • #1 Breast lumps pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Breast_lumps_pathophysiology
    It is understood that breast lumps are the result of hormonal events: Prevalence of benign breast lesion in post-menopausal women receiving estrogen with or without progesteron for more than 8 years raise by 1.7 fold. Estrogen and progesterone increase rate of benign proliferative breast disease to 74%. Anti-estrogen drugs such as tamoxifen, decrease prevalence of breast lesions such as adenosis, cysts, hyperplasia, duct ectasia to 28%. […] Although estrogen receptors (ER) and progesterone-receptor (PR) attributed to weak prognosis, they may predict patients’ response to endocrine therapy. Assessment of presence of ER and PR are required in invasive breast cancers. ER-positive result is present in 70% of breast cancers and PR-positive result is present in 60% of breast cancers. […] HER2/neu is a proto-oncogene which involves in breast regulatory pathways such as proliferation, cell motility and invasion. In 10% to 34% of breast cancers, overexpression and amplification of HER2 is reported. In 90% of cases, overexpression, amplification, and surface membrane protein expressions of HER2/neu may be seen.
  • #1 Rheumatoid nodule – Wikipedia
    https://en.wikipedia.org/wiki/Rheumatoid_nodule
    Although the exact process is unknown, there are a few hypotheses for the generation of rheumatoid nodules. It has been observed that rheumatoid nodules frequently form over extensor sites and areas vulnerable to trauma. The trauma causes inflammatory particles to build up and leads to a secondary inflammatory response which ultimately causes fibrin release and necrosis. Another hypothesis suggests that the inflammation of blood vessels activates complement components, which leads to the deposit of rheumatoid factors and fibrin. […] The rheumatoid nodule is the most common cutaneous manifestation of rheumatoid arthritis. Rheumatoid arthritis involves chronic inflammation of synovial membranes, which leads to degradation of articular cartilage and the juxta-articular bone. Inflammation is caused by T cells, B cells, and monocytes when endothelial cells are activated. Neovascularization, the growth of new blood vessels, serves as an additional marker for rheumatoid arthritis. A hyperplastic synovial lining layer can be caused by the expansion of synovial fibroblast and macrophage cells. This expansion of the synovial membrane, sometimes referred to as „pannus”, can lead to bony erosions and cartilage degradation at the site of the cartilage-bone junction in the periarticular bone.
  • #1 Researchers uncover a fundamental mechanism in breast cancer – Institute for Bioengineering of Catalonia
    https://ibecbarcelona.eu/researchers-uncover-a-fundamental-mechanism-in-breast-cancer/
    As every woman knows, an early test for breast cancer is feeling for lumps. What the doctor or patient herself is actually looking for when she does this is one of the first signs of tumor development: an unusual stiffening of the tissue. […] In healthy breast cells, we have shown that the adhesive properties of integrins lead cells to reduce the force they apply to their environment if the tissue is stiffer than normal, says Pere Roca-Cusachs, group leader at IBEC and assistant professor at the University of Barcelona, who led the study. […] However, cancer cells in the breast express a different type of integrin with different adhesive properties. This other integrin leads cells to apply higher forces as tissue stiffness increases, creating a feedback mechanism that can eventually lead to the hard lumps characteristic of breast tumors.
  • #1 Researchers uncover a fundamental mechanism in breast cancer – Institute for Bioengineering of Catalonia
    https://ibecbarcelona.eu/researchers-uncover-a-fundamental-mechanism-in-breast-cancer/
    Our study is the first time ever that a molecular mechanism of rigidity sensing by cells has been described, and its been demonstrated in healthy and unhealthy human breast cells, says Pere. […] This means that mechanical changes induced by altered integrin expression could be a key aspect behind the onset of several diseases. […] If so, this would have an enormous potential for possible therapies designed to prevent malignant alterations in tissue stiffness.
  • #1 Hidradenitis suppurativa: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/hidradenitis-suppurativa/
    Hidradenitis suppurativa, also known as acne inversa, is a chronic skin disease characterized by recurrent boil-like lumps (nodules) under the skin. […] The condition probably results from a combination of genetic and environmental factors. Originally, researchers believed that the disorder was caused by the blockage (occlusion) of specialized sweat glands called apocrine glands. However, recent studies have shown that the condition actually begins with a blockage of hair follicles in areas of the body that also contain a high concentration of apocrine glands (such as the armpits and groin). […] Genetic factors clearly play a role in causing hidradenitis suppurativa. Some cases have been found to result from variants (also known as mutations) in the NCSTN, PSEN1, or PSENEN gene. […] Although little is known about the mechanism, abnormal Notch signaling appears to promote the development of nodules and lead to inflammation in the skin. […] Researchers have studied many other possible risk factors for hidradenitis suppurativa. Obesity and smoking both appear to increase the risk of the disorder, and obesity is also associated with increased severity of signs and symptoms in affected individuals.
  • #1 Hidradenitis suppurativa – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/hidradenitis-suppurativa/symptoms-causes/syc-20352306
    Hidradenitis suppurativa (hi-drad-uh-NIE-tis sup-yoo-ruh-TIE-vuh), also known as acne inversa, is a condition that causes small, painful lumps to form under the skin. The lumps usually develop in areas where your skin rubs together, such as the armpits, groin, buttocks and breasts. The lumps heal slowly, recur, and can lead to tunnels under the skin and scarring. […] Hidradenitis suppurativa develops when hair follicles become blocked, but why this blockage occurs isn’t known. Experts think it could be connected to hormones, genetic predisposition, cigarette smoking or excess weight. […] The condition occurs most in Black people, possibly due to genetic factors. […] Persistent and severe hidradenitis suppurativa can cause complications, including: […] Squamous cell carcinoma has been reported with long-term hidradenitis suppurativa, particularly in people whose condition involves the perianal area. This area consists of the tissues around the anus. […] Hidradenitis suppurativa is more common and severe in people who are overweight. It also has an association with severe acne, arthritis, diabetes, metabolic syndrome and inflammatory bowel disease.
  • #1 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infections display a diverse array of clinical manifestations, including both temporary and chronic subclinical infections, and death in severe cases. The virus’s incubation period after successful transmission to the host varies from 7 to 28 days. LSD initially manifests with fever (40 °C to 41.5 °C), depression, decreased appetite, and reduced physical activity. Within 5–7 days, numerous well-defined skin lesions (nodules) appear, ranging from 2 to 7 cm in diameter. These lesions, characterized by flat-topped papules and nodules, affect the dermis and epidermis, occasionally extending to the hypodermis and rarely to the adjacent striated muscle. LSDV can persist in various reservoirs, including skin lesions, blood, scabs, oral and nasal secretions, semen, and sometimes in animal skin without apparent symptoms. It is widely distributed across several tissues, with painful nodules initially appearing near the head, mouth, nose, and eyes, then spreading to the cervical region, extremities, perineum, mammary gland, and reproductive organs. During the initial phases of viral infection, these nodules exhibit a grayish-white internal coloration and may secrete serum. Around 14 days post-infection, nodules may develop a central core of necrotic material known as the “sit-fast.” These necrotic cores provide an opportunity for secondary bacterial infection. As ulcers form in the infected nodules, LSDV can invade various body fluids, such as saliva, nasal and ocular secretions, and vaginal discharge. Consequently, infected bovines often show significant emaciation and fragility, leading to prolonged productivity losses and potential skin damage.
  • #1 Caseous Lymphadenitis of Sheep and Goats – Circulatory System – Merck Veterinary Manual
    https://www.merckvetmanual.com/circulatory-system/lymphadenitis-and-lymphangitis-of-large-animals/caseous-lymphadenitis-of-sheep-and-goats
    C pseudotuberculosis is a gram-positive, facultative, intracellular coccobacillus. Two biotypes have been identified based on the ability of the bacteria to reduce nitrate: a nitrate-negative group that infects sheep and goats, and a nitrate-positive group that infects horses. […] All strains produce an exotoxin, called phospholipase D, that enhances dissemination of the bacteria by damaging endothelial cells and increasing vascular permeability. […] C pseudotuberculosis has a second virulence factor, which is an external lipid coat that provides protection from hydrolytic enzymes in host phagocytes. The bacteria replicate in the phagocytes, which then rupture and release the bacteria. The ongoing process of bacterial replication, followed by attraction and subsequent death of inflammatory cells, forms the characteristic abscesses associated with CL.
  • #1 Caseous Lymphadenitis of Sheep and Goats – Circulatory System – Merck Veterinary Manual
    https://www.merckvetmanual.com/circulatory-system/lymphadenitis-and-lymphangitis-of-large-animals/caseous-lymphadenitis-of-sheep-and-goats
    To establish infection, C pseudotuberculosis must penetrate skin or mucous membranes. The most common site of entry is the skin after an injury that may result from shearing, tagging, tail docking, castration, or other environmental hazards. […] After entering the body, the bacteria move to the lymph nodes via the regional draining lymphatic system. Internally, the bacteria establish infection not only in the lymph nodes but also in the viscera. The incubation period varies from 1 to 3 months, culminating in the development of encapsulated abscesses. […] C pseudotuberculosis is hardy in the environment and can survive on fomites such as bedding and wood for 2 months and in soil for 8 months. The presence of organic material, shade, and moisture enhance survival of the organism.
  • #1 Biopsy Overview
    https://www.radiologyinfo.org/en/info/biopgen
    A biopsy is the removal of tissue to examine it for disease. The tissue samples can be taken from any part of the body. Biopsies are performed in several different ways. Some biopsies involve removing a small amount of tissue with a needle while others involve surgically removing an entire lump, or nodule, that is suspicious. […] A biopsy may be necessary when imaging exams cannot clearly define the abnormality. […] Biopsies are frequently used to diagnose cancer, but they can help identify other conditions such as infections and inflammatory and autoimmune disorders. […] Abdominal biopsy is used to diagnose whether a lump in the abdomen is cancerous or benign. […] Bone biopsy is used to diagnose cancer or infection in the bones. […] Breast biopsy is used to determine if a lump in the breast is cancerous or benign.
  • #1 Biopsy Overview
    https://www.radiologyinfo.org/en/info/biopgen
    Testicular biopsy is used to determine underlying causes of male infertility. […] Thyroid biopsy is used to find the cause of a nodule in the thyroid gland. […] In some cases, the amount of tissue obtained from a needle biopsy may not be sufficient and the biopsy may have to be repeated. […] Rarely, less invasive breast biopsy procedures may be unable to detect some lesions or determine the extent of disease present. […] Any imaging-guided procedure will not be able to be used unless the area of abnormality can be seen.
  • #1 Lumps: Types, Causes, and Treatment | Doctor
    https://patient.info/doctor/lumps
    The most likely diagnoses will be determined by the features of the lump, the anatomical site and the suspected aetiology. […] This will depend on a number of factors such as the site of the lump, the features of the lump and, ultimately, the suspected diagnosis. […] The management of some lumps (particularly some sites and clinical findings) may be usefully discussed with consultant colleagues. A typical example is lymphadenopathy in the neck. Benign pathology can present in an alarming fashion with hard, fixed and rapidly growing lumps which suggest malignancy. Urgent referral for further investigation is needed to make a diagnosis and, hopefully, allay anxiety. […] Malignant change is very rare (suspect if there is rapid growth, or if hardening or vascularisation occurs). […] Suspicion will be aroused generally speaking by rapid growth and the hard consistency of these tumours.
  • #1 Rheumatoid nodules in rheumatoid arthritis (RA) | NRAS
    https://nras.org.uk/resource/rheumatoid-nodules/
    Rheumatoid nodules are firm lumps that appear under the skin in up to 20% of patients with RA. […] Rheumatoid nodules are very firm and are made of inflammatory tissue but under the microscope show intense inflammatory changes that are different from the ones that are found within the joints. This explains why disease-modifying drugs and biological therapies may not reduce the size of the nodules even though they may have an excellent effect on controlling joint disease. […] Combination disease-modifying therapies and the biological therapies, in particular rituximab, seem to have reduced the incidence of nodule formation. […] If micronodules develop while on methotrexate, then the addition of hydroxychloroquine and other disease-modifying drugs, including prednisolone, may reduce their size. […] Occasionally, injection of steroid into or just under the nodule can reduce their size.
  • #1 Ganglionic Cysts – Pathophysiology – Management – TeachMeSurgery
    https://teachmesurgery.com/orthopaedic/wrist-and-hand/ganglionic-cysts/
    Most ganglion cysts can be diagnosed clinically. A plain film radiograph may assist in ruling out osteoarthritis or bone malignancies as differentials if suspected. […] If the cyst does not cause any pain, the usual recommended treatment is to simply monitor, as cysts often disappear spontaneously without further intervention. […] If the cyst causes pain or severely limits range of movement, there are two main interventions that can be performed: Aspiration +/- steroid injection, although this is associated with infection and a higher rate of recurrence; Cyst excision, removing the cyst capsule along with a portion of the associated tendon sheath (recurrence is less than with aspiration, but still possible). […] Ganglionic cysts are non-cancerous soft tissue lumps that occur along any joint or tendon. They appear as smooth spherical painless lumps, that are soft and transilluminate on examination. Diagnosis is clinical and most cases will be managed conservatively, intervention only indicated in symptomatic cases or those limiting range of movement.
  • #2 Lumps and Bumps of the Gingiva: A Pathological Miscellany
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6404662/
    Lesions of the gingivae are amongst the commonest lesions seen in patients and the vast majority are reactive hyperplasias, related to a number of chronic irritant stimuli. […] The purpose of this paper is to discuss the clinical and histological differential diagnoses when presented with a lump on the gingivae, including the approach to diagnosis and diagnostic pitfalls. […] The majority of these lesions are reactive (with varied appearance), but other developmental and neoplastic conditions can also present in the gingiva, giving rise to areas of clinical and histological uncertainty in diagnosis. […] The descriptions below will cover the most salient features of a range of different pathologies of the gingival tissues. […] Histology shows hyperplastic and usually keratinized epithelium overlying nodular fibrous connective tissue.
  • #2 Lipoma: Causes, symptoms, and treatment
    https://www.medicalnewstoday.com/articles/322551
    A lipoma is a lump under the skin that occurs due to an overgrowth of fat cells. […] Experts do not fully understand what causes a lipoma. […] Some people inherit a faulty gene from their parents that can cause one or more lipomas. This is rare and is known as familial multiple lipomatosis. […] Researchers associate lipomas with some medical conditions, including Gardners syndrome, Cowden syndrome, Madelungs disease, and adiposis dolorosa. […] Some lipomas may also result from an injury that involves a substantial impact on the area. […] Lipomas are benign masses of fat cells. […] Lipomas are not the same as liposarcomas. Liposarcomas are a cancerous mass of fat cells. Lipomas cannot turn into liposarcomas, but the two types of tumors can look very similar. […] Fatty tumors can be benign or cancerous. However, most experts agree that lipomas do not usually become cancerous.
  • #2 Lumps and Bumps of the Gingiva: A Pathological Miscellany
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6404662/
    Histologically, the mineralizing component consists of trabeculae or drop-like calcifications resembling woven bone or cementum in a background of active cellular stroma. […] The recurrence rate of such lesions is higher than for other forms of fibrous epulis. […] The vascular epulis (syn. pyogenic granuloma) is a reactive vascular lesion, which, in the mouth, is most common on the gingiva. […] These lesions develop as a result of trauma or recurrent irritation, most commonly in females. […] The clinical differential diagnosis includes peripheral giant cell granuloma, as both lesions tend to be vascular in nature. […] The characteristic feature is of a destructive vasculitis. […] Affected vessels show inflammatory cells throughout the wall and these may be associated with vessel obliteration creating areas of necrosis.
  • #2 Lumps and Bumps of the Gingiva: A Pathological Miscellany
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6404662/
    The extent of collagenisation and vascularity of the body of the lesion will depend on its maturity and the presence or absence of inflammation. […] The fibroblast component is bland and in most cases comprises fine spindle shaped cells, with most lesions relatively paucicellular. […] However, in some cases, the fibroblasts may be large and stellate in morphology, and occasionally multinucleated, albeit cytologically bland. […] Up to a third of such lesions on the gingiva contain trabeculae of metaplastic bone, particularly those on the maxillary labial gingiva, and which are or have been ulcerated. […] Such lesions are termed peripheral ossifying fibroma. […] The use of this terminology varies geographically, as does the viewpoint that this represents a separate diagnostic entity.
  • #2 Common lumps and bumps on and under the skin: what are they? – Dermatology Research Centre – University of Queensland
    https://dermatology-research.centre.uq.edu.au/blog/2022/04/common-lumps-and-bumps-and-under-skin-what-are-they
    Some cysts form when a hair follicle, sweat duct or mucous gland becomes blocked and fluid builds up behind the blockage. […] Haemangiomas are another benign, usually painless skin lesion, formed from an excessive growth of blood vessels in the skin. […] Rarely, angiomas mimic amelanotic (non-pigmented) nodular melanomas. These need to be excised for further testing. […] Dermatofibromas are caused by a benign proliferation of fibroblast cells (the main cells in connective tissue), perhaps in response to a mild skin injury, but its not clear why this happens. […] Like seborrhoeic keratoses, dermatofibromas are harmless but can be annoying. […] Lipomas are actually slow-growing tumours of fat cells surrounded by a fibrous capsule. […] Some lipomas might arise after a blunt injury to the site, but the mechanism causing that is not well understood. […] Any lump, bump or lesion on your skin is worth showing to a doctor if its worrying you, but there are some red flags that should prompt you to make the appointment sooner rather than later.
  • #2 Ganglion Cyst: Practice Essentials, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/1243454-overview
    Although no definitive etiology has been established, the theory that the ganglion is the degeneration of the mucoid connective tissue, specifically collagen, has dominated since 1893, when Ledderhose described it as such. […] The etiology of the ganglion cyst has been described as an outpouching of synovium; as an irritation of articular tissue, creating a new formation; and, the most common and accepted theory, as a degeneration of connective tissue and cystic space formation. It has also been suggested that degeneration of the connective tissue is caused by an irritation or chronic damage causing the mesenchymal cells or fibroblasts to produce mucin. […] Although ganglion cysts can be unilobulated, they are most often multilobulated, with septa made from connective tissue separating the lobes or cavities. Thornburg pointed out that because there is no epithelial lining of the cyst wall, a ganglion cyst is not a true cyst; because of this histologic observation, the theories of synovial herniation or synovial tumor formation are not supported and may be disputed.
  • #2 Breast lumps pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Breast_lumps_pathophysiology
    Breast development is influenced by different hormones such as estrogen, progesterone, prolactin, and estradiol. The pathophysiology of breast lumps depends on the histological subtypes. Histological findings of breast lumps are different from each other which lead to diagnosis. It is thought that breast lumps are the result of hormonal events and genetic mutations. Estrogen and progesterone may increase risk of benign proliferative disease to 74% and benign breast lesion in post-menopausal women receiving estrogen with or without progesteron for more than 8 years raise by 1.7 fold. Gene mutations are classified into 3 categories based on cancer risk such as BRCA1, BRCA2, TP53 considered as high risk mutations, Homozygous ataxia-telangiectasia, somatic mutation in CHEK2, BRIP1, PALB2 moderate risk mutations, and low risk genes mutation are not determined yet.
  • #2 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infection initiates a cascade of events including viral replication, viremia, fever, cutaneous localization, and nodule formation. Experimental studies following intradermal viral injection outlined specific timelines for various outcomes: between 4 and 7 days post-infection (DPI), nodules or plaques of 1 to 3 cm appeared at the inoculation site; between 6 and 18 DPI, viral shedding occurred through oral and nasal routes, along with viremia; between 7 and 19 DPI, regional lymphadenopathy and generalized skin nodules developed; and 42 days after fever onset, the virus was detected in semen. Virus replication within macrophages, endothelial cells, pericytes, and fibroblasts resulted in vasculitis and lymphangitis. Due to humoral immune deficiency, lactating cows, newborn calves, and underweight animals are more susceptible to natural infections, while animals that survive after virus exposure develop lifelong immunity. Maternal antibodies provide passive immunity to calves, which can help protect them from infection during the first few months of life. However, once a calf is infected with LSDV, these maternal antibodies can still play a role in modulating the disease’s severity. While they do not prevent the infection itself, maternal antibodies may help reduce the intensity of clinical symptoms and support the calf’s immune response in combating the virus. This protective effect is particularly important in young animals, as their immune systems are still developing. Thus, while maternal antibodies do not prevent infection, they can mitigate the impact of the disease in already infected calves. Infected animals with LSDV typically recover completely, and there are no documented carriers of the virus. Understanding the evolution and clinical manifestations of LSDV includes tracing the progression from the initial signs to subsequent symptoms.
  • #2 What Is Cancer? – NCI
    https://www.cancer.gov/about-cancer/understanding/what-is-cancer
    Cancer is a disease in which some of the bodys cells grow uncontrollably and spread to other parts of the body. […] Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldnt. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous or not cancerous (benign). […] Cancer is caused by changes to DNA. Most cancer-causing DNA changes occur in sections of DNA called genes. These changes are also called genetic changes. […] A DNA change can cause genes involved in normal cell growth to become oncogenes. Unlike normal genes, oncogenes cannot be turned off, so they cause uncontrolled cell growth. […] In normal cells, tumor suppressor genes prevent cancer by slowing or stopping cell growth. DNA changes that inactivate tumor suppressor genes can lead to uncontrolled cell growth and cancer. […] Cancer cells can break away from the original tumor and travel through the blood or lymph system to distant locations in the body, where they exit the vessels to form additional tumors. This is called metastasis.
  • #2 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Soft-tissue tumors constitute a large and heterogeneous group of neoplasms. […] However, histomorphologic, immunohistochemical, and experimental data suggest that most, if not all, sarcomas arise from primitive, multipotential mesenchymal cells, which in the course of neoplastic transformation differentiate along one or more lines. […] Although most soft-tissue tumors of various histogenetic types are classified as either benign or malignant, many are of an intermediate nature, which typically implies aggressive local behavior with a low-to-moderate propensity for metastasis. […] Current achievements in the field of soft-tissue tumors are the result of advances in molecular biology, oncogenetics, imaging techniques, immunochemistry, diagnosis by fine-needle aspiration (FNA), surgical reconstruction, radiation therapy, and tissue banking.
  • #2 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Future advances in molecular oncology may further improve diagnostic, prognostic, and treatment protocols for patients with soft-tissue sarcomas. […] Generally, soft-tissue tumors grow centripetally, though some benign tumors (eg, fibrous lesions) may grow longitudinally along tissue planes. […] Once the tumor reaches the anatomic limits of the compartment, the tumor is more likely to breach compartmental boundaries. […] The peripheral portion of the tumor compresses surrounding, normal soft tissue because of centripetal expansile growth. […] A thin layer of tissue called the reactive zone surrounds the compression zone, especially in higher-grade tumors. […] Some extremely aggressive lesions with infiltrative growth patterns, such as childhood rhabdomyosarcoma, may not respect anatomic compartmental boundaries and frequently will invade fascial planes.
  • #2 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Soft-tissue sarcomas have a propensity for local recurrence. […] The pseudocapsule provides surgeons with a more or less obvious plane of dissection; however, such an excision can leave behind microscopic or occasionally gross tumor. […] The addition of postoperative radiation therapy decreases the risk of recurrence associated with a marginal resection. […] The pattern of recurrence generally is predictable, and most tumors destined to recur do so within the first 2-3 years. […] Adjuvant radiation therapy clearly minimizes local recurrence, but its ability to increase overall chances of survival, though likely, is not certain. […] Many patients with high-grade soft-tissue sarcomas, as well as a few with the low-grade type, progress to metastatic disease, even after adequate local control of the primary tumor has been achieved.
  • #2 Lipoma Benign Lump | Other Conditions | Cancer Research UK
    https://www.cancerresearchuk.org/about-cancer/other-conditions/lipoma
    A lipoma is a non cancerous (benign) lump that forms due to an overgrowth of fat cells. […] Lipomas are not cancer. Cancerous tumours of the fat cells are called liposarcomas. […] We dont know what causes them, but some people develop them because of an inherited faulty gene. This condition is known as familial multiple lipomatosis and is not common. […] Rarely, doctors cant tell for certain whether the lump is a lipoma or not. Lipomas can be confused with malignant (cancerous) tumours, called liposarcomas. […] Your doctor may feel it is best to remove it or take a biopsy so that they can be certain it is a lipoma. […] Lipomas dont usually need removing. But in some cases, your doctor, or you, might want your lipoma removed. […] The removed lipoma should then be sent to the laboratory to be looked at under the microscope.
  • #2 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Although most patients do not have clinically evident metastases at the time of presentation, they may have occult micrometastases that eventually manifest clinically. […] Good evidence exists suggesting that certain genetic disorders and gene mutations are predisposing factors for some benign and malignant soft-tissue tumors. […] The pathogenetic mechanism is the emergence of radiation-induced genetic mutations that encourage neoplastic transformation. […] An association between exposure to various carcinogens and an increased incidence of soft-tissue tumors has been reported. […] A classic example of an infection-induced soft-tissue tumor is Kaposi sarcoma resulting from human herpesvirus type 8 in patients with human immunodeficiency virus (HIV). […] The relation between trauma and soft-tissue tumors appears to be coincidental.
  • #2 Nodular vasculitis
    https://dermnetnz.org/topics/nodular-vasculitis
    Nodular vasculitis refers to a group of poorly defined conditions causing nodules on the legs in which inflamed blood vessels (vasculitis) are found on biopsy. […] The exact cause of nodular vasculitis is unknown but the patchy inflammation in the blood vessels and lymphatics in the deep dermis and subcutaneous fat appears to relate to a slowed circulation. […] Slowing of the flow in the deep vessels can also encourage deposition of bacteria from the bloodstream, including tubercle bacilli, and in some patients, nodular vasculitis is a sign of tuberculosis, when it may be called erythema induratum or Bazin disease. […] Skin biopsy of the nodules reveals panniculitis, with varying degrees of inflammation of the blood vessels and lymphatics in the deep dermis and subcutaneous tissue. […] Painful lumps are usually due to a form of panniculitis and/or vasculitis.
  • #2 Breast lumps pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Breast_lumps_pathophysiology
    It is understood that breast lumps are the result of hormonal events: Prevalence of benign breast lesion in post-menopausal women receiving estrogen with or without progesteron for more than 8 years raise by 1.7 fold. Estrogen and progesterone increase rate of benign proliferative breast disease to 74%. Anti-estrogen drugs such as tamoxifen, decrease prevalence of breast lesions such as adenosis, cysts, hyperplasia, duct ectasia to 28%. […] Although estrogen receptors (ER) and progesterone-receptor (PR) attributed to weak prognosis, they may predict patients’ response to endocrine therapy. Assessment of presence of ER and PR are required in invasive breast cancers. ER-positive result is present in 70% of breast cancers and PR-positive result is present in 60% of breast cancers. […] HER2/neu is a proto-oncogene which involves in breast regulatory pathways such as proliferation, cell motility and invasion. In 10% to 34% of breast cancers, overexpression and amplification of HER2 is reported. In 90% of cases, overexpression, amplification, and surface membrane protein expressions of HER2/neu may be seen.
  • #2 Rheumatoid nodule – Wikipedia
    https://en.wikipedia.org/wiki/Rheumatoid_nodule
    Although the exact process is unknown, there are a few hypotheses for the generation of rheumatoid nodules. It has been observed that rheumatoid nodules frequently form over extensor sites and areas vulnerable to trauma. The trauma causes inflammatory particles to build up and leads to a secondary inflammatory response which ultimately causes fibrin release and necrosis. Another hypothesis suggests that the inflammation of blood vessels activates complement components, which leads to the deposit of rheumatoid factors and fibrin. […] The rheumatoid nodule is the most common cutaneous manifestation of rheumatoid arthritis. Rheumatoid arthritis involves chronic inflammation of synovial membranes, which leads to degradation of articular cartilage and the juxta-articular bone. Inflammation is caused by T cells, B cells, and monocytes when endothelial cells are activated. Neovascularization, the growth of new blood vessels, serves as an additional marker for rheumatoid arthritis. A hyperplastic synovial lining layer can be caused by the expansion of synovial fibroblast and macrophage cells. This expansion of the synovial membrane, sometimes referred to as „pannus”, can lead to bony erosions and cartilage degradation at the site of the cartilage-bone junction in the periarticular bone.
  • #2 Researchers uncover a fundamental mechanism in breast cancer – Institute for Bioengineering of Catalonia
    https://ibecbarcelona.eu/researchers-uncover-a-fundamental-mechanism-in-breast-cancer/
    As every woman knows, an early test for breast cancer is feeling for lumps. What the doctor or patient herself is actually looking for when she does this is one of the first signs of tumor development: an unusual stiffening of the tissue. […] In healthy breast cells, we have shown that the adhesive properties of integrins lead cells to reduce the force they apply to their environment if the tissue is stiffer than normal, says Pere Roca-Cusachs, group leader at IBEC and assistant professor at the University of Barcelona, who led the study. […] However, cancer cells in the breast express a different type of integrin with different adhesive properties. This other integrin leads cells to apply higher forces as tissue stiffness increases, creating a feedback mechanism that can eventually lead to the hard lumps characteristic of breast tumors.
  • #2 Researchers uncover a fundamental mechanism in breast cancer – Institute for Bioengineering of Catalonia
    https://ibecbarcelona.eu/researchers-uncover-a-fundamental-mechanism-in-breast-cancer/
    Our study is the first time ever that a molecular mechanism of rigidity sensing by cells has been described, and its been demonstrated in healthy and unhealthy human breast cells, says Pere. […] This means that mechanical changes induced by altered integrin expression could be a key aspect behind the onset of several diseases. […] If so, this would have an enormous potential for possible therapies designed to prevent malignant alterations in tissue stiffness.
  • #2 Hidradenitis suppurativa: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/hidradenitis-suppurativa/
    Hidradenitis suppurativa, also known as acne inversa, is a chronic skin disease characterized by recurrent boil-like lumps (nodules) under the skin. […] The condition probably results from a combination of genetic and environmental factors. Originally, researchers believed that the disorder was caused by the blockage (occlusion) of specialized sweat glands called apocrine glands. However, recent studies have shown that the condition actually begins with a blockage of hair follicles in areas of the body that also contain a high concentration of apocrine glands (such as the armpits and groin). […] Genetic factors clearly play a role in causing hidradenitis suppurativa. Some cases have been found to result from variants (also known as mutations) in the NCSTN, PSEN1, or PSENEN gene. […] Although little is known about the mechanism, abnormal Notch signaling appears to promote the development of nodules and lead to inflammation in the skin. […] Researchers have studied many other possible risk factors for hidradenitis suppurativa. Obesity and smoking both appear to increase the risk of the disorder, and obesity is also associated with increased severity of signs and symptoms in affected individuals.
  • #2 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infections display a diverse array of clinical manifestations, including both temporary and chronic subclinical infections, and death in severe cases. The virus’s incubation period after successful transmission to the host varies from 7 to 28 days. LSD initially manifests with fever (40 °C to 41.5 °C), depression, decreased appetite, and reduced physical activity. Within 5–7 days, numerous well-defined skin lesions (nodules) appear, ranging from 2 to 7 cm in diameter. These lesions, characterized by flat-topped papules and nodules, affect the dermis and epidermis, occasionally extending to the hypodermis and rarely to the adjacent striated muscle. LSDV can persist in various reservoirs, including skin lesions, blood, scabs, oral and nasal secretions, semen, and sometimes in animal skin without apparent symptoms. It is widely distributed across several tissues, with painful nodules initially appearing near the head, mouth, nose, and eyes, then spreading to the cervical region, extremities, perineum, mammary gland, and reproductive organs. During the initial phases of viral infection, these nodules exhibit a grayish-white internal coloration and may secrete serum. Around 14 days post-infection, nodules may develop a central core of necrotic material known as the “sit-fast.” These necrotic cores provide an opportunity for secondary bacterial infection. As ulcers form in the infected nodules, LSDV can invade various body fluids, such as saliva, nasal and ocular secretions, and vaginal discharge. Consequently, infected bovines often show significant emaciation and fragility, leading to prolonged productivity losses and potential skin damage.
  • #2 Caseous Lymphadenitis of Sheep and Goats – Circulatory System – Merck Veterinary Manual
    https://www.merckvetmanual.com/circulatory-system/lymphadenitis-and-lymphangitis-of-large-animals/caseous-lymphadenitis-of-sheep-and-goats
    C pseudotuberculosis is a gram-positive, facultative, intracellular coccobacillus. Two biotypes have been identified based on the ability of the bacteria to reduce nitrate: a nitrate-negative group that infects sheep and goats, and a nitrate-positive group that infects horses. […] All strains produce an exotoxin, called phospholipase D, that enhances dissemination of the bacteria by damaging endothelial cells and increasing vascular permeability. […] C pseudotuberculosis has a second virulence factor, which is an external lipid coat that provides protection from hydrolytic enzymes in host phagocytes. The bacteria replicate in the phagocytes, which then rupture and release the bacteria. The ongoing process of bacterial replication, followed by attraction and subsequent death of inflammatory cells, forms the characteristic abscesses associated with CL.
  • #2 Caseous Lymphadenitis of Sheep and Goats – Circulatory System – Merck Veterinary Manual
    https://www.merckvetmanual.com/circulatory-system/lymphadenitis-and-lymphangitis-of-large-animals/caseous-lymphadenitis-of-sheep-and-goats
    To establish infection, C pseudotuberculosis must penetrate skin or mucous membranes. The most common site of entry is the skin after an injury that may result from shearing, tagging, tail docking, castration, or other environmental hazards. […] After entering the body, the bacteria move to the lymph nodes via the regional draining lymphatic system. Internally, the bacteria establish infection not only in the lymph nodes but also in the viscera. The incubation period varies from 1 to 3 months, culminating in the development of encapsulated abscesses. […] C pseudotuberculosis is hardy in the environment and can survive on fomites such as bedding and wood for 2 months and in soil for 8 months. The presence of organic material, shade, and moisture enhance survival of the organism.
  • #2 Biopsy Overview
    https://www.radiologyinfo.org/en/info/biopgen
    A biopsy is the removal of tissue to examine it for disease. The tissue samples can be taken from any part of the body. Biopsies are performed in several different ways. Some biopsies involve removing a small amount of tissue with a needle while others involve surgically removing an entire lump, or nodule, that is suspicious. […] A biopsy may be necessary when imaging exams cannot clearly define the abnormality. […] Biopsies are frequently used to diagnose cancer, but they can help identify other conditions such as infections and inflammatory and autoimmune disorders. […] Abdominal biopsy is used to diagnose whether a lump in the abdomen is cancerous or benign. […] Bone biopsy is used to diagnose cancer or infection in the bones. […] Breast biopsy is used to determine if a lump in the breast is cancerous or benign.
  • #2 Lumps: Types, Causes, and Treatment | Doctor
    https://patient.info/doctor/lumps
    The most likely diagnoses will be determined by the features of the lump, the anatomical site and the suspected aetiology. […] This will depend on a number of factors such as the site of the lump, the features of the lump and, ultimately, the suspected diagnosis. […] The management of some lumps (particularly some sites and clinical findings) may be usefully discussed with consultant colleagues. A typical example is lymphadenopathy in the neck. Benign pathology can present in an alarming fashion with hard, fixed and rapidly growing lumps which suggest malignancy. Urgent referral for further investigation is needed to make a diagnosis and, hopefully, allay anxiety. […] Malignant change is very rare (suspect if there is rapid growth, or if hardening or vascularisation occurs). […] Suspicion will be aroused generally speaking by rapid growth and the hard consistency of these tumours.
  • #3
    https://link.springer.com/article/10.1007/s12105-019-01000-w
    Lesions of the gingivae are amongst the commonest lesions seen in patients and the vast majority are reactive hyperplasias, related to a number of chronic irritant stimuli. […] The majority of these lesions are reactive (with varied appearance), but other developmental and neoplastic conditions can also present in the gingiva, giving rise to areas of clinical and histological uncertainty in diagnosis. […] The clinical differential diagnosis most often includes other reactive lesions of the gingiva including pyogenic granuloma and peripheral giant cell granuloma. […] Up to a third of such lesions on the gingiva contain trabeculae of metaplastic bone, particularly those on the maxillary labial gingiva, and which are or have been ulcerated. […] The vascular epulis (syn. pyogenic granuloma) is a reactive vascular lesion, which, in the mouth, is most common on the gingiva.
  • #3 Ganglion Cyst: Practice Essentials, Anatomy, Pathophysiology
    https://emedicine.medscape.com/article/1243454-overview
    Although no definitive etiology has been established, the theory that the ganglion is the degeneration of the mucoid connective tissue, specifically collagen, has dominated since 1893, when Ledderhose described it as such. […] The etiology of the ganglion cyst has been described as an outpouching of synovium; as an irritation of articular tissue, creating a new formation; and, the most common and accepted theory, as a degeneration of connective tissue and cystic space formation. It has also been suggested that degeneration of the connective tissue is caused by an irritation or chronic damage causing the mesenchymal cells or fibroblasts to produce mucin. […] Although ganglion cysts can be unilobulated, they are most often multilobulated, with septa made from connective tissue separating the lobes or cavities. Thornburg pointed out that because there is no epithelial lining of the cyst wall, a ganglion cyst is not a true cyst; because of this histologic observation, the theories of synovial herniation or synovial tumor formation are not supported and may be disputed.
  • #3 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infection initiates a cascade of events including viral replication, viremia, fever, cutaneous localization, and nodule formation. Experimental studies following intradermal viral injection outlined specific timelines for various outcomes: between 4 and 7 days post-infection (DPI), nodules or plaques of 1 to 3 cm appeared at the inoculation site; between 6 and 18 DPI, viral shedding occurred through oral and nasal routes, along with viremia; between 7 and 19 DPI, regional lymphadenopathy and generalized skin nodules developed; and 42 days after fever onset, the virus was detected in semen. Virus replication within macrophages, endothelial cells, pericytes, and fibroblasts resulted in vasculitis and lymphangitis. Due to humoral immune deficiency, lactating cows, newborn calves, and underweight animals are more susceptible to natural infections, while animals that survive after virus exposure develop lifelong immunity. Maternal antibodies provide passive immunity to calves, which can help protect them from infection during the first few months of life. However, once a calf is infected with LSDV, these maternal antibodies can still play a role in modulating the disease’s severity. While they do not prevent the infection itself, maternal antibodies may help reduce the intensity of clinical symptoms and support the calf’s immune response in combating the virus. This protective effect is particularly important in young animals, as their immune systems are still developing. Thus, while maternal antibodies do not prevent infection, they can mitigate the impact of the disease in already infected calves. Infected animals with LSDV typically recover completely, and there are no documented carriers of the virus. Understanding the evolution and clinical manifestations of LSDV includes tracing the progression from the initial signs to subsequent symptoms.
  • #3 What Is Cancer? – NCI
    https://www.cancer.gov/about-cancer/understanding/what-is-cancer
    Cancer is a disease in which some of the bodys cells grow uncontrollably and spread to other parts of the body. […] Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldnt. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous or not cancerous (benign). […] Cancer is caused by changes to DNA. Most cancer-causing DNA changes occur in sections of DNA called genes. These changes are also called genetic changes. […] A DNA change can cause genes involved in normal cell growth to become oncogenes. Unlike normal genes, oncogenes cannot be turned off, so they cause uncontrolled cell growth. […] In normal cells, tumor suppressor genes prevent cancer by slowing or stopping cell growth. DNA changes that inactivate tumor suppressor genes can lead to uncontrolled cell growth and cancer. […] Cancer cells can break away from the original tumor and travel through the blood or lymph system to distant locations in the body, where they exit the vessels to form additional tumors. This is called metastasis.
  • #3 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Future advances in molecular oncology may further improve diagnostic, prognostic, and treatment protocols for patients with soft-tissue sarcomas. […] Generally, soft-tissue tumors grow centripetally, though some benign tumors (eg, fibrous lesions) may grow longitudinally along tissue planes. […] Once the tumor reaches the anatomic limits of the compartment, the tumor is more likely to breach compartmental boundaries. […] The peripheral portion of the tumor compresses surrounding, normal soft tissue because of centripetal expansile growth. […] A thin layer of tissue called the reactive zone surrounds the compression zone, especially in higher-grade tumors. […] Some extremely aggressive lesions with infiltrative growth patterns, such as childhood rhabdomyosarcoma, may not respect anatomic compartmental boundaries and frequently will invade fascial planes.
  • #3 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Soft-tissue sarcomas have a propensity for local recurrence. […] The pseudocapsule provides surgeons with a more or less obvious plane of dissection; however, such an excision can leave behind microscopic or occasionally gross tumor. […] The addition of postoperative radiation therapy decreases the risk of recurrence associated with a marginal resection. […] The pattern of recurrence generally is predictable, and most tumors destined to recur do so within the first 2-3 years. […] Adjuvant radiation therapy clearly minimizes local recurrence, but its ability to increase overall chances of survival, though likely, is not certain. […] Many patients with high-grade soft-tissue sarcomas, as well as a few with the low-grade type, progress to metastatic disease, even after adequate local control of the primary tumor has been achieved.
  • #3 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Although most patients do not have clinically evident metastases at the time of presentation, they may have occult micrometastases that eventually manifest clinically. […] Good evidence exists suggesting that certain genetic disorders and gene mutations are predisposing factors for some benign and malignant soft-tissue tumors. […] The pathogenetic mechanism is the emergence of radiation-induced genetic mutations that encourage neoplastic transformation. […] An association between exposure to various carcinogens and an increased incidence of soft-tissue tumors has been reported. […] A classic example of an infection-induced soft-tissue tumor is Kaposi sarcoma resulting from human herpesvirus type 8 in patients with human immunodeficiency virus (HIV). […] The relation between trauma and soft-tissue tumors appears to be coincidental.
  • #3 Nodular vasculitis
    https://dermnetnz.org/topics/nodular-vasculitis
    Nodular vasculitis refers to a group of poorly defined conditions causing nodules on the legs in which inflamed blood vessels (vasculitis) are found on biopsy. […] The exact cause of nodular vasculitis is unknown but the patchy inflammation in the blood vessels and lymphatics in the deep dermis and subcutaneous fat appears to relate to a slowed circulation. […] Slowing of the flow in the deep vessels can also encourage deposition of bacteria from the bloodstream, including tubercle bacilli, and in some patients, nodular vasculitis is a sign of tuberculosis, when it may be called erythema induratum or Bazin disease. […] Skin biopsy of the nodules reveals panniculitis, with varying degrees of inflammation of the blood vessels and lymphatics in the deep dermis and subcutaneous tissue. […] Painful lumps are usually due to a form of panniculitis and/or vasculitis.
  • #3 Breast lumps pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Breast_lumps_pathophysiology
    It is understood that breast lumps are the result of hormonal events: Prevalence of benign breast lesion in post-menopausal women receiving estrogen with or without progesteron for more than 8 years raise by 1.7 fold. Estrogen and progesterone increase rate of benign proliferative breast disease to 74%. Anti-estrogen drugs such as tamoxifen, decrease prevalence of breast lesions such as adenosis, cysts, hyperplasia, duct ectasia to 28%. […] Although estrogen receptors (ER) and progesterone-receptor (PR) attributed to weak prognosis, they may predict patients’ response to endocrine therapy. Assessment of presence of ER and PR are required in invasive breast cancers. ER-positive result is present in 70% of breast cancers and PR-positive result is present in 60% of breast cancers. […] HER2/neu is a proto-oncogene which involves in breast regulatory pathways such as proliferation, cell motility and invasion. In 10% to 34% of breast cancers, overexpression and amplification of HER2 is reported. In 90% of cases, overexpression, amplification, and surface membrane protein expressions of HER2/neu may be seen.
  • #3 Rheumatoid nodule – Wikipedia
    https://en.wikipedia.org/wiki/Rheumatoid_nodule
    Although the exact process is unknown, there are a few hypotheses for the generation of rheumatoid nodules. It has been observed that rheumatoid nodules frequently form over extensor sites and areas vulnerable to trauma. The trauma causes inflammatory particles to build up and leads to a secondary inflammatory response which ultimately causes fibrin release and necrosis. Another hypothesis suggests that the inflammation of blood vessels activates complement components, which leads to the deposit of rheumatoid factors and fibrin. […] The rheumatoid nodule is the most common cutaneous manifestation of rheumatoid arthritis. Rheumatoid arthritis involves chronic inflammation of synovial membranes, which leads to degradation of articular cartilage and the juxta-articular bone. Inflammation is caused by T cells, B cells, and monocytes when endothelial cells are activated. Neovascularization, the growth of new blood vessels, serves as an additional marker for rheumatoid arthritis. A hyperplastic synovial lining layer can be caused by the expansion of synovial fibroblast and macrophage cells. This expansion of the synovial membrane, sometimes referred to as „pannus”, can lead to bony erosions and cartilage degradation at the site of the cartilage-bone junction in the periarticular bone.
  • #3 Researchers uncover a fundamental mechanism in breast cancer – Institute for Bioengineering of Catalonia
    https://ibecbarcelona.eu/researchers-uncover-a-fundamental-mechanism-in-breast-cancer/
    As every woman knows, an early test for breast cancer is feeling for lumps. What the doctor or patient herself is actually looking for when she does this is one of the first signs of tumor development: an unusual stiffening of the tissue. […] In healthy breast cells, we have shown that the adhesive properties of integrins lead cells to reduce the force they apply to their environment if the tissue is stiffer than normal, says Pere Roca-Cusachs, group leader at IBEC and assistant professor at the University of Barcelona, who led the study. […] However, cancer cells in the breast express a different type of integrin with different adhesive properties. This other integrin leads cells to apply higher forces as tissue stiffness increases, creating a feedback mechanism that can eventually lead to the hard lumps characteristic of breast tumors.
  • #3 Hidradenitis suppurativa: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/hidradenitis-suppurativa/
    Hidradenitis suppurativa, also known as acne inversa, is a chronic skin disease characterized by recurrent boil-like lumps (nodules) under the skin. […] The condition probably results from a combination of genetic and environmental factors. Originally, researchers believed that the disorder was caused by the blockage (occlusion) of specialized sweat glands called apocrine glands. However, recent studies have shown that the condition actually begins with a blockage of hair follicles in areas of the body that also contain a high concentration of apocrine glands (such as the armpits and groin). […] Genetic factors clearly play a role in causing hidradenitis suppurativa. Some cases have been found to result from variants (also known as mutations) in the NCSTN, PSEN1, or PSENEN gene. […] Although little is known about the mechanism, abnormal Notch signaling appears to promote the development of nodules and lead to inflammation in the skin. […] Researchers have studied many other possible risk factors for hidradenitis suppurativa. Obesity and smoking both appear to increase the risk of the disorder, and obesity is also associated with increased severity of signs and symptoms in affected individuals.
  • #3 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infections display a diverse array of clinical manifestations, including both temporary and chronic subclinical infections, and death in severe cases. The virus’s incubation period after successful transmission to the host varies from 7 to 28 days. LSD initially manifests with fever (40 °C to 41.5 °C), depression, decreased appetite, and reduced physical activity. Within 5–7 days, numerous well-defined skin lesions (nodules) appear, ranging from 2 to 7 cm in diameter. These lesions, characterized by flat-topped papules and nodules, affect the dermis and epidermis, occasionally extending to the hypodermis and rarely to the adjacent striated muscle. LSDV can persist in various reservoirs, including skin lesions, blood, scabs, oral and nasal secretions, semen, and sometimes in animal skin without apparent symptoms. It is widely distributed across several tissues, with painful nodules initially appearing near the head, mouth, nose, and eyes, then spreading to the cervical region, extremities, perineum, mammary gland, and reproductive organs. During the initial phases of viral infection, these nodules exhibit a grayish-white internal coloration and may secrete serum. Around 14 days post-infection, nodules may develop a central core of necrotic material known as the “sit-fast.” These necrotic cores provide an opportunity for secondary bacterial infection. As ulcers form in the infected nodules, LSDV can invade various body fluids, such as saliva, nasal and ocular secretions, and vaginal discharge. Consequently, infected bovines often show significant emaciation and fragility, leading to prolonged productivity losses and potential skin damage.
  • #3 Caseous Lymphadenitis of Sheep and Goats – Circulatory System – Merck Veterinary Manual
    https://www.merckvetmanual.com/circulatory-system/lymphadenitis-and-lymphangitis-of-large-animals/caseous-lymphadenitis-of-sheep-and-goats
    C pseudotuberculosis is a gram-positive, facultative, intracellular coccobacillus. Two biotypes have been identified based on the ability of the bacteria to reduce nitrate: a nitrate-negative group that infects sheep and goats, and a nitrate-positive group that infects horses. […] All strains produce an exotoxin, called phospholipase D, that enhances dissemination of the bacteria by damaging endothelial cells and increasing vascular permeability. […] C pseudotuberculosis has a second virulence factor, which is an external lipid coat that provides protection from hydrolytic enzymes in host phagocytes. The bacteria replicate in the phagocytes, which then rupture and release the bacteria. The ongoing process of bacterial replication, followed by attraction and subsequent death of inflammatory cells, forms the characteristic abscesses associated with CL.
  • #4 What Is Cancer? – NCI
    https://www.cancer.gov/about-cancer/understanding/what-is-cancer
    Cancer is a disease in which some of the bodys cells grow uncontrollably and spread to other parts of the body. […] Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldnt. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous or not cancerous (benign). […] Cancer is caused by changes to DNA. Most cancer-causing DNA changes occur in sections of DNA called genes. These changes are also called genetic changes. […] A DNA change can cause genes involved in normal cell growth to become oncogenes. Unlike normal genes, oncogenes cannot be turned off, so they cause uncontrolled cell growth. […] In normal cells, tumor suppressor genes prevent cancer by slowing or stopping cell growth. DNA changes that inactivate tumor suppressor genes can lead to uncontrolled cell growth and cancer. […] Cancer cells can break away from the original tumor and travel through the blood or lymph system to distant locations in the body, where they exit the vessels to form additional tumors. This is called metastasis.
  • #4 Benign and Malignant Soft-Tissue Tumors: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1253816-overview
    Although most patients do not have clinically evident metastases at the time of presentation, they may have occult micrometastases that eventually manifest clinically. […] Good evidence exists suggesting that certain genetic disorders and gene mutations are predisposing factors for some benign and malignant soft-tissue tumors. […] The pathogenetic mechanism is the emergence of radiation-induced genetic mutations that encourage neoplastic transformation. […] An association between exposure to various carcinogens and an increased incidence of soft-tissue tumors has been reported. […] A classic example of an infection-induced soft-tissue tumor is Kaposi sarcoma resulting from human herpesvirus type 8 in patients with human immunodeficiency virus (HIV). […] The relation between trauma and soft-tissue tumors appears to be coincidental.
  • #4 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infections display a diverse array of clinical manifestations, including both temporary and chronic subclinical infections, and death in severe cases. The virus’s incubation period after successful transmission to the host varies from 7 to 28 days. LSD initially manifests with fever (40 °C to 41.5 °C), depression, decreased appetite, and reduced physical activity. Within 5–7 days, numerous well-defined skin lesions (nodules) appear, ranging from 2 to 7 cm in diameter. These lesions, characterized by flat-topped papules and nodules, affect the dermis and epidermis, occasionally extending to the hypodermis and rarely to the adjacent striated muscle. LSDV can persist in various reservoirs, including skin lesions, blood, scabs, oral and nasal secretions, semen, and sometimes in animal skin without apparent symptoms. It is widely distributed across several tissues, with painful nodules initially appearing near the head, mouth, nose, and eyes, then spreading to the cervical region, extremities, perineum, mammary gland, and reproductive organs. During the initial phases of viral infection, these nodules exhibit a grayish-white internal coloration and may secrete serum. Around 14 days post-infection, nodules may develop a central core of necrotic material known as the “sit-fast.” These necrotic cores provide an opportunity for secondary bacterial infection. As ulcers form in the infected nodules, LSDV can invade various body fluids, such as saliva, nasal and ocular secretions, and vaginal discharge. Consequently, infected bovines often show significant emaciation and fragility, leading to prolonged productivity losses and potential skin damage.
  • #5 Lumpy Skin Disease: Insights into Molecular Pathogenesis and Control Strategies
    https://www.mdpi.com/2306-7381/11/11/561
    LSDV infections display a diverse array of clinical manifestations, including both temporary and chronic subclinical infections, and death in severe cases. The virus’s incubation period after successful transmission to the host varies from 7 to 28 days. LSD initially manifests with fever (40 °C to 41.5 °C), depression, decreased appetite, and reduced physical activity. Within 5–7 days, numerous well-defined skin lesions (nodules) appear, ranging from 2 to 7 cm in diameter. These lesions, characterized by flat-topped papules and nodules, affect the dermis and epidermis, occasionally extending to the hypodermis and rarely to the adjacent striated muscle. LSDV can persist in various reservoirs, including skin lesions, blood, scabs, oral and nasal secretions, semen, and sometimes in animal skin without apparent symptoms. It is widely distributed across several tissues, with painful nodules initially appearing near the head, mouth, nose, and eyes, then spreading to the cervical region, extremities, perineum, mammary gland, and reproductive organs. During the initial phases of viral infection, these nodules exhibit a grayish-white internal coloration and may secrete serum. Around 14 days post-infection, nodules may develop a central core of necrotic material known as the “sit-fast.” These necrotic cores provide an opportunity for secondary bacterial infection. As ulcers form in the infected nodules, LSDV can invade various body fluids, such as saliva, nasal and ocular secretions, and vaginal discharge. Consequently, infected bovines often show significant emaciation and fragility, leading to prolonged productivity losses and potential skin damage.

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