Rak wargi
Patofizjologia i mechanizm

Rak wargi, najczęstszy nowotwór jamy ustnej (25-30% przypadków), to głównie rak płaskonabłonkowy wywodzący się z nabłonka warg. Patogeneza jest wieloczynnikowa, z kluczowymi czynnikami ryzyka: ekspozycją na promieniowanie UV (szczególnie wargi dolnej), używaniem tytoniu (papierosy, fajki, żucie tytoniu) i nadmiernym spożyciem alkoholu, które w synergii mogą zwiększyć ryzyko nawet 30-krotnie. Inne istotne czynniki to jasna karnacja, infekcja HPV (szczególnie genotypy wysokiego ryzyka), stany immunosupresji oraz przewlekły stan zapalny. Na poziomie molekularnym dominują mutacje i inaktywacja genów supresorowych nowotworów (TP53, P16), nadekspresja onkogenów (PRAD1, H-ras) oraz receptorów wzrostu (EGFR), które aktywują szlaki sygnałowe MAPK, PI3K/AKT/mTOR i inne, sprzyjając proliferacji, progresji i inwazji guza. Przewlekły stan zapalny i mikrobiom jamy ustnej, zwłaszcza obecność Fusobacterium nucleatum, również odgrywają rolę w patogenezie poprzez indukcję uszkodzeń DNA i modulację mikrośrodowiska nowotworowego.

Patogeneza raka wargi

Rak wargi to rodzaj nowotworu głowy i szyi, który rozwija się, gdy komórki tworzące wargę namnażają się w sposób niekontrolowany, tworząc zmiany patologiczne lub guzy. Jest to najczęstszy nowotwór jamy ustnej, stanowiący 25-30% wszystkich przypadków nowotworów tej lokalizacji12. Rak wargi najczęściej rozwija się z komórek płaskich nabłonka (komórek płaskonabłonkowych), które wyściełają wargi i inne obszary jamy ustnej. Ten typ nowotworu określany jest jako rak płaskonabłonkowy wargi (squamous cell carcinoma)34.

Czynniki ryzyka rozwoju raka wargi

Patogeneza raka wargi jest procesem złożonym i wieloczynnikowym, obejmującym interakcję między różnymi czynnikami ryzyka5. Główne czynniki etiologiczne związane z rozwojem tego nowotworu to:

  • Ekspozycja na promieniowanie ultrafioletowe (UV) – długotrwałe narażenie na światło słoneczne jest specyficznym czynnikiem ryzyka dla raka wargi, szczególnie wargi dolnej (suchej)678
  • Używanie tytoniu – palenie papierosów, fajki, cygar lub żucie tytoniu zwiększa ryzyko rozwoju raka wargi, szczególnie wargi wewnętrznej (mokrej)910
  • Nadmierne spożycie alkoholu – zwiększa ryzyko rozwoju raka wargi wewnętrznej11
  • Współistniejące używanie tytoniu i alkoholu może zwiększyć ryzyko raka wargi nawet 30-krotnie12
  • Jasna karnacja skóry13
  • Infekcja wirusem brodawczaka ludzkiego (HPV) – choć jej rola w patogenezie raka wargi nie jest tak dobrze zdefiniowana jak w przypadku innych lokalizacji w jamie ustnej14
  • Stany immunosupresji, które mogą predysponować do wyższego ryzyka rozwoju raka wargi15

Mechanizmy molekularne patogenezy

Rozwój raka wargi na poziomie molekularnym obejmuje złożone mechanizmy związane z uszkodzeniem DNA i zaburzeniami regulacji cyklu komórkowego16. Kluczowe procesy patogenetyczne obejmują:

  • Zmiany genetyczne – w raku płaskonabłonkowym jamy ustnej (w tym wargi) zidentyfikowano zmiany chromosomalne sugerujące zaangażowanie genów supresorowych nowotworów (TSGs), szczególnie w chromosomach 3, 9, 11 i 1717
  • Inaktywacja genów supresorowych nowotworów, zwłaszcza P16 na chromosomie 9 i TP53 na chromosomie 17, co prowadzi do zaburzenia mechanizmów kontroli wzrostu1819
  • Uszkodzenie onkogenów zaangażowanych w kontrolę wzrostu komórkowego, szczególnie tych uczestniczących w przekazywaniu sygnałów komórkowych, takich jak PRAD1 na chromosomie 11 i Harvey ras (H-ras) na chromosomie 1720
  • Aberracje genetyczne dotyczące chromosomów 9, 3, 17, 13 i 11, z inaktywacją TSGs (szczególnie P16 i TP53) oraz nadekspresją onkogenów (zwłaszcza PRAD1)21
  • Nadekspresja cykliny D1, która reguluje cykl komórkowy i jest związana z agresywnością i progresją guza22

Rola receptora naskórkowego czynnika wzrostu (EGFR)

EGFR odgrywa kluczową rolę w onkogenezie raka wargi poprzez regulację szlaków sygnałowych, takich jak MAPK i PI3K, oraz poprzez promowanie proliferacji i aktywację onkogenu cykliny D123. Liczne badania wskazują, że czynniki takie jak naskórkowy czynnik wzrostu, wodór, promieniowanie UV i promieniowanie jonizujące mogą powodować translokację EGFR do jądra komórkowego, gdzie wchodzi on w interakcje z licznymi czynnikami transkrypcyjnymi i wpływa na aktywację genów zaangażowanych w proliferację komórek, progresję guza i naprawę DNA24.

Rola przewlekłego stanu zapalnego

Przewlekły stan zapalny może odgrywać istotną rolę w patogenezie raka wargi25. Mechanizm rozwoju raka płaskonabłonkowego w następstwie urazu błony śluzowej może obejmować wiele czynników, takich jak uszkodzenie DNA, cytokiny, infekcja HPV, zmiany genetyczne, palenie tytoniu, alkohol i inne26. Przewlekłe zapalenie może indukować trwałe uszkodzenie tkanek i zmiany w typach komórek zapalnych27.

Mediatory zapalne, w tym czynnik jądrowy kappa B, naczyniowo-śródbłonkowy czynnik wzrostu, cytokiny zapalne, szlaki prostaglandynowe, p53, reaktywne formy tlenu i azotu oraz mikroRNA, są głównymi elementami patogenezy raka jamy ustnej28. Przewlekły stan zapalny może prowadzić do kluczowego uszkodzenia DNA, które dalej postępuje do rozwoju raka29. Zatem przewlekłe zapalenie może wpływać na inicjację, progresję, inwazję i przerzutowanie guza poprzez zmiany w populacjach komórek zapalnych i poziomach cytokin w tkankach lokalnych30.

Rola tytoniu w patogenezie

Tytoń jest jednym z najważniejszych czynników ryzyka przedwczesnej śmierci na całym świecie i jest silnie związany z rozwojem raka płaskonabłonkowego jamy ustnej, w tym wargi3132. Mechanizmy karcinogenezy indukowanej przez tytoń mogą być wieloaspektowe:

  • Tytoń jako ważny czynnik ryzyka może powodować epigenetyczne zmiany komórek nabłonka jamy ustnej3334
  • Hamowanie wielu systemowych funkcji immunologicznych gospodarza, co zwiększa podatność na rozwój nowotworów – częstość występowania nowotworów złośliwych u pacjentów z immunosupresją jest 100 razy wyższa niż u osób z prawidłową odpornością3536
  • Toksyczne metabolity tytoniu mogą powodować stres oksydacyjny w tkankach i indukować raka płaskonabłonkowego jamy ustnej – udowodniono, że rak jamy ustnej jest związany ze stresem oksydacyjnym3738
  • Uszkodzenie DNA przez toksyczne metabolity tytoniu, co prowadzi do indukcji raka3940

Rola HPV w patogenezie

Wirus brodawczaka ludzkiego (HPV) jest wirusem DNA, który specyficznie atakuje komórki podstawne nabłonka błony śluzowej. Genotypy takie jak HPV1 infekują komórki naskórka, podczas gdy HPV6, 11, 16 i 18 infekują komórki nabłonkowe jamy ustnej i inne powierzchnie błon śluzowych41.

Zaangażowanie HPV w onkogenezę jamy ustnej, w tym wargi, opiera się na następujących dowodach42:

  • Silnie ustanowiona rola etiologiczna HPV w raku płaskonabłonkowym szyjki macicy
  • Tropizm nabłonkowy HPV
  • Podobieństwo między nabłonkiem jamy ustnej a narządów płciowych
  • Wykrycie genotypów HPV w próbkach raka płaskonabłonkowego jamy ustnej

Uważa się, że jednym z głównych wydarzeń w kancerogenezie indukowanej przez HPV jest integracja genomu HPV do chromosomu gospodarza43. Integracja genomu HPV często występuje w pobliżu miejsc łamliwych genomu ludzkiego, ale nie ma wyraźnych miejsc integracji ani dowodów na mutagenezę insercyjną44.

Infekcja HPV stanowi około 5,2% globalnego obciążenia nowotworami u ludzi45. Karcynogeneza indukowana przez HPV zachodzi jako wieloetapowy proces, który rozpoczyna się od pierwotnej infekcji proliferujących komórek podstawnych nabłonka płaskiego. Jeśli infekcja jest spowodowana przez typ HPV wysokiego ryzyka (HR-HPV), a dodatkowo występuje niewydolność układu odpornościowego w kontrolowaniu i usuwaniu infekcji oraz obecność niektórych kofaktorów, po pewnym czasie zakażenie HPV prowadzi do akumulacji wystarczającej niestabilności genomowej, co skutkuje transformacją nowotworową nabłonka46.

HPV jest karcynogenny częściowo dlatego, że białka E6 i E7 powodują nieprawidłową regulację p53 i Rb, kontrolę apoptozy i regulację cyklu komórkowego47. Uważa się, że kolisty genom jest linearyzowany i integrowany jako późne zdarzenie w procesie infekcji, niszcząc region genu E1/E2, niszcząc gen E2, uwalniając supresję genomu wirusowego, prowadząc do nadekspresji wirusów E6 i genów E7 w celu utrzymania fenotypu złośliwego48.

Rola mikroflory jamy ustnej

Mikroflora jamy ustnej może odgrywać rolę w patogenezie raka wargi. Czynniki ryzyka raka jamy ustnej, takie jak palenie tytoniu, nadużywanie alkoholu i infekcja HPV, wpływają na mikrobiom jamy ustnej49. Niektóre gatunki bakterii zostały powiązane z rozwojem raka jamy ustnej5051.

Badania z wykorzystaniem sekwencjonowania nowej generacji ujawniły różnice w obfitości bakterii, przy czym Fusobacterium nucleatum wyłania się jako potencjalny biomarker mikrobiologiczny znacząco związany z rakiem jamy ustnej52. Funkcjonalna analiza wskazała na wzbogacenie szlaków związanych ze stanem zapalnym i proliferacją komórek w przypadkach raka, co sugeruje udział mikrobiomu jamy ustnej w lokalnym mikrośrodowisku53.

Integracja mechanizmów patogenetycznych

Patogeneza raka wargi nie wydaje się być ograniczona do pojedynczego czynnika, ale raczej do złożonego, wieloetapowego procesu interakcji między potencjalnymi czynnikami ryzyka54. Różnice geograficzne w profilach molekularnych sugerują genetyczne zróżnicowanie, które może wyjaśniać podatność określonych grup na raka wargi55.

Zmiany molekularne występujące w raku płaskonabłonkowym jamy ustnej z krajów zachodnich (np. Wielkiej Brytanii, Stanów Zjednoczonych, Australii), szczególnie mutacje TP53, są rzadko spotykane w krajach wschodnich (np. Indiach, Azji Południowo-Wschodniej), gdzie częstsze jest zaangażowanie onkogenów ras56.

Karcinogeneza raka wargi obejmuje utrzymanie proliferacji, unikanie supresorów wzrostu, oporność na śmierć komórkową, nieśmiertelność, angiogenezę, inwazję, przerzuty, deregulację równowagi energetycznej i unikanie zniszczenia przez układ odpornościowy57.

Szlaki sygnałowe w patogenezie

Onkogenne szlaki sygnałowe, w tym szlak EGFR, szlak PI3K/AKT/mTOR, szlak JAK/STAT, szlak MET, szlak Wnt/-katenina i szlak RAS/RAF/MAPK, są nieprawidłowo aktywowane i nadregulowane, co sprzyja progresji raka płaskonabłonkowego jamy ustnej, w tym wargi58.

Około 80% raków głowy i szyi HPV-negatywnych ma zmutowane białko p53 (TP53), co prowadzi do dysfunkcji genu59. Podobnie jak mutacje w szlaku TP53, mutacje szlaku retinoblastoma (RB) są wczesnymi manifestacjami raków głowy i szyi60.

Sygnalizacja Notch została wykazana jako supresor nowotworowy w nowotworach złośliwych płaskonabłonkowych nabłonka (nowotwory płuc, pęcherza moczowego i przełyku) oraz w kilku modelach in vivo61.

Metylacja DNA w patogenezie

Rozwój i rokowanie raka wargi są związane z nieprawidłowościami metylacji DNA62. Hipermetylacja może prowadzić do supresji genów zaangażowanych w progresję i przerzutowanie raka płaskonabłonkowego jamy ustnej63.

Hipoksja w patogenezie

Rak płaskonabłonkowy jamy ustnej, w tym wargi, jest miejscowo agresywnym guzem o podwyższonym poziomie hipoksji, co skutkuje rozsiewem, nawrotem i słabą odpowiedzią terapeutyczną64. Zmniejszenie poziomów mRNA E-kadheryny indukowane hipoksją zwiększa zdolność migracyjną komórek raka65.

Rola enzymów metaloproteazowych

Metaloproteinazy macierzy (MMPs) są enzymami proteolitycznymi, które uczestniczą w przebudowie macierzy pozakomórkowej (ECM). MMPs niszczą macierz pozakomórkową, powodując wzrost guza i przerzuty. MMPs są zaangażowane w rozprzestrzenianie się i przerzutowanie raka jamy ustnej. Wysokie poziomy MMPs i raka płaskonabłonkowego jamy ustnej zostały powiązane z rokowaniem nowotworowym66.

Polimorfizm genów MMP został niedawno zidentyfikowany jako jeden z czynników przewidujących podatność lub ryzyko w rozwoju raka jamy ustnej67.

Podsumowanie mechanizmów patogenetycznych

Patogeneza raka wargi jest procesem złożonym i wieloczynnikowym, obejmującym interakcje między czynnikami środowiskowymi, genetycznymi i molekularnymi. Główne mechanizmy patogenetyczne obejmują:

  • Ekspozycję na promieniowanie UV, tytoń i alkohol jako główne czynniki ryzyka
  • Zmiany genetyczne, w tym mutacje genów supresorowych nowotworów (TP53, P16) i onkogenów (PRAD1, H-ras)
  • Nadekspresję receptora naskórkowego czynnika wzrostu (EGFR) i jego rolę w regulacji szlaków sygnałowych
  • Przewlekły stan zapalny i jego wpływ na uszkodzenie DNA
  • Infekcję HPV i jej rolę w transformacji komórek nabłonkowych
  • Dysbiozę mikroflory jamy ustnej i jej potencjalny wpływ na rozwój raka
  • Nieprawidłowości metylacji DNA i ich wpływ na ekspresję genów
  • Hipoksję i jej wpływ na inwazyjność guza
  • Remodelowanie macierzy pozakomórkowej przez metaloproteinazy

Zrozumienie tych złożonych mechanizmów patogenetycznych jest niezbędne do rozwoju skutecznych strategii diagnostycznych, profilaktycznych i terapeutycznych dla raka wargi68.

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  1. 13.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1
    https://med.uth.edu/orl/2009/12/11/lip-cancer/
    Lip cancer is the most common malignant lesion of the oral cavity, constituting 25-30% of all oral cavity cancer cases. […] Unlike other sub-sites of the oral cavity, sun exposure is a well established risk factor for development of lip cancer. […] HPV has been associated with lip malignancy, but its role in the pathogenesis of the disease is not as defined as with other sub-sites in the oral cavity and oropharynx. […] Even in early stages lip cancers can gain access to the mental nerve and involve the mandible by direct extension, perineural invasion or lymphatic spread into the mental foramen. This, in turn, affects treatment required and prognosis. […] Incisional biopsy is the preferred diagnostic method as this will allow the pathologist to determine patterns of invasion as well as the presence of perineural invasion.
  • #2 Lip Cancer: Lip Melanoma & Squamous Cell Carcinoma | Memorial Sloan Kettering Cancer Center
    https://www.mskcc.org/cancer-care/types/mouth/types-mouth/lip
    Lip cancer is a type of head and neck cancer that begins when the cells that make up the lip grow out of control and form lesions or tumors. It is the most common cancer of the mouth. […] Lip cancer usually develops in the thin, flat cells called squamous cells that line the lips and other areas of the mouth. Lip cancer from squamous cells is called squamous cell carcinoma. […] Lip cancer can affect anyone. The causes of most lip cancers and melanomas are linked to smoking or chewing tobacco, drinking alcohol, and being exposed to ultraviolet light, such as sunlight, for long periods of time. […] The best ways to prevent lip cancer are to limit how much alcohol you drink and try to quit or cut down on smoking and chewing tobacco. Its also important to stay out of the sun (UV light) for long periods of time, including tanning beds.
  • #3 Lip Cancer: Lip Melanoma & Squamous Cell Carcinoma | Memorial Sloan Kettering Cancer Center
    https://www.mskcc.org/cancer-care/types/mouth/types-mouth/lip
    Lip cancer is a type of head and neck cancer that begins when the cells that make up the lip grow out of control and form lesions or tumors. It is the most common cancer of the mouth. […] Lip cancer usually develops in the thin, flat cells called squamous cells that line the lips and other areas of the mouth. Lip cancer from squamous cells is called squamous cell carcinoma. […] Lip cancer can affect anyone. The causes of most lip cancers and melanomas are linked to smoking or chewing tobacco, drinking alcohol, and being exposed to ultraviolet light, such as sunlight, for long periods of time. […] The best ways to prevent lip cancer are to limit how much alcohol you drink and try to quit or cut down on smoking and chewing tobacco. Its also important to stay out of the sun (UV light) for long periods of time, including tanning beds.
  • #4 9 things to know about lip cancer | MD Anderson Cancer Center
    https://www.mdanderson.org/cancerwise/9-things-to-know-about-lip-cancer.h00-159700701.html
    Most lip cancers start in the squamous cells, which line the surface of the mouth, tongue, gum and lips. Cancers on the wet lip are almost always squamous cell carcinomas. […] Lip cancer can be linked to the following risk factors: excessive sun exposure (cancers on the dry lip), smoking and tobacco use (cancers on the wet lip), heavy alcohol use (cancers on the wet lip). […] Lip cancer can spread, but typically it doesn’t spread very quickly. It most often spreads to the lymph nodes in the neck. Sometimes it can spread to distant parts of the body, usually the lungs. […] Lip cancer is curable in many cases. We can cure lip cancer that is localized or even lip cancer that has spread to the lymph nodes. […] Surgery is the standard treatment for lip cancer. A surgeon will remove the cancer and then repair or reconstruct the lip.
  • #5 Etiology of cancer of the lip | CoLab
    https://colab.ws/articles/10.1016%2Fs0901-5027%2898%2980010-6
    A range of environmental and host factors has been identified to explain the etiopathogenesis of squamous cell carcinoma of the lip. However, the definitive pathogenic pathway remains unclear. […] Carcinogenesis does not seem to be limited to a single agent, but rather to a complex multistep process of interactions between putative risk factors. […] In this paper, the currently available data regarding risk factors, considered to be causally related to the onset of lip cancer, are reviewed.
  • #6 Lip Cancer: Symptoms, Causes, Treatment & Survival Rate
    https://www.cancercenter.com/cancer-types/oral-cancer/types/lip-cancer
    A persistent sore or lump on your lip may be an early symptom of lip cancer, a type of oral cancer. […] This type typically results when the squamous cells on the surface layer of the mouth and lips begin to grow abnormally. […] Too much exposure to sun or ultraviolet (UV) light from tanning equipment is a risk factor thats specific to lip cancer, as is having fair skin. […] Risk factors for this group of cancers include: Tobacco use, whether it be cigarette, pipe or cigar smoking, or chewing tobacco. […] If you have a history of tobacco and/or heavy alcohol use, its possible to simultaneously develop cancer in more than one area of your body. […] Progression for lip and oral cavity cancers range from stage 0, also called carcinoma in situ, which is when abnormal cells exist on the surface but have not grown into neighboring tissue, all the way to stage 4C, which is when cancer has spread to distant parts of your body. […] A clinical trial of hyperthermia, another therapeutic approach, may be used for recurrent lip cancer. During this technique, tumor cells are heated to kill them or impede their growth or make them more susceptible to radiation and chemotherapy.
  • #7
    https://med.uth.edu/orl/2009/12/11/lip-cancer/
    Lip cancer is the most common malignant lesion of the oral cavity, constituting 25-30% of all oral cavity cancer cases. […] Unlike other sub-sites of the oral cavity, sun exposure is a well established risk factor for development of lip cancer. […] HPV has been associated with lip malignancy, but its role in the pathogenesis of the disease is not as defined as with other sub-sites in the oral cavity and oropharynx. […] Even in early stages lip cancers can gain access to the mental nerve and involve the mandible by direct extension, perineural invasion or lymphatic spread into the mental foramen. This, in turn, affects treatment required and prognosis. […] Incisional biopsy is the preferred diagnostic method as this will allow the pathologist to determine patterns of invasion as well as the presence of perineural invasion.
  • #8 9 things to know about lip cancer | MD Anderson Cancer Center
    https://www.mdanderson.org/cancerwise/9-things-to-know-about-lip-cancer.h00-159700701.html
    Most lip cancers start in the squamous cells, which line the surface of the mouth, tongue, gum and lips. Cancers on the wet lip are almost always squamous cell carcinomas. […] Lip cancer can be linked to the following risk factors: excessive sun exposure (cancers on the dry lip), smoking and tobacco use (cancers on the wet lip), heavy alcohol use (cancers on the wet lip). […] Lip cancer can spread, but typically it doesn’t spread very quickly. It most often spreads to the lymph nodes in the neck. Sometimes it can spread to distant parts of the body, usually the lungs. […] Lip cancer is curable in many cases. We can cure lip cancer that is localized or even lip cancer that has spread to the lymph nodes. […] Surgery is the standard treatment for lip cancer. A surgeon will remove the cancer and then repair or reconstruct the lip.
  • #9 9 things to know about lip cancer | MD Anderson Cancer Center
    https://www.mdanderson.org/cancerwise/9-things-to-know-about-lip-cancer.h00-159700701.html
    Most lip cancers start in the squamous cells, which line the surface of the mouth, tongue, gum and lips. Cancers on the wet lip are almost always squamous cell carcinomas. […] Lip cancer can be linked to the following risk factors: excessive sun exposure (cancers on the dry lip), smoking and tobacco use (cancers on the wet lip), heavy alcohol use (cancers on the wet lip). […] Lip cancer can spread, but typically it doesn’t spread very quickly. It most often spreads to the lymph nodes in the neck. Sometimes it can spread to distant parts of the body, usually the lungs. […] Lip cancer is curable in many cases. We can cure lip cancer that is localized or even lip cancer that has spread to the lymph nodes. […] Surgery is the standard treatment for lip cancer. A surgeon will remove the cancer and then repair or reconstruct the lip.
  • #10 Lip Cancer: Symptoms, Causes, Treatment & Survival Rate
    https://www.cancercenter.com/cancer-types/oral-cancer/types/lip-cancer
    A persistent sore or lump on your lip may be an early symptom of lip cancer, a type of oral cancer. […] This type typically results when the squamous cells on the surface layer of the mouth and lips begin to grow abnormally. […] Too much exposure to sun or ultraviolet (UV) light from tanning equipment is a risk factor thats specific to lip cancer, as is having fair skin. […] Risk factors for this group of cancers include: Tobacco use, whether it be cigarette, pipe or cigar smoking, or chewing tobacco. […] If you have a history of tobacco and/or heavy alcohol use, its possible to simultaneously develop cancer in more than one area of your body. […] Progression for lip and oral cavity cancers range from stage 0, also called carcinoma in situ, which is when abnormal cells exist on the surface but have not grown into neighboring tissue, all the way to stage 4C, which is when cancer has spread to distant parts of your body. […] A clinical trial of hyperthermia, another therapeutic approach, may be used for recurrent lip cancer. During this technique, tumor cells are heated to kill them or impede their growth or make them more susceptible to radiation and chemotherapy.
  • #11 9 things to know about lip cancer | MD Anderson Cancer Center
    https://www.mdanderson.org/cancerwise/9-things-to-know-about-lip-cancer.h00-159700701.html
    Most lip cancers start in the squamous cells, which line the surface of the mouth, tongue, gum and lips. Cancers on the wet lip are almost always squamous cell carcinomas. […] Lip cancer can be linked to the following risk factors: excessive sun exposure (cancers on the dry lip), smoking and tobacco use (cancers on the wet lip), heavy alcohol use (cancers on the wet lip). […] Lip cancer can spread, but typically it doesn’t spread very quickly. It most often spreads to the lymph nodes in the neck. Sometimes it can spread to distant parts of the body, usually the lungs. […] Lip cancer is curable in many cases. We can cure lip cancer that is localized or even lip cancer that has spread to the lymph nodes. […] Surgery is the standard treatment for lip cancer. A surgeon will remove the cancer and then repair or reconstruct the lip.
  • #12 Lip Cancer: Symptoms, Stages & Treatment
    https://my.clevelandclinic.org/health/diseases/21933-lip-cancer
    Lip cancer occurs when abnormal cells grow out of control, resulting in tumors (solid tissue masses) or lesions (abnormal areas of skin) on your lips. […] As with all cancers, errors in cell DNA cause normal cells to become cancer cells that multiply out of control. The abnormal cancer cells can spread and damage healthy tissue. […] Most lip cancers are linked to tobacco use. […] You increase your risk of lip cancer by up to 30 times if you use tobacco and also consume excessive amounts of alcohol. […] The best treatment for you depends on the size of the tumor or lesion and the cancer stage. […] Lip cancer treatments include surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy. […] Squamous cell carcinoma (the most common type of lip cancer) tends to spread slowly. […] Because lip cancer lesions develop in easily seen locations, this type of cancer is detected and treated early in most cases.
  • #13 Lip Cancer: Symptoms, Causes, Treatment & Survival Rate
    https://www.cancercenter.com/cancer-types/oral-cancer/types/lip-cancer
    A persistent sore or lump on your lip may be an early symptom of lip cancer, a type of oral cancer. […] This type typically results when the squamous cells on the surface layer of the mouth and lips begin to grow abnormally. […] Too much exposure to sun or ultraviolet (UV) light from tanning equipment is a risk factor thats specific to lip cancer, as is having fair skin. […] Risk factors for this group of cancers include: Tobacco use, whether it be cigarette, pipe or cigar smoking, or chewing tobacco. […] If you have a history of tobacco and/or heavy alcohol use, its possible to simultaneously develop cancer in more than one area of your body. […] Progression for lip and oral cavity cancers range from stage 0, also called carcinoma in situ, which is when abnormal cells exist on the surface but have not grown into neighboring tissue, all the way to stage 4C, which is when cancer has spread to distant parts of your body. […] A clinical trial of hyperthermia, another therapeutic approach, may be used for recurrent lip cancer. During this technique, tumor cells are heated to kill them or impede their growth or make them more susceptible to radiation and chemotherapy.
  • #14
    https://med.uth.edu/orl/2009/12/11/lip-cancer/
    Lip cancer is the most common malignant lesion of the oral cavity, constituting 25-30% of all oral cavity cancer cases. […] Unlike other sub-sites of the oral cavity, sun exposure is a well established risk factor for development of lip cancer. […] HPV has been associated with lip malignancy, but its role in the pathogenesis of the disease is not as defined as with other sub-sites in the oral cavity and oropharynx. […] Even in early stages lip cancers can gain access to the mental nerve and involve the mandible by direct extension, perineural invasion or lymphatic spread into the mental foramen. This, in turn, affects treatment required and prognosis. […] Incisional biopsy is the preferred diagnostic method as this will allow the pathologist to determine patterns of invasion as well as the presence of perineural invasion.
  • #15 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1075729-overview
    The genetic aberrations involve, in order of decreasing frequency, chromosomes 9, 3, 17, 13, and 11 in particular, and probably other chromosomes, and involve inactivated TSGs, especially P16, and TP53 and overexpressed oncogenes, especially PRAD1. […] The molecular changes found in oral SCC from Western countries (eg, United Kingdom, United States, Australia), particularly TP53 mutations, are infrequent in Eastern countries (eg, India, Southeast Asia), where the involvement of ras oncogenes is more common, suggesting genetic differences that might be involved in explaining the susceptibility of certain groups to oral SCC. […] Carcinogen-metabolizing enzymes are implicated in some patients. […] Tobacco is a potent risk factor for oral cancer. […] An immune deficiency state may predispose one to a higher risk of developing oral SCC, especially lip cancer.
  • #16 Lip Cancer: Symptoms, Stages & Treatment
    https://my.clevelandclinic.org/health/diseases/21933-lip-cancer
    Lip cancer occurs when abnormal cells grow out of control, resulting in tumors (solid tissue masses) or lesions (abnormal areas of skin) on your lips. […] As with all cancers, errors in cell DNA cause normal cells to become cancer cells that multiply out of control. The abnormal cancer cells can spread and damage healthy tissue. […] Most lip cancers are linked to tobacco use. […] You increase your risk of lip cancer by up to 30 times if you use tobacco and also consume excessive amounts of alcohol. […] The best treatment for you depends on the size of the tumor or lesion and the cancer stage. […] Lip cancer treatments include surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy. […] Squamous cell carcinoma (the most common type of lip cancer) tends to spread slowly. […] Because lip cancer lesions develop in easily seen locations, this type of cancer is detected and treated early in most cases.
  • #17 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1075729-overview
    In oral SCC, modern DNA technology, especially allelic imbalance (loss of heterozygosity) studies, have identified chromosomal changes suggestive of the involvement of tumor suppressor genes (TSGs), particularly in chromosomes 3, 9, 11, and 17. Functional TSGs seem to assist growth control, while their mutation can unbridle these control mechanisms. […] The regions most commonly identified thus far have included some on the short arm of chromosome 3, a TSG termed P16 on chromosome 9, and the TSG termed TP53 on chromosome 17, but multiple other genes are being discovered. […] As well as damage to TSGs, cancer may also involve damage to other genes involved in growth control, mainly those involved in cell signaling (oncogenes), especially some on chromosome 11 (PRAD1 in particular) and chromosome 17 (Harvey ras [H-ras]). Changes in these and other oncogenes can disrupt cell growth control, ultimately leading to the uncontrolled growth of cancer.
  • #18 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1075729-overview
    In oral SCC, modern DNA technology, especially allelic imbalance (loss of heterozygosity) studies, have identified chromosomal changes suggestive of the involvement of tumor suppressor genes (TSGs), particularly in chromosomes 3, 9, 11, and 17. Functional TSGs seem to assist growth control, while their mutation can unbridle these control mechanisms. […] The regions most commonly identified thus far have included some on the short arm of chromosome 3, a TSG termed P16 on chromosome 9, and the TSG termed TP53 on chromosome 17, but multiple other genes are being discovered. […] As well as damage to TSGs, cancer may also involve damage to other genes involved in growth control, mainly those involved in cell signaling (oncogenes), especially some on chromosome 11 (PRAD1 in particular) and chromosome 17 (Harvey ras [H-ras]). Changes in these and other oncogenes can disrupt cell growth control, ultimately leading to the uncontrolled growth of cancer.
  • #19 Pathogenesis and Therapy of Oral Carcinogenesis
    https://www.mdpi.com/1422-0067/25/12/6343
    The proteins p53 and cyclin D1 are of critical importance in OSCC, with p53 mutations often leading to overexpression in the early stages of carcinogenesis, while overexpression of cyclin D1 regulates the cell cycle and is associated with aggressiveness and tumor progression. […] Tarle, M. and colleagues conducted a retrospective study that included immunohistochemical analysis of nuclear EGFR (nEGFR) expression and other markers such as Ki-67, p53, cyclin D1, and ABCG2 in samples of healthy oral mucosa, premalignant changes, and OSCC. […] Cetuximab, an antibody targeting EGFR, can be combined with inhibitors of PI3K/Akt signaling to enhance the effect. […] Lysyl oxidase (LOX) promotes extracellular matrix maturation and tumor invasiveness, while its propeptide (LOX-PP) inhibits tumor growth. […] Cholesterol also plays an important role in carcinogenesis as it is used for membrane biogenesis and cell signaling. […] Chan, N.N. et al. investigated the role of cholesterol in regulating the localization of caveolin-1 (CAV1) and cell migration in OSCC.
  • #20 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1075729-overview
    In oral SCC, modern DNA technology, especially allelic imbalance (loss of heterozygosity) studies, have identified chromosomal changes suggestive of the involvement of tumor suppressor genes (TSGs), particularly in chromosomes 3, 9, 11, and 17. Functional TSGs seem to assist growth control, while their mutation can unbridle these control mechanisms. […] The regions most commonly identified thus far have included some on the short arm of chromosome 3, a TSG termed P16 on chromosome 9, and the TSG termed TP53 on chromosome 17, but multiple other genes are being discovered. […] As well as damage to TSGs, cancer may also involve damage to other genes involved in growth control, mainly those involved in cell signaling (oncogenes), especially some on chromosome 11 (PRAD1 in particular) and chromosome 17 (Harvey ras [H-ras]). Changes in these and other oncogenes can disrupt cell growth control, ultimately leading to the uncontrolled growth of cancer.
  • #21 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1075729-overview
    The genetic aberrations involve, in order of decreasing frequency, chromosomes 9, 3, 17, 13, and 11 in particular, and probably other chromosomes, and involve inactivated TSGs, especially P16, and TP53 and overexpressed oncogenes, especially PRAD1. […] The molecular changes found in oral SCC from Western countries (eg, United Kingdom, United States, Australia), particularly TP53 mutations, are infrequent in Eastern countries (eg, India, Southeast Asia), where the involvement of ras oncogenes is more common, suggesting genetic differences that might be involved in explaining the susceptibility of certain groups to oral SCC. […] Carcinogen-metabolizing enzymes are implicated in some patients. […] Tobacco is a potent risk factor for oral cancer. […] An immune deficiency state may predispose one to a higher risk of developing oral SCC, especially lip cancer.
  • #22 Pathogenesis and Therapy of Oral Carcinogenesis
    https://www.mdpi.com/1422-0067/25/12/6343
    The proteins p53 and cyclin D1 are of critical importance in OSCC, with p53 mutations often leading to overexpression in the early stages of carcinogenesis, while overexpression of cyclin D1 regulates the cell cycle and is associated with aggressiveness and tumor progression. […] Tarle, M. and colleagues conducted a retrospective study that included immunohistochemical analysis of nuclear EGFR (nEGFR) expression and other markers such as Ki-67, p53, cyclin D1, and ABCG2 in samples of healthy oral mucosa, premalignant changes, and OSCC. […] Cetuximab, an antibody targeting EGFR, can be combined with inhibitors of PI3K/Akt signaling to enhance the effect. […] Lysyl oxidase (LOX) promotes extracellular matrix maturation and tumor invasiveness, while its propeptide (LOX-PP) inhibits tumor growth. […] Cholesterol also plays an important role in carcinogenesis as it is used for membrane biogenesis and cell signaling. […] Chan, N.N. et al. investigated the role of cholesterol in regulating the localization of caveolin-1 (CAV1) and cell migration in OSCC.
  • #23 Pathogenesis and Therapy of Oral Carcinogenesis
    https://www.mdpi.com/1422-0067/25/12/6343
    OSCC develops from the epithelium of the oral cavity mucosa under the influence of genetic, epigenetic, and environmental factors, as well as precancerous lesions such as leukoplakia and erythroplakia. […] Key features of cancer include maintenance of proliferation, evasion of growth suppressors, resistance to cell death, immortality, angiogenesis, invasion, metastasis, deregulation of energy balance, and evasion of destruction by the immune system. […] EGFR plays a key role in oral carcinogenesis by regulating signaling pathways such as MAPK and PI3K and by promoting proliferation and activation of the oncogene cyclin D1. […] Numerous studies indicate that factors such as epidermal growth factor, hydrogen, UV radiation, and ionizing radiation can cause translocation of EGFR to the nucleus, where it interacts with numerous transcription factors and influences the activation of genes involved in cell proliferation, tumor progression, and DNA repair.
  • #24 Pathogenesis and Therapy of Oral Carcinogenesis
    https://www.mdpi.com/1422-0067/25/12/6343
    OSCC develops from the epithelium of the oral cavity mucosa under the influence of genetic, epigenetic, and environmental factors, as well as precancerous lesions such as leukoplakia and erythroplakia. […] Key features of cancer include maintenance of proliferation, evasion of growth suppressors, resistance to cell death, immortality, angiogenesis, invasion, metastasis, deregulation of energy balance, and evasion of destruction by the immune system. […] EGFR plays a key role in oral carcinogenesis by regulating signaling pathways such as MAPK and PI3K and by promoting proliferation and activation of the oncogene cyclin D1. […] Numerous studies indicate that factors such as epidermal growth factor, hydrogen, UV radiation, and ionizing radiation can cause translocation of EGFR to the nucleus, where it interacts with numerous transcription factors and influences the activation of genes involved in cell proliferation, tumor progression, and DNA repair.
  • #25 Chronic Oral Mucosal Trauma and Oral Cancer: A Series of Cases
    https://www.scientificarchives.com/article/chronic-oral-mucosal-trauma-and-oral-cancer-a-series-of-cases
    Oral mucosal lesions affect the quality of life of many patients and are an apparent indicator of oral and general health. […] Indeed, chronic mucosal trauma resulting from sharp teeth and faulty restorations has been associated with the development of oral cancer. […] Although not all the risk factors for developing oral squamous cell carcinoma (OSCC) have been determined, it is likely that malignant transformation has a multifactorial etiology. […] Some of the oral manifestations of the cases presented here might explain the possible link to the pathogenesis of OSCC. […] The mechanism of developing OSCC following mucosal trauma may involve multiple factors, such as DNA damage, cytokines, human papillomavirus infection, genetic changes, smoking, alcohol, and others. […] Chronic inflammation can induce persistent tissue damage and changes in types of inflammatory cells.
  • #26 Chronic Oral Mucosal Trauma and Oral Cancer: A Series of Cases
    https://www.scientificarchives.com/article/chronic-oral-mucosal-trauma-and-oral-cancer-a-series-of-cases
    Oral mucosal lesions affect the quality of life of many patients and are an apparent indicator of oral and general health. […] Indeed, chronic mucosal trauma resulting from sharp teeth and faulty restorations has been associated with the development of oral cancer. […] Although not all the risk factors for developing oral squamous cell carcinoma (OSCC) have been determined, it is likely that malignant transformation has a multifactorial etiology. […] Some of the oral manifestations of the cases presented here might explain the possible link to the pathogenesis of OSCC. […] The mechanism of developing OSCC following mucosal trauma may involve multiple factors, such as DNA damage, cytokines, human papillomavirus infection, genetic changes, smoking, alcohol, and others. […] Chronic inflammation can induce persistent tissue damage and changes in types of inflammatory cells.
  • #27 Chronic Oral Mucosal Trauma and Oral Cancer: A Series of Cases
    https://www.scientificarchives.com/article/chronic-oral-mucosal-trauma-and-oral-cancer-a-series-of-cases
    Oral mucosal lesions affect the quality of life of many patients and are an apparent indicator of oral and general health. […] Indeed, chronic mucosal trauma resulting from sharp teeth and faulty restorations has been associated with the development of oral cancer. […] Although not all the risk factors for developing oral squamous cell carcinoma (OSCC) have been determined, it is likely that malignant transformation has a multifactorial etiology. […] Some of the oral manifestations of the cases presented here might explain the possible link to the pathogenesis of OSCC. […] The mechanism of developing OSCC following mucosal trauma may involve multiple factors, such as DNA damage, cytokines, human papillomavirus infection, genetic changes, smoking, alcohol, and others. […] Chronic inflammation can induce persistent tissue damage and changes in types of inflammatory cells.
  • #28 Chronic Oral Mucosal Trauma and Oral Cancer: A Series of Cases
    https://www.scientificarchives.com/article/chronic-oral-mucosal-trauma-and-oral-cancer-a-series-of-cases
    Moreover, the inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer. […] The concept of chronic inflammation results in crucial DNA damage, which further progresses to development of carcinoma has been reported in one study. […] Therefore, chronic inflammation may influence tumor initiation, progression, invasion, and metastasis via changes in inflammatory-cell populations and cytokine levels in local tissues. […] Taken together, a series of our cases provide clinical evidence of chronic irritation, chronic inflammation and poor oral hygiene as risk factors for oral epithelial dysplasia and OSCC.
  • #29 Chronic Oral Mucosal Trauma and Oral Cancer: A Series of Cases
    https://www.scientificarchives.com/article/chronic-oral-mucosal-trauma-and-oral-cancer-a-series-of-cases
    Moreover, the inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer. […] The concept of chronic inflammation results in crucial DNA damage, which further progresses to development of carcinoma has been reported in one study. […] Therefore, chronic inflammation may influence tumor initiation, progression, invasion, and metastasis via changes in inflammatory-cell populations and cytokine levels in local tissues. […] Taken together, a series of our cases provide clinical evidence of chronic irritation, chronic inflammation and poor oral hygiene as risk factors for oral epithelial dysplasia and OSCC.
  • #30 Chronic Oral Mucosal Trauma and Oral Cancer: A Series of Cases
    https://www.scientificarchives.com/article/chronic-oral-mucosal-trauma-and-oral-cancer-a-series-of-cases
    Moreover, the inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer. […] The concept of chronic inflammation results in crucial DNA damage, which further progresses to development of carcinoma has been reported in one study. […] Therefore, chronic inflammation may influence tumor initiation, progression, invasion, and metastasis via changes in inflammatory-cell populations and cytokine levels in local tissues. […] Taken together, a series of our cases provide clinical evidence of chronic irritation, chronic inflammation and poor oral hygiene as risk factors for oral epithelial dysplasia and OSCC.
  • #31
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-a-review-of-carcinogenic-pathways,105844,0,2.html
    Tobacco is one of the most important risk factors for premature death globally. […] A vast quantity of scientific, clinical and epidemiological data shows that tobacco is associated with the development of oral squamous cell carcinoma, and its carcinogenic pathways may be complicated. […] Tobacco as an important risk factor can cause epigenetic alteration of oral epithelial cells, inhibit multiple systemic immune functions of the host, and its toxic metabolites can cause oxidative stress on tissues and induce OSCC. […] It is widely accepted that tobacco is one the most important carcinogenic factors of OSCC, and its carcinogenic pathways may be multifaceted. […] The epigenetic alteration of these genes is a common event in oral malignancy, and is an inchoate change discovered in oral mucosa of these patients.
  • #32
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-A-review-of-ncarcinogenic-pathways,105844,0,2.html
    Tobacco is one of the most important risk factors for premature death globally. […] A vast quantity of scientific, clinical and epidemiological data shows that tobacco is associated with the development of oral squamous cell carcinoma, and its carcinogenic pathways may be complicated. […] Tobacco as an important risk factor can cause epigenetic alteration of oral epithelial cells, inhibit multiple systemic immune functions of the host, and its toxic metabolites can cause oxidative stress on tissues and induce OSCC. […] It is widely accepted that tobacco is one the most important carcinogenic factors of OSCC, and its carcinogenic pathways may be multifaceted. […] The epigenetic alteration of these genes is a common event in oral malignancy, and is an inchoate change discovered in oral mucosa of these patients.
  • #33
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-a-review-of-carcinogenic-pathways,105844,0,2.html
    Tobacco is one of the most important risk factors for premature death globally. […] A vast quantity of scientific, clinical and epidemiological data shows that tobacco is associated with the development of oral squamous cell carcinoma, and its carcinogenic pathways may be complicated. […] Tobacco as an important risk factor can cause epigenetic alteration of oral epithelial cells, inhibit multiple systemic immune functions of the host, and its toxic metabolites can cause oxidative stress on tissues and induce OSCC. […] It is widely accepted that tobacco is one the most important carcinogenic factors of OSCC, and its carcinogenic pathways may be multifaceted. […] The epigenetic alteration of these genes is a common event in oral malignancy, and is an inchoate change discovered in oral mucosa of these patients.
  • #34
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-A-review-of-ncarcinogenic-pathways,105844,0,2.html
    Tobacco is one of the most important risk factors for premature death globally. […] A vast quantity of scientific, clinical and epidemiological data shows that tobacco is associated with the development of oral squamous cell carcinoma, and its carcinogenic pathways may be complicated. […] Tobacco as an important risk factor can cause epigenetic alteration of oral epithelial cells, inhibit multiple systemic immune functions of the host, and its toxic metabolites can cause oxidative stress on tissues and induce OSCC. […] It is widely accepted that tobacco is one the most important carcinogenic factors of OSCC, and its carcinogenic pathways may be multifaceted. […] The epigenetic alteration of these genes is a common event in oral malignancy, and is an inchoate change discovered in oral mucosa of these patients.
  • #35
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-A-review-of-ncarcinogenic-pathways,105844,0,2.html
    The incidence of malignancy in immunocompromised patients is 100 times higher than in normal ones. […] The immunosuppressive effects may exist in tobacco-related OSCC. […] It has been proven that oral cancer is related to oxidative stress. […] Tobacco is an important risk factor, which through its toxic metabolites, can cause DNA damage that induces OSCC. […] In conclusion, it can be assumed that tobacco induces the occurrence of OSCC by inducing EBV reactivation, similar to NCP.
  • #36
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-a-review-of-carcinogenic-pathways,105844,0,2.html
    The incidence of malignancy in immunocompromised patients is 100 times higher than in normal ones. […] It has been proven that oral cancer is related to oxidative stress. […] Tobacco is an important risk factor, which through its toxic metabolites, can cause DNA damage that induces OSCC. […] In conclusion, it can be assumed that tobacco induces the occurrence of OSCC by inducing EBV reactivation, similar to NCP.
  • #37
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-a-review-of-carcinogenic-pathways,105844,0,2.html
    The incidence of malignancy in immunocompromised patients is 100 times higher than in normal ones. […] It has been proven that oral cancer is related to oxidative stress. […] Tobacco is an important risk factor, which through its toxic metabolites, can cause DNA damage that induces OSCC. […] In conclusion, it can be assumed that tobacco induces the occurrence of OSCC by inducing EBV reactivation, similar to NCP.
  • #38
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-A-review-of-ncarcinogenic-pathways,105844,0,2.html
    The incidence of malignancy in immunocompromised patients is 100 times higher than in normal ones. […] The immunosuppressive effects may exist in tobacco-related OSCC. […] It has been proven that oral cancer is related to oxidative stress. […] Tobacco is an important risk factor, which through its toxic metabolites, can cause DNA damage that induces OSCC. […] In conclusion, it can be assumed that tobacco induces the occurrence of OSCC by inducing EBV reactivation, similar to NCP.
  • #39
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-a-review-of-carcinogenic-pathways,105844,0,2.html
    The incidence of malignancy in immunocompromised patients is 100 times higher than in normal ones. […] It has been proven that oral cancer is related to oxidative stress. […] Tobacco is an important risk factor, which through its toxic metabolites, can cause DNA damage that induces OSCC. […] In conclusion, it can be assumed that tobacco induces the occurrence of OSCC by inducing EBV reactivation, similar to NCP.
  • #40
    https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-A-review-of-ncarcinogenic-pathways,105844,0,2.html
    The incidence of malignancy in immunocompromised patients is 100 times higher than in normal ones. […] The immunosuppressive effects may exist in tobacco-related OSCC. […] It has been proven that oral cancer is related to oxidative stress. […] Tobacco is an important risk factor, which through its toxic metabolites, can cause DNA damage that induces OSCC. […] In conclusion, it can be assumed that tobacco induces the occurrence of OSCC by inducing EBV reactivation, similar to NCP.
  • #41 Role of human papillomavirus in the pathogenesis of oral squamous cell carcinoma
    https://www.wjgnet.com/2220-315X/full/v2/i4/65.htm
    The human papillomavirus (HPV) family consists of more than 100 genotypes, classified in accordance with the ability to infect and transform epithelial cells. HPVs are DNA viruses that specifically target the basal cells of the epithelial mucosa. Genotypes, such as HPV1 infect epidermal cells, whereas HPV6, 11, 16 and 18 infect epithelial cells of the oral cavity and other mucosal surfaces. The ability of HPV to transform epithelial cells is divided into high-risk and low-risk types. Low-risk types are associated with development of benign lesions such as warts, while infections with high-risk types may progress to malignant lesions. The HPV involvement in oral carcinogenesis was supported on the basis of the following evidences: (1) the strongly established etiological role of HPV in cervical SCC; (2) the epithelial tropism of HPV; (3) the similarity between oral and genital epithelia; and (4) the detection of HPV genotypes in samples of OSCC.
  • #42 Role of human papillomavirus in the pathogenesis of oral squamous cell carcinoma
    https://www.wjgnet.com/2220-315X/full/v2/i4/65.htm
    The human papillomavirus (HPV) family consists of more than 100 genotypes, classified in accordance with the ability to infect and transform epithelial cells. HPVs are DNA viruses that specifically target the basal cells of the epithelial mucosa. Genotypes, such as HPV1 infect epidermal cells, whereas HPV6, 11, 16 and 18 infect epithelial cells of the oral cavity and other mucosal surfaces. The ability of HPV to transform epithelial cells is divided into high-risk and low-risk types. Low-risk types are associated with development of benign lesions such as warts, while infections with high-risk types may progress to malignant lesions. The HPV involvement in oral carcinogenesis was supported on the basis of the following evidences: (1) the strongly established etiological role of HPV in cervical SCC; (2) the epithelial tropism of HPV; (3) the similarity between oral and genital epithelia; and (4) the detection of HPV genotypes in samples of OSCC.
  • #43 Role of human papillomavirus in the pathogenesis of oral squamous cell carcinoma
    https://www.wjgnet.com/2220-315X/full/v2/i4/65.htm
    It is believed that one of the major events of HPV-induced carcinogenesis is the integration of the HPV genome into a host chromosome. HPV genome integration often occurs near fragile sites of the human genome, but there are no apparent sites for integration and no evidence for insertional mutagenesis. […] The vast amounts of epidemiological, molecular pathological and experimental data are consistent with the hypothesis that HPV does indeed have a causal role in oral carcinogenesis. However, HPV alone appears to be insufficient as the cause of OSCC but requires other co-factors. Although a viral association within a subset of OSCC has been shown, the molecular and histopathological characteristics of these tumors have yet to be clearly defined.
  • #44 Role of human papillomavirus in the pathogenesis of oral squamous cell carcinoma
    https://www.wjgnet.com/2220-315X/full/v2/i4/65.htm
    It is believed that one of the major events of HPV-induced carcinogenesis is the integration of the HPV genome into a host chromosome. HPV genome integration often occurs near fragile sites of the human genome, but there are no apparent sites for integration and no evidence for insertional mutagenesis. […] The vast amounts of epidemiological, molecular pathological and experimental data are consistent with the hypothesis that HPV does indeed have a causal role in oral carcinogenesis. However, HPV alone appears to be insufficient as the cause of OSCC but requires other co-factors. Although a viral association within a subset of OSCC has been shown, the molecular and histopathological characteristics of these tumors have yet to be clearly defined.
  • #45 The Presence of HPV in Dental Calculus: It’s Role in Pathogenesis of Oral and Cervical Cancer | IntechOpen
    https://www.intechopen.com/chapters/77238
    Human papillomavirus (HPV) infection accounts for approximately 5.2% of the worldwide human cancer burden. Molecular epidemiologic evidence clearly indicates that certain types of HPV are the principal cause of both cervical and oral cancers. Major oncoproteins E6 and E7 can inactivate p53 and pRB proteins because it happened genome instability and dysregulation host cell cycles. This virus is an epithelial tropism, vulnerable area mainly at the basal layer and epithelial stem cell, because it still has a high proliferation capacity, so it can support the replication of the virus. […] HPV is a small double-stranded circular DNA virus that commonly infects humans. HPV is almost entirely acquired from sexual exposure, when it enters the skin and mucous membranes of the mouth, anus, penis, and female reproductive tract. Infections with different strains are linked to a variety of skin manifestations, ranging from common warts to malignancies. HPV infection accounts for approximately 5.2% of human cancer burden worldwide, including the cancers of the anus, genital tract, and oropharynx.
  • #46 The Presence of HPV in Dental Calculus: It’s Role in Pathogenesis of Oral and Cervical Cancer | IntechOpen
    https://www.intechopen.com/chapters/77238
    HPV-induced carcinogenesis occurs as a multi-step process. It begins by primary infection of the proliferating basal cells of the squamous epithelium. If the infection is caused by a HR-HPV type, and there are presence of failure of the immune system to control and clear the infection plus the presence of some co-factors, after a period of time, HPV infection continues to accumulate sufficient genomic instability and leads to epithelial neoplastic transformation. HPV is carcinogenic, partly because proteins E6 and E7 cause abnormal regulation of p53 and Rb, control of apoptosis and regulation of cell cycle. It is believed that the circular genome is linearized and integrated as a late event in the infection process, destroying the region of the E1/E2 gene, destroying the E2 gene, releasing the suppression of the viral genome, leading to the overexpression of E6 viruses and E7 genes to maintain the malignant phenotype. […] In oral cavity, exposed areas of the basal layer will be very susceptible to HPV infection. The presence of HPV in the oral cavity is thought to be the etiologic of oral cancer in those who do not have bad habits such as smoking, betel chewing or poor oral hygiene.
  • #47 The Presence of HPV in Dental Calculus: It’s Role in Pathogenesis of Oral and Cervical Cancer | IntechOpen
    https://www.intechopen.com/chapters/77238
    HPV-induced carcinogenesis occurs as a multi-step process. It begins by primary infection of the proliferating basal cells of the squamous epithelium. If the infection is caused by a HR-HPV type, and there are presence of failure of the immune system to control and clear the infection plus the presence of some co-factors, after a period of time, HPV infection continues to accumulate sufficient genomic instability and leads to epithelial neoplastic transformation. HPV is carcinogenic, partly because proteins E6 and E7 cause abnormal regulation of p53 and Rb, control of apoptosis and regulation of cell cycle. It is believed that the circular genome is linearized and integrated as a late event in the infection process, destroying the region of the E1/E2 gene, destroying the E2 gene, releasing the suppression of the viral genome, leading to the overexpression of E6 viruses and E7 genes to maintain the malignant phenotype. […] In oral cavity, exposed areas of the basal layer will be very susceptible to HPV infection. The presence of HPV in the oral cavity is thought to be the etiologic of oral cancer in those who do not have bad habits such as smoking, betel chewing or poor oral hygiene.
  • #48 The Presence of HPV in Dental Calculus: It’s Role in Pathogenesis of Oral and Cervical Cancer | IntechOpen
    https://www.intechopen.com/chapters/77238
    HPV-induced carcinogenesis occurs as a multi-step process. It begins by primary infection of the proliferating basal cells of the squamous epithelium. If the infection is caused by a HR-HPV type, and there are presence of failure of the immune system to control and clear the infection plus the presence of some co-factors, after a period of time, HPV infection continues to accumulate sufficient genomic instability and leads to epithelial neoplastic transformation. HPV is carcinogenic, partly because proteins E6 and E7 cause abnormal regulation of p53 and Rb, control of apoptosis and regulation of cell cycle. It is believed that the circular genome is linearized and integrated as a late event in the infection process, destroying the region of the E1/E2 gene, destroying the E2 gene, releasing the suppression of the viral genome, leading to the overexpression of E6 viruses and E7 genes to maintain the malignant phenotype. […] In oral cavity, exposed areas of the basal layer will be very susceptible to HPV infection. The presence of HPV in the oral cavity is thought to be the etiologic of oral cancer in those who do not have bad habits such as smoking, betel chewing or poor oral hygiene.
  • #49 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Notch signaling has been demonstrated as a tumor suppressor in epithelial SCC malignancies (lung, bladder, and esophageal tumors) and several in vivo models. […] The development and prognosis of OSCC are affected by DNA methylation abnormalities. […] Hypermethylation can also lead to the suppression of genes involved in the progression and metastasis of OSCC. […] OSCC is a locally aggressive tumor with an elevated hypoxia level, resulting in dissemination, relapse, and poor therapeutic response. […] Hypoxia-induced decreases in E-cadherin mRNA levels boost the migration capability of OSCC cells. […] The oral microbiome is affected by OSCC risk factors such as smoking, alcohol abuse, and HPV infection. […] Certain bacterial species have been linked to the development of oral carcinoma.
  • #50 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Notch signaling has been demonstrated as a tumor suppressor in epithelial SCC malignancies (lung, bladder, and esophageal tumors) and several in vivo models. […] The development and prognosis of OSCC are affected by DNA methylation abnormalities. […] Hypermethylation can also lead to the suppression of genes involved in the progression and metastasis of OSCC. […] OSCC is a locally aggressive tumor with an elevated hypoxia level, resulting in dissemination, relapse, and poor therapeutic response. […] Hypoxia-induced decreases in E-cadherin mRNA levels boost the migration capability of OSCC cells. […] The oral microbiome is affected by OSCC risk factors such as smoking, alcohol abuse, and HPV infection. […] Certain bacterial species have been linked to the development of oral carcinoma.
  • #51 THE ROLE OF THE ORAL MICROBIOME IN ORAL CANCER PATHOGENESIS | Journal of Population Therapeutics and Clinical Pharmacology
    https://jptcp.com/index.php/jptcp/article/view/3988
    This quantitative research explores the intricate relationship between the oral microbiome and oral cancer, aiming to elucidate microbial markers indicative of disease pathogenesis. […] A case-control study involving 120 participants (60 oral cancer cases and 60 controls) revealed a significant reduction in microbial diversity among oral cancer cases, highlighting microbial dysbiosis. […] Next-generation sequencing unveiled differential abundances, with Fusobacterium nucleatum emerging as a potential microbial biomarker significantly associated with oral cancer. […] Functional analysis indicated enrichment in pathways related to inflammation and cell proliferation in cancer cases, implicating the oral microbiome in the local microenvironment. […] Importantly, Fusobacterium nucleatum exhibited diagnostic promise, displaying a fourfold increase in abundance in oral cancer cases. […] The positive correlation between its abundance and disease severity underscores its prognostic potential. […] This study contributes valuable insights into the quantitative aspects of the oral microbiome in oral cancer, paving the way for personalized diagnostic and therapeutic strategies.
  • #52 THE ROLE OF THE ORAL MICROBIOME IN ORAL CANCER PATHOGENESIS | Journal of Population Therapeutics and Clinical Pharmacology
    https://jptcp.com/index.php/jptcp/article/view/3988
    This quantitative research explores the intricate relationship between the oral microbiome and oral cancer, aiming to elucidate microbial markers indicative of disease pathogenesis. […] A case-control study involving 120 participants (60 oral cancer cases and 60 controls) revealed a significant reduction in microbial diversity among oral cancer cases, highlighting microbial dysbiosis. […] Next-generation sequencing unveiled differential abundances, with Fusobacterium nucleatum emerging as a potential microbial biomarker significantly associated with oral cancer. […] Functional analysis indicated enrichment in pathways related to inflammation and cell proliferation in cancer cases, implicating the oral microbiome in the local microenvironment. […] Importantly, Fusobacterium nucleatum exhibited diagnostic promise, displaying a fourfold increase in abundance in oral cancer cases. […] The positive correlation between its abundance and disease severity underscores its prognostic potential. […] This study contributes valuable insights into the quantitative aspects of the oral microbiome in oral cancer, paving the way for personalized diagnostic and therapeutic strategies.
  • #53 THE ROLE OF THE ORAL MICROBIOME IN ORAL CANCER PATHOGENESIS | Journal of Population Therapeutics and Clinical Pharmacology
    https://jptcp.com/index.php/jptcp/article/view/3988
    This quantitative research explores the intricate relationship between the oral microbiome and oral cancer, aiming to elucidate microbial markers indicative of disease pathogenesis. […] A case-control study involving 120 participants (60 oral cancer cases and 60 controls) revealed a significant reduction in microbial diversity among oral cancer cases, highlighting microbial dysbiosis. […] Next-generation sequencing unveiled differential abundances, with Fusobacterium nucleatum emerging as a potential microbial biomarker significantly associated with oral cancer. […] Functional analysis indicated enrichment in pathways related to inflammation and cell proliferation in cancer cases, implicating the oral microbiome in the local microenvironment. […] Importantly, Fusobacterium nucleatum exhibited diagnostic promise, displaying a fourfold increase in abundance in oral cancer cases. […] The positive correlation between its abundance and disease severity underscores its prognostic potential. […] This study contributes valuable insights into the quantitative aspects of the oral microbiome in oral cancer, paving the way for personalized diagnostic and therapeutic strategies.
  • #54 Etiology of cancer of the lip | CoLab
    https://colab.ws/articles/10.1016%2Fs0901-5027%2898%2980010-6
    A range of environmental and host factors has been identified to explain the etiopathogenesis of squamous cell carcinoma of the lip. However, the definitive pathogenic pathway remains unclear. […] Carcinogenesis does not seem to be limited to a single agent, but rather to a complex multistep process of interactions between putative risk factors. […] In this paper, the currently available data regarding risk factors, considered to be causally related to the onset of lip cancer, are reviewed.
  • #55 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1075729-overview
    The genetic aberrations involve, in order of decreasing frequency, chromosomes 9, 3, 17, 13, and 11 in particular, and probably other chromosomes, and involve inactivated TSGs, especially P16, and TP53 and overexpressed oncogenes, especially PRAD1. […] The molecular changes found in oral SCC from Western countries (eg, United Kingdom, United States, Australia), particularly TP53 mutations, are infrequent in Eastern countries (eg, India, Southeast Asia), where the involvement of ras oncogenes is more common, suggesting genetic differences that might be involved in explaining the susceptibility of certain groups to oral SCC. […] Carcinogen-metabolizing enzymes are implicated in some patients. […] Tobacco is a potent risk factor for oral cancer. […] An immune deficiency state may predispose one to a higher risk of developing oral SCC, especially lip cancer.
  • #56 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1075729-overview
    The genetic aberrations involve, in order of decreasing frequency, chromosomes 9, 3, 17, 13, and 11 in particular, and probably other chromosomes, and involve inactivated TSGs, especially P16, and TP53 and overexpressed oncogenes, especially PRAD1. […] The molecular changes found in oral SCC from Western countries (eg, United Kingdom, United States, Australia), particularly TP53 mutations, are infrequent in Eastern countries (eg, India, Southeast Asia), where the involvement of ras oncogenes is more common, suggesting genetic differences that might be involved in explaining the susceptibility of certain groups to oral SCC. […] Carcinogen-metabolizing enzymes are implicated in some patients. […] Tobacco is a potent risk factor for oral cancer. […] An immune deficiency state may predispose one to a higher risk of developing oral SCC, especially lip cancer.
  • #57 Pathogenesis and Therapy of Oral Carcinogenesis
    https://www.mdpi.com/1422-0067/25/12/6343
    OSCC develops from the epithelium of the oral cavity mucosa under the influence of genetic, epigenetic, and environmental factors, as well as precancerous lesions such as leukoplakia and erythroplakia. […] Key features of cancer include maintenance of proliferation, evasion of growth suppressors, resistance to cell death, immortality, angiogenesis, invasion, metastasis, deregulation of energy balance, and evasion of destruction by the immune system. […] EGFR plays a key role in oral carcinogenesis by regulating signaling pathways such as MAPK and PI3K and by promoting proliferation and activation of the oncogene cyclin D1. […] Numerous studies indicate that factors such as epidermal growth factor, hydrogen, UV radiation, and ionizing radiation can cause translocation of EGFR to the nucleus, where it interacts with numerous transcription factors and influences the activation of genes involved in cell proliferation, tumor progression, and DNA repair.
  • #58 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Persistent exposure to these risk factors results in genetic alterations, epigenetic modifications, and a dysregulated tumor microenvironment, all of which contribute to the occurrence and transformation of OPMDs to OSCC. […] Genetic mutations contribute to aberrant activation of oncogenic signaling and inactivation of suppressor signaling, promoting the transformation and uncontrolled proliferation of OSCC cells. […] Oncogenic signaling pathways, including the EGFR pathway, PI3K/AKT/mTOR pathway, JAK/STAT pathway, MET pathway, Wnt/-catenin pathway, and RAS/RAF/MAPK pathway, are aberrantly activated and upregulated to promote the progression of OSCC. […] Approximately 80% of HPV- HNSCC have muted tumor protein p53 (TP53), resulting in gene dysfunction. […] Similar to mutations in the TP53 pathway, retinoblastoma (RB) pathway mutations are early manifestations of HNSCC.
  • #59 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Persistent exposure to these risk factors results in genetic alterations, epigenetic modifications, and a dysregulated tumor microenvironment, all of which contribute to the occurrence and transformation of OPMDs to OSCC. […] Genetic mutations contribute to aberrant activation of oncogenic signaling and inactivation of suppressor signaling, promoting the transformation and uncontrolled proliferation of OSCC cells. […] Oncogenic signaling pathways, including the EGFR pathway, PI3K/AKT/mTOR pathway, JAK/STAT pathway, MET pathway, Wnt/-catenin pathway, and RAS/RAF/MAPK pathway, are aberrantly activated and upregulated to promote the progression of OSCC. […] Approximately 80% of HPV- HNSCC have muted tumor protein p53 (TP53), resulting in gene dysfunction. […] Similar to mutations in the TP53 pathway, retinoblastoma (RB) pathway mutations are early manifestations of HNSCC.
  • #60 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Persistent exposure to these risk factors results in genetic alterations, epigenetic modifications, and a dysregulated tumor microenvironment, all of which contribute to the occurrence and transformation of OPMDs to OSCC. […] Genetic mutations contribute to aberrant activation of oncogenic signaling and inactivation of suppressor signaling, promoting the transformation and uncontrolled proliferation of OSCC cells. […] Oncogenic signaling pathways, including the EGFR pathway, PI3K/AKT/mTOR pathway, JAK/STAT pathway, MET pathway, Wnt/-catenin pathway, and RAS/RAF/MAPK pathway, are aberrantly activated and upregulated to promote the progression of OSCC. […] Approximately 80% of HPV- HNSCC have muted tumor protein p53 (TP53), resulting in gene dysfunction. […] Similar to mutations in the TP53 pathway, retinoblastoma (RB) pathway mutations are early manifestations of HNSCC.
  • #61 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Notch signaling has been demonstrated as a tumor suppressor in epithelial SCC malignancies (lung, bladder, and esophageal tumors) and several in vivo models. […] The development and prognosis of OSCC are affected by DNA methylation abnormalities. […] Hypermethylation can also lead to the suppression of genes involved in the progression and metastasis of OSCC. […] OSCC is a locally aggressive tumor with an elevated hypoxia level, resulting in dissemination, relapse, and poor therapeutic response. […] Hypoxia-induced decreases in E-cadherin mRNA levels boost the migration capability of OSCC cells. […] The oral microbiome is affected by OSCC risk factors such as smoking, alcohol abuse, and HPV infection. […] Certain bacterial species have been linked to the development of oral carcinoma.
  • #62 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Notch signaling has been demonstrated as a tumor suppressor in epithelial SCC malignancies (lung, bladder, and esophageal tumors) and several in vivo models. […] The development and prognosis of OSCC are affected by DNA methylation abnormalities. […] Hypermethylation can also lead to the suppression of genes involved in the progression and metastasis of OSCC. […] OSCC is a locally aggressive tumor with an elevated hypoxia level, resulting in dissemination, relapse, and poor therapeutic response. […] Hypoxia-induced decreases in E-cadherin mRNA levels boost the migration capability of OSCC cells. […] The oral microbiome is affected by OSCC risk factors such as smoking, alcohol abuse, and HPV infection. […] Certain bacterial species have been linked to the development of oral carcinoma.
  • #63 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Notch signaling has been demonstrated as a tumor suppressor in epithelial SCC malignancies (lung, bladder, and esophageal tumors) and several in vivo models. […] The development and prognosis of OSCC are affected by DNA methylation abnormalities. […] Hypermethylation can also lead to the suppression of genes involved in the progression and metastasis of OSCC. […] OSCC is a locally aggressive tumor with an elevated hypoxia level, resulting in dissemination, relapse, and poor therapeutic response. […] Hypoxia-induced decreases in E-cadherin mRNA levels boost the migration capability of OSCC cells. […] The oral microbiome is affected by OSCC risk factors such as smoking, alcohol abuse, and HPV infection. […] Certain bacterial species have been linked to the development of oral carcinoma.
  • #64 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Notch signaling has been demonstrated as a tumor suppressor in epithelial SCC malignancies (lung, bladder, and esophageal tumors) and several in vivo models. […] The development and prognosis of OSCC are affected by DNA methylation abnormalities. […] Hypermethylation can also lead to the suppression of genes involved in the progression and metastasis of OSCC. […] OSCC is a locally aggressive tumor with an elevated hypoxia level, resulting in dissemination, relapse, and poor therapeutic response. […] Hypoxia-induced decreases in E-cadherin mRNA levels boost the migration capability of OSCC cells. […] The oral microbiome is affected by OSCC risk factors such as smoking, alcohol abuse, and HPV infection. […] Certain bacterial species have been linked to the development of oral carcinoma.
  • #65 Oral squamous cell carcinomas: state of the field and emerging directions | International Journal of Oral Science
    https://www.nature.com/articles/s41368-023-00249-w
    Notch signaling has been demonstrated as a tumor suppressor in epithelial SCC malignancies (lung, bladder, and esophageal tumors) and several in vivo models. […] The development and prognosis of OSCC are affected by DNA methylation abnormalities. […] Hypermethylation can also lead to the suppression of genes involved in the progression and metastasis of OSCC. […] OSCC is a locally aggressive tumor with an elevated hypoxia level, resulting in dissemination, relapse, and poor therapeutic response. […] Hypoxia-induced decreases in E-cadherin mRNA levels boost the migration capability of OSCC cells. […] The oral microbiome is affected by OSCC risk factors such as smoking, alcohol abuse, and HPV infection. […] Certain bacterial species have been linked to the development of oral carcinoma.
  • #66 Matrix Metalloproteinases in Oral Cancer Pathogenesis and their Use in Therapy – Maurya – Anti-Cancer Agents in Medicinal Chemistry
    https://vietnamjournal.ru/1871-5206/article/view/643671
    Matrix metalloproteinases (MMPs) are proteolytic enzymes that aid in extracellular matrix (ECM) remodeling. MMPs destroy the extracellular matrix, causing tumor growth and metastasis. MMPs are involved in the spread and metastasis of oral cancer. High levels of MMPs and oral squamous cell carcinoma have been linked to cancer prognosis. […] MMP gene polymorphism has recently been identified as one of the factors predicting susceptibility or risk in the development of oral carcinoma. […] The genetic polymorphism in MMP genes and its predictive value in risk evaluation have been elaborated. […] Matrix metalloproteinases in oral squamous cell carcinoma – A review.
  • #67 Matrix Metalloproteinases in Oral Cancer Pathogenesis and their Use in Therapy – Maurya – Anti-Cancer Agents in Medicinal Chemistry
    https://vietnamjournal.ru/1871-5206/article/view/643671
    Matrix metalloproteinases (MMPs) are proteolytic enzymes that aid in extracellular matrix (ECM) remodeling. MMPs destroy the extracellular matrix, causing tumor growth and metastasis. MMPs are involved in the spread and metastasis of oral cancer. High levels of MMPs and oral squamous cell carcinoma have been linked to cancer prognosis. […] MMP gene polymorphism has recently been identified as one of the factors predicting susceptibility or risk in the development of oral carcinoma. […] The genetic polymorphism in MMP genes and its predictive value in risk evaluation have been elaborated. […] Matrix metalloproteinases in oral squamous cell carcinoma – A review.
  • #68 Etiology and Pathogenesis of Oral Cancer (EPOC) | Evans Center for Interdisciplinary Biomedical Research
    https://www.bumc.bu.edu/evanscenteribr/the-arcs/recent-past-arc-programs-evolved-into-university-and-or-agency-funded-programs/etiology-and-pathogenesis-of-oral-cancer-epoc/
    Oral squamous cell carcinoma (OSCC) is among the most morbid cancers with poor survival rates, whose incidence is on the rise. The overall goal of this multidisciplinary ARC application is to determine the molecular mechanisms underlying the Etiology and Pathogenesis of Oral Cancer (EPOC), to identify novel biomarkers predictive of disease initiation, progression and morbidity, to evaluate responses to environmental carcinogens and the role of oral microbiome, and to examine the effectiveness of novel therapeutics in preclinical testing using orthotopic nude mouse models of non-metastatic and metastatic tongue cancers. […] Our studies will generate new knowledge of high impact and translational relevance to oral cancer. Further, information derived from these studies will be relevant to other malignancies and provide a platform for future exploration of new biomarkers and therapeutics for other cancers.