Rak podjęzykowy – Patofizjologia i mechanizm

Rak podjęzykowy
Patofizjologia i mechanizm

Rak podjęzykowy, stanowiący około 90% raków płaskonabłonkowych jamy ustnej, rozwija się w tkance między żuchwą a kością gnykową i charakteryzuje się akumulacją licznych zmian genetycznych i epigenetycznych, w tym aktywacją onkogenów (EGFR, K-ras, c-myc, PRAD-1) oraz inaktywacją genów supresorowych (p53, p16, Rb). Proces kancerogenezy obejmuje niestabilność genomową (LOH, MSI) oraz modyfikacje epigenetyczne, które prowadzą do nieprawidłowej aktywacji szlaków onkogennych (EGFR, Wnt/β-katenina, JAK/STAT, NOTCH, PI3K/AKT/mTOR, MET, RAS/RAF/MAPK) i zaburzeń szlaków supresorowych (TP53/RB, p16/Cyclin D1/Rb). Czynniki ryzyka to głównie ekspozycja na tytoń i alkohol (zwiększające ryzyko 15-krotnie przy jednoczesnym stosowaniu), przewlekły stan zapalny, infekcje wirusowe (szczególnie HPV, choć w raku dna jamy ustnej jego rola jest ograniczona) oraz dysbioza mikrobiomu jamy ustnej, z istotnym udziałem Fusobacterium nucleatum, którego ilość koreluje ze stopniem zaawansowania choroby. Histologicznie nowotwór przechodzi od hyperplazji, przez dysplazję i raka in situ, do inwazyjnego raka płaskonabłonkowego, często manifestując się jako wrzodziejący guz o szybkim wzroście i tendencji do przerzutów.

Patogeneza raka podjęzykowego

Modyfikacje genetyczne w patogenezie
Szlaki sygnałowe w onkogenezie
Mikrobiom jamy ustnej a rak podjęzykowy

Mechanizmy rozwoju raka podjęzykowego

Wieloetapowy proces kancerogenezy
Rola czynników ryzyka w patogenezie
Specyfika anatomiczna dna jamy ustnej
Rola wirusa HPV
Mechanizmy śmiertelności

Morfologia i postęp raka podjęzykowego

Formy wzrostu guza
Głębokość inwazji
Objawy kliniczne
Rokowanie
Kolejne rozdziały

Patogeneza raka podjęzykowego

Rak podjęzykowy (rak dna jamy ustnej) rozwija się, gdy komórki znajdujące się pod językiem ulegają zmianom w swoim DNA. W zdrowych komórkach DNA zawiera instrukcje dotyczące kontrolowanego wzrostu, namnażania się i obumierania w określonym czasie. W komórkach nowotworowych zmiany w DNA prowadzą do innych instrukcji, nakazujących komórkom szybsze namnażanie się oraz zapobiegających ich zaprogramowanej śmierci. Powoduje to nadmierną akumulację komórek, które mogą tworzyć guz. Guz ten może naciekać i niszczyć zdrowe tkanki, a w miarę postępu choroby komórki nowotworowe mogą się odrywać i rozprzestrzeniać do innych części ciała, tworząc przerzuty.¹²

Rak podjęzykowy jest w około 90% przypadków rakiem płaskonabłonkowym (squamous cell carcinoma), co oznacza, że rozwija się on w najbardziej powierzchownej warstwie błony śluzowej jamy ustnej.³ Nowotwór ten pojawia się w tkance pomiędzy żuchwą a kością gnykową i może rozprzestrzeniać się do sąsiednich tkanek, a w zaawansowanym stadium tworzyć przerzuty w węzłach chłonnych, potencjalnie wpływając na inne ważne narządy poprzez układ limfatyczny.⁴

Modyfikacje genetyczne w patogenezie

Rozwój raka podjęzykowego, podobnie jak innych nowotworów jamy ustnej, jest procesem wieloetapowym wymagającym akumulacji licznych zmian genetycznych i epigenetycznych w kluczowych genach regulatorowych. Proces ten jest zależny zarówno od predyspozycji genetycznych pacjenta, jak i od czynników środowiskowych, takich jak ekspozycja na tytoń, alkohol, przewlekły stan zapalny i infekcje wirusowe.⁵⁶

Zmiany genetyczne w raku podjęzykowym obejmują:

Aktywację onkogenów, takich jak naskórkowy receptor czynnika wzrostu (EGFR), K-ras, c-myc, int-2, PRAD-1 (Parathyroid adenomatosis 1) oraz onkogeny podobne do bcl (B-cell lymphoma)⁷
Inaktywację genów supresorowych nowotworów (TSGs), szczególnie p53, p16 i Rb⁸⁹
Niestabilność genomową, w tym utratę heterozygotyczności (LOH) i niestabilność mikrosatelitarną (MSI)¹⁰
Modyfikacje epigenetyczne, takie jak metylacja DNA, modyfikacje kowalencyjne histonów, przebudowa chromatyny i regulacja genów przez niekodujące RNA (ncRNAs)¹¹

Najczęściej obserwowane aberracje chromosomalne w raku podjęzykowym i innych nowotworach głowy i szyi dotyczą chromosomów 9, 3, 17, 13 i 11. Szczególnie istotną rolę odgrywają inaktywowane geny supresorowe nowotworów, zwłaszcza P16 i TP53, oraz nadekspresja onkogenów, szczególnie PRAD1.¹²

Szlaki sygnałowe w onkogenezie

Zmiany genetyczne w raku podjęzykowym prowadzą do nieprawidłowej aktywacji szlaków onkogennych, takich jak:¹³

EGFR (receptor naskórkowego czynnika wzrostu)
Wnt/β-katenina
JAK/STAT
NOTCH
PI3K/AKT/mTOR
MET
RAS/RAF/MAPK

Jednocześnie dochodzi do zakłóceń szlaków supresorowych, takich jak TP53/RB i p16/Cyclin D1/Rb, co znacząco przyczynia się do progresji raka.¹⁴ Mutacje w genach supresorowych nowotworów mogą być związane z genotypami cytochromu P450 i predysponować do rozwoju raka płaskonabłonkowego jamy ustnej.¹⁵

Mikrobiom jamy ustnej a rak podjęzykowy

Badania wykazały, że mikrobiom jamy ustnej może odgrywać rolę w patogenezie raka jamy ustnej, w tym raka podjęzykowego. U pacjentów z rakiem jamy ustnej obserwuje się znaczne zmniejszenie różnorodności mikrobiologicznej, co wskazuje na dysbiozę mikrobiologiczną.¹⁶

Szczególnie istotną rolę może odgrywać Fusobacterium nucleatum, którego zwiększoną ilość (czterokrotnie wyższą) obserwuje się u pacjentów z rakiem jamy ustnej. Dodatkowo stwierdzono pozytywną korelację między ilością tej bakterii a stopniem zaawansowania choroby, co podkreśla jej potencjalne znaczenie prognostyczne.¹⁷ Analiza funkcjonalna wykazała wzbogacenie szlaków związanych ze stanem zapalnym i proliferacją komórek w przypadkach raka, co sugeruje udział mikrobiomu jamy ustnej w lokalnym mikrośrodowisku nowotworowym.¹⁸

Mechanizmy rozwoju raka podjęzykowego

Wieloetapowy proces kancerogenezy

Rozwój raka podjęzykowego jest rezultatem wieloetapowego procesu, który histologicznie postępuje od normalnego nabłonka do hyperplazji, następnie dysplazji i raka in situ, poprzedzając rozwój inwazyjnego raka płaskonabłonkowego.¹⁹ Proces ten charakteryzuje się mutacjami związanymi ze zmianami liczby kopii genów oraz modyfikacjami epigenetycznymi.²⁰

Kancerogeneza w dnie jamy ustnej wiąże się z wieloogniskowymi zmianami, co oznacza, że rak może rozwijać się w wielu miejscach jednocześnie. Koncepcja pola kanceryzacji (field cancerization) sugeruje, że długotrwała ekspozycja na czynniki środowiskowe i egzogenne może prowadzić do wieloogniskowych prezentacji i ekspresji mutacji genów supresorowych nowotworów, co utrudnia chirurgiczne usunięcie zmian przedrakowych.²¹

Rola czynników ryzyka w patogenezie

Do głównych czynników ryzyka rozwoju raka podjęzykowego należą:²²²³

Tytoń i alkohol – Użytkowanie wyrobów tytoniowych, szczególnie tytoniu do żucia, oraz regularne spożywanie dużych ilości alkoholu znacząco zwiększa ryzyko rozwoju raka podjęzykowego. Jednoczesne używanie obu tych substancji zwiększa ryzyko 15-krotnie.²⁴
Żucie betelu (orzechów betelowych) – Praktyka popularna szczególnie w Azji Południowo-Wschodniej
Przewlekły stan zapalny spowodowany źle dopasowanymi protezami lub ostrymi krawędziami zębów
Infekcje wirusowe, zwłaszcza HPV (wirus brodawczaka ludzkiego)
Nieleczone stany przedrakowe, np. leukoplakia
Słaba higiena jamy ustnej

Szczególnie interesujący jest związek między rakiem dna jamy ustnej a paleniem tytoniu i spożywaniem alkoholu. Rak podjęzykowy wydaje się być prawie wyłącznie związany z konwencjonalnym paleniem i intensywnym spożyciem alkoholu.²⁵ Ryzyko to jest związane z lokalną ekspozycją, co przypisuje się gromadzeniu się karcynogenów w ślinie, która predysponuje cienką i niezrogowaciałą błonę śluzową dna jamy ustnej do powtarzającej się ekspozycji na karcynogeny.²⁶

Specyfika anatomiczna dna jamy ustnej

Struktura dna jamy ustnej może wyjaśniać, dlaczego jest ona bardziej wrażliwa na karcynogeny. Poszczególne obszary jamy ustnej różnią się składem tkanek, ekspresją markerów molekularnych i szybkością odnowy nabłonka. Dno jamy ustnej ma cienką, niezrogowaciałą błonę śluzową, a karcynogeny mają tendencję do gromadzenia się po zmieszaniu ze śliną, co wydłuża czas kontaktu z szkodliwymi substancjami.²⁷

Ze względu na brak bariery ochronnej, jaką stanowi zrogowaciały nabłonek, dno jamy ustnej jest bardziej wrażliwe na działanie karcynogenów i ciepło dymu tytoniowego. Podczas gdy raki płaskonabłonkowe niezrogowaciałego nabłonka wyściełającego dno jamy ustnej i błonę śluzową policzka są powiązane z konsumpcją tytoniu i alkoholu, raki wywodzące się ze zrogowaciałego nabłonka żującego dziąseł i podniebienia twardego częściej występują u kobiet bez czynników ryzyka.²⁸

Rola wirusa HPV

Infekcja wirusem brodawczaka ludzkiego (HPV), szczególnie typem 16, jest uznanym czynnikiem ryzyka i czynnikiem przyczynowym raka jamy ustnej.²⁹ Jednakże w przypadku raka dna jamy ustnej, rola HPV nie wydaje się być znacząca w patogenezie.³⁰

Raki podjęzykowe zwykle charakteryzują się niską częstością występowania DNA HPV, co sugeruje, że wirus ten nie odgrywa istotnej roli w patogenezie raka dna jamy ustnej.³¹

Mechanizmy śmiertelności

Rak płaskonabłonkowy jamy ustnej, w tym rak podjęzykowy, może prowadzić do śmierci poprzez różne mechanizmy. Progresja nowotworu, miejscowa inwazja sąsiednich narządów i odległe przerzuty są głównymi przyczynami zgonu.³²

Agresywny wzrost zmiany może szybko naciekać i uszkadzać otaczające struktury, takie jak drogi oddechowe, prowadząc do niedrożności dróg oddechowych, krwawienia i ciężkich infekcji. Odległe przerzuty, szczególnie do narządów ważnych dla życia, takich jak płuca, znacząco wpływają na wskaźniki przeżywalności tej choroby.³³

Pacjenci poddawani resekcji z powodu raka płaskonabłonkowego jamy ustnej są narażeni na wysokie ryzyko powikłań sercowo-naczyniowych i oddechowych, uznawanych za istotne czynniki śmiertelności.³⁴

Morfologia i postęp raka podjęzykowego

Formy wzrostu guza

Około 99% guzów dna jamy ustnej ma formę wrzodziejącą. Oznacza to, że guz wnika głęboko w istniejącą tkankę, pozostawiając „krater”. Guzy tego typu rosną niezwykle szybko i często są już dość zaawansowane w momencie postawienia diagnozy. Ponadto, guzy wrzodziejące mają tendencję do tworzenia przerzutów, co powoduje, że rokowanie dla tej formy choroby jest raczej negatywne.³⁵

Tylko w około 1% wszystkich raków płaskonabłonkowych dna jamy ustnej guz rośnie na zewnątrz w stopniowym tempie. Ta forma progresji zwykle nie prowadzi do rozwoju przerzutów.³⁶

Głębokość inwazji

Głębokość inwazji (DOI – Depth of Invasion) jest istotnym czynnikiem prognostycznym w raku podjęzykowym. 8. edycja Podręcznika Klasyfikacji Nowotworów AJCC dodała DOI do kryteriów klasyfikacji T raka jamy ustnej od T1 do T4a, ponieważ patologiczna głębokość inwazji jest silnie związana z przerzutami do węzłów chłonnych szyi, które są najważniejszym czynnikiem prognostycznym.³⁷

W przypadku raka dna jamy ustnej, niewykrywalność w obrazowaniu MRI sugeruje zmianę powierzchowną i wskazuje na małą głębokość inwazji (≤3 mm). DOI raka dna jamy ustnej może być ważnym wskaźnikiem przy określaniu kombinacji resekcji miejscowej i rekonstrukcji płatowej.³⁸

Objawy kliniczne

Najczęstszym objawem raka dna jamy ustnej jest rana w jamie ustnej, która stale się powiększa. Inne objawy raka podjęzykowego to:³⁹⁴⁰

Białe lub czerwone plamy lub zmiany wrzodziejące na dnie jamy ustnej
Ból lub drętwienie w jamie ustnej
Guzek na szyi

Rak podjęzykowy często pojawia się jako owrzodzenie w jamie ustnej, które nie goi się, i może być mylony z aftą.⁴¹

Rokowanie

Rokowanie zależy znacząco od tego, jak zaawansowany jest nowotwór w momencie diagnozy:⁴²

Jeśli węzły chłonne nie zostały jeszcze zajęte, średni wskaźnik pięcioletniego przeżycia wynosi około 70%.
Jeśli w węzłach chłonnych utworzyły się przerzuty, wskaźnik przeżycia spada do około 20-25%.

Rak dna jamy ustnej jest wysoce uleczalny, gdy zostanie zdiagnozowany wcześnie. Leczenie często obejmuje operację przeprowadzaną przez chirurga specjalizującego się w nowotworach głowy i szyi. Jeśli nowotwór jest bardziej zaawansowany, radioterapia, chemioterapia lub obie te metody mogą być stosowane do zmniejszenia guza przed lub po operacji w celu zmniejszenia ryzyka nawrotu nowotworu.⁴³

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Materiały źródłowe

#1 Floor of the mouth cancer – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/floor-mouth-cancer/symptoms-causes/syc-20354179
Floor of the mouth cancer happens when cells under the tongue develop changes in their DNA. A cell’s DNA holds the instructions that tell a cell what to do. In healthy cells, the DNA gives instructions to grow and multiply at a set rate. The instructions also tell the cells to die at a set time. In cancer cells, the DNA changes give different instructions. The changes tell the cancer cells to make many more cells quickly. Cancer cells can keep living when healthy cells would die. This causes too many cells. […] The cancer cells might form a mass called a tumor. The tumor can grow to invade and destroy healthy body tissue. In time, cancer cells can break away and spread to other parts of the body. When cancer spreads, it’s called metastatic cancer.
#2 Mouth cancer – Symptoms and causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/mouth-cancer/symptoms-causes/syc-20350997
Mouth cancer happens when cells on the lips or in the mouth develop changes in their DNA. […] These are flat, thin cells that line the lips and the inside of the mouth. Most oral cancers are squamous cell carcinomas. […] The changes tell the cancer cells to grow and multiply quickly. Cancer cells can keep living when healthy cells would die. This causes too many cells. […] The cancer cells might form a mass called a tumor. The tumor can grow to invade and destroy healthy body tissue. In time, the cancer cells can break away and spread to other parts of the body. When cancer spreads, it’s called metastatic cancer.
#3 Floor of the mouth cancer: Symptoms, treatment and prognosis | CURAPROX
https://curaprox.us/blog/post/interesting-facts-about-floor-of-the-mouth-cancer?srsltid=AfmBOooXrmQJL-aDEvj-x6hpcYDumOIdEUVwJZ2Bwd13vqyEHgWlxeF0
Floor of the mouth cancer is a malignant tumour that forms on the oral mucosa between the lower jaw and the hyoid bone. […] The tumour spreads to neighbouring tissue and can, at an advanced stage, form metastases in the lymph nodes, potentially impacting other vital organs via the lymphatic system. […] In around 90 percent of cases, floor of the mouth cancer is a squamous cell carcinoma. This means that the tumour is located on the uppermost layer of the oral mucosa. […] Floor of the mouth cancer occurs when cells with altered genetic information multiply and are not recognised by the immune system. These altered cancer cells gradually displace healthy cells and form a tumour, which grows either quickly or slowly depending on the type of tumour. […] When tumour cells migrate and settle in the lymph nodes, for example, doctors say the cancer has „metastasised”.
#4 Floor of the mouth cancer: Symptoms, treatment and prognosis | CURAPROX
https://curaprox.us/blog/post/interesting-facts-about-floor-of-the-mouth-cancer?srsltid=AfmBOooXrmQJL-aDEvj-x6hpcYDumOIdEUVwJZ2Bwd13vqyEHgWlxeF0
Floor of the mouth cancer is a malignant tumour that forms on the oral mucosa between the lower jaw and the hyoid bone. […] The tumour spreads to neighbouring tissue and can, at an advanced stage, form metastases in the lymph nodes, potentially impacting other vital organs via the lymphatic system. […] In around 90 percent of cases, floor of the mouth cancer is a squamous cell carcinoma. This means that the tumour is located on the uppermost layer of the oral mucosa. […] Floor of the mouth cancer occurs when cells with altered genetic information multiply and are not recognised by the immune system. These altered cancer cells gradually displace healthy cells and form a tumour, which grows either quickly or slowly depending on the type of tumour. […] When tumour cells migrate and settle in the lymph nodes, for example, doctors say the cancer has „metastasised”.
#5 Oral Cancer: Risk Factors and Molecular Pathogenesis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3177522/
Oral cancer is one of the most common cancers and it constitutes a major health problem particularly in developing countries. […] The development of oral cancer is a multistep process involving the accumulation of genetic and epigenetic alterations in key regulatory genes. […] Use of genetic and proteomic approach in recent years have revealed the molecular pathological picture of OC. There is active search to identify genetic alterations in oncogenes or tumour suppressor genes, role of genomic instability and epigenetic modifications and to generate a gene expression profile in oral oncogenesis. […] Understanding these genetic changes and gene expression patterns are keys to the understanding of molecular pathogenesis of OC. […] Genetic alterations define molecular basis of carcinogenesis which includes point mutations, amplifications, rearrangements, and deletions. Several oncogenes have also been implicated in oral carcinogenesis.
#6 KEGG DISEASE: Oral cancer
https://www.genome.jp/dbget-bin/www_bget?ds:H00016
Oral cancer refers to a subgroup of head and neck malignancies that develop at the lips, tongue, salivary glands, gingiva, floor of the mouth, oropharynx, buccal surfaces and other intra-oral locations, according to the International Classification of Diseases. […] The development of OSCC is a multistep process requiring the accumulation of multiple genetic alterations, influenced by a patient’s genetic predisposition as well as by environmental influences, including tobacco, alcohol, chronic inflammation, and viral infection. […] The genetic changes include activation of the epidermal growth factor receptor (EGFR), alterations of tumor suppressors p53 and p16, and cyclin D1 overexpression.
#7 Oral Cancer: Risk Factors and Molecular Pathogenesis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3177522/
Aberrant expression of epidermal growth factor receptor (EGFR), K-ras, c-myc, int-2, Parathyroid adenomatosis 1 (PRAD-1) and B-cell lymphoma (bcl) like oncogenes have been reported in OC development. […] More than 50% of all primary HNSCC harbour p53 mutation. […] The most commonly deleted region in HNC is located at chromosome 9p21-22. […] Loss of chromosome 9p21 occurs in the majority of invasive tumors in head and neck cancer. […] Genomic instability such as loss of heterozygosity (LOH) and microsatellite instability (MSI) are frequently observed in cancer and such instability has been investigated and several reports are available in OC. […] The major epigenetic modification in tumours is methylation. Changes in the methylation patterns can play an important role in tumorigenesis. […] Methylation patterns of p16, methylguanine-DNA methyltransferase (MGMT) and Death-associated protein kinase (DAP-K) genes in smears of patients suffering from head and neck cancer showed abnormal hypermethylation patterns by a methylation specific polymerase chain reaction.
#8 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.
#9 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
Oral squamous cell carcinoma (OSCC) develops on the mucosal epithelium of the oral cavity. […] Persistent exposure to various risk factors, including tobacco, alcohol, betel quid (BQ), and human papillomavirus (HPV), will lead to the development of oral potentially malignant disorders (OPMDs), which are oral mucosal lesions with an increased risk of developing into OSCC. […] Complex and multifactorial, the oncogenesis process involves genetic alteration, epigenetic modification, and a dysregulated tumor microenvironment. […] Understanding the mechanism of malignancies will facilitate the identification of therapeutic and prognostic factors, thereby improving the efficacy of treatment for OSCC patients. […] The genetic alterations result in the aberrant activation of oncogenic pathways, such as EGFR, Wnt/-catenin, JAK/STAT, NOTCH, PI3K/AKT/mTOR, MET, and RAS/RAF/MAPK, as well as disruptions of suppressor pathways, such as TP53/RB, p16/Cyclin D1/Rb, which significantly contribute to the progression of OSCC.
#10 Oral Cancer: Risk Factors and Molecular Pathogenesis
https://pmc.ncbi.nlm.nih.gov/articles/PMC3177522/
Aberrant expression of epidermal growth factor receptor (EGFR), K-ras, c-myc, int-2, Parathyroid adenomatosis 1 (PRAD-1) and B-cell lymphoma (bcl) like oncogenes have been reported in OC development. […] More than 50% of all primary HNSCC harbour p53 mutation. […] The most commonly deleted region in HNC is located at chromosome 9p21-22. […] Loss of chromosome 9p21 occurs in the majority of invasive tumors in head and neck cancer. […] Genomic instability such as loss of heterozygosity (LOH) and microsatellite instability (MSI) are frequently observed in cancer and such instability has been investigated and several reports are available in OC. […] The major epigenetic modification in tumours is methylation. Changes in the methylation patterns can play an important role in tumorigenesis. […] Methylation patterns of p16, methylguanine-DNA methyltransferase (MGMT) and Death-associated protein kinase (DAP-K) genes in smears of patients suffering from head and neck cancer showed abnormal hypermethylation patterns by a methylation specific polymerase chain reaction.
#11 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
Epigenetic modifications, such as DNA methylation, histone covalent modification, chromatin remodeling, and gene regulation by non-coding RNAs (ncRNAs), participate in OSCC formation and development. […] 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.
#12 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. […] Mutations in some TSGs may be related to cytochrome P450 genotypes and predispose to oral SCC. […] 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.
#13 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
Oral squamous cell carcinoma (OSCC) develops on the mucosal epithelium of the oral cavity. […] Persistent exposure to various risk factors, including tobacco, alcohol, betel quid (BQ), and human papillomavirus (HPV), will lead to the development of oral potentially malignant disorders (OPMDs), which are oral mucosal lesions with an increased risk of developing into OSCC. […] Complex and multifactorial, the oncogenesis process involves genetic alteration, epigenetic modification, and a dysregulated tumor microenvironment. […] Understanding the mechanism of malignancies will facilitate the identification of therapeutic and prognostic factors, thereby improving the efficacy of treatment for OSCC patients. […] The genetic alterations result in the aberrant activation of oncogenic pathways, such as EGFR, Wnt/-catenin, JAK/STAT, NOTCH, PI3K/AKT/mTOR, MET, and RAS/RAF/MAPK, as well as disruptions of suppressor pathways, such as TP53/RB, p16/Cyclin D1/Rb, which significantly contribute to the progression of OSCC.
#14 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
Oral squamous cell carcinoma (OSCC) develops on the mucosal epithelium of the oral cavity. […] Persistent exposure to various risk factors, including tobacco, alcohol, betel quid (BQ), and human papillomavirus (HPV), will lead to the development of oral potentially malignant disorders (OPMDs), which are oral mucosal lesions with an increased risk of developing into OSCC. […] Complex and multifactorial, the oncogenesis process involves genetic alteration, epigenetic modification, and a dysregulated tumor microenvironment. […] Understanding the mechanism of malignancies will facilitate the identification of therapeutic and prognostic factors, thereby improving the efficacy of treatment for OSCC patients. […] The genetic alterations result in the aberrant activation of oncogenic pathways, such as EGFR, Wnt/-catenin, JAK/STAT, NOTCH, PI3K/AKT/mTOR, MET, and RAS/RAF/MAPK, as well as disruptions of suppressor pathways, such as TP53/RB, p16/Cyclin D1/Rb, which significantly contribute to the progression of OSCC.
#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. […] Mutations in some TSGs may be related to cytochrome P450 genotypes and predispose to oral SCC. […] 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 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.
#17 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.
#18 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.
#19 Biomedicines | Special Issue : Oral Cancer: From Pathophysiology to Novel Therapeutic Approaches
https://www.mdpi.com/journal/biomedicines/special_issues/oral_cancer_therapy
Oral cancer is a commonly occurring head and neck cancer, 90% of cases of which are diagnosed as oral squamous cell carcinoma (OSCC). This lethal malignancy is a debilitating disease that impacts patientsâ physical appearance, causing disfiguration and devastating their self-esteem. Despite improvements in diagnostic facilities and patient management, the prognosis of OSCC remains poor. […] Histologically, OSCC is derived from a multistep mechanism known as oral carcinogenesis, which progresses from normal epithelium to hyperplasia, followed by dysplasia and carcinoma in situ and precedes the development of invasive squamous cell carcinoma. Caused by exposure to carcinogens, such as smoking and excessive alcohol drinking and HPV infections, this multistep mechanism is characterized by mutations related to copy number alteration and epigenetic modifications.
#20 Biomedicines | Special Issue : Oral Cancer: From Pathophysiology to Novel Therapeutic Approaches
https://www.mdpi.com/journal/biomedicines/special_issues/oral_cancer_therapy
Oral cancer is a commonly occurring head and neck cancer, 90% of cases of which are diagnosed as oral squamous cell carcinoma (OSCC). This lethal malignancy is a debilitating disease that impacts patientsâ physical appearance, causing disfiguration and devastating their self-esteem. Despite improvements in diagnostic facilities and patient management, the prognosis of OSCC remains poor. […] Histologically, OSCC is derived from a multistep mechanism known as oral carcinogenesis, which progresses from normal epithelium to hyperplasia, followed by dysplasia and carcinoma in situ and precedes the development of invasive squamous cell carcinoma. Caused by exposure to carcinogens, such as smoking and excessive alcohol drinking and HPV infections, this multistep mechanism is characterized by mutations related to copy number alteration and epigenetic modifications.
#21
http://waocp.com/journal/index.php/apjcb/article/view/1221
Oral carcinogenesis is a multifocal process involving genetic alterations in squamous epithelial cells, which can be detected through various molecular biology techniques. High-throughput methods are being used to search for oral cancer biomarkers in biofluids like saliva and serum. The concept of field cancerization suggests that cancer can develop at multiple sites, and research has shown that mutations in the p53 gene are linked to smoking and increase the risk of oral carcinoma. Long-term exposure to environmental and exogenous factors may lead to multi-focal presentations and mutational expressions of tumor suppressor genes, making it difficult to surgically remove premalignant lesions.
#22 Floor of the mouth cancer: Symptoms, treatment and prognosis | CURAPROX
https://curaprox.co.uk/blog/post/interesting-facts-about-floor-of-the-mouth-cancer?srsltid=AfmBOopR8nT9eA5RihokjHNYRIjSDB3lWyRIy_PsIx4bxesw1-pQoObG
Floor of the mouth cancer occurs when cells with altered genetic information multiply and are not recognised by the immune system. These altered cancer cells gradually displace healthy cells and form a tumour, which grows either quickly or slowly depending on the type of tumour. […] It is not yet known why this type of cell mutation occurs. However, there are a number of risk factors that increase the likelihood of developing floor of the mouth cancer. […] The main risk factors for floor of the mouth cancer are: Drinking and smoking (also the use of „smokeless” tobacco products), Betel chewing (use of betel nuts; especially in Southeast Asia), Chronic inflammation due to poorly fitting dentures or sharp-edged teeth, Virus infections (especially HPV), Untreated preliminary stages (e.g. leukoplakia), Poor oral hygiene.
#23 Floor of the mouth cancer: Symptoms, treatment and prognosis | CURAPROX
https://curaprox.us/blog/post/interesting-facts-about-floor-of-the-mouth-cancer?srsltid=AfmBOooXrmQJL-aDEvj-x6hpcYDumOIdEUVwJZ2Bwd13vqyEHgWlxeF0
The main risk factors for floor of the mouth cancer are: Drinking and smoking (also the use of „smokeless” tobacco products), Betel chewing (use of betel nuts; especially in Southeast Asia), Chronic inflammation due to poorly fitting dentures or sharp-edged teeth, Virus infections (especially HPV), Untreated preliminary stages (e.g. leukoplakia), Poor oral hygiene. […] Treatment of floor of the mouth cancer may vary significantly depending on its location, size, form of progression and stage. […] The most common forms of treatment for squamous cell carcinomas of the floor of the mouth are presented below: Surgery, Radiotherapy, Chemotherapy. […] If the tumour needs to be removed surgically, chemotherapy and/or radiotherapy treatment may be prescribed either before or after surgery. […] About 99 percent of floor of the mouth tumours have an ulcerous form. This means that the tumour invades deep into existing tissue, leaving a „crater”.
#24
https://www.tobaccoinduceddiseases.org/Oral-squamous-cell-carcinoma-Effect-of-tobacco-and-alcohol-on-cancer-location,189303,0,2.html
In 519 patients, tumors occurred most often in the tongue (51%), gingiva (21%), or floor of the mouth (FOM; 15%). FOM had 26-fold greater odds for a history of smoking and alcohol use than other tumor sites (OR=25.78; 95% CI: 8.0282.95; p […] OSCC of oral cavity sites has notable differences in etiology. FOM seems to be related almost exclusively to conventional smoking and heavy alcohol use. […] The combined use of both increases the risk of OSCC by 15-fold, especially for floor-of-mouth (FOM) cancer. […] The risk of tobacco and alcohol is connected to local exposure. This is attributed to pooling the carcinogens with saliva, which predisposes the thin and non-keratinized mucosa of FOM to repeated exposure to carcinogens. […] The structure of FOM could explain why it is more sensitive to carcinogens. The oral cavity sites differ in tissue composition, molecular marker expression, and epithelial turnover rates. FOM has thin, non-keratinized mucosa, and the carcinogens tend to pool when mixed with saliva, allowing more contact time with noxious substances.
#25
https://www.tobaccoinduceddiseases.org/Oral-squamous-cell-carcinoma-Effect-of-tobacco-and-alcohol-on-cancer-location,189303,0,2.html
Since FOM lacks this barrier, it is more sensitive to carcinogens and the heat of tobacco smoke. […] OSCCs of the non-keratinized lining epithelium of the FOM and buccal mucosa have been linked to tobacco and alcohol consumption, the OSCCs originating from the keratinized masticatory epithelium of the gingiva and hard palate are more commonly seen in women with no risk behavior. […] The differences in the etiology of these cancers remain partly unknown, but examining whether FOM has structural and/or molecular differences from the tongue that could attenuate the effect of these risk factors should be elucidated. […] FOM carcinomas usually also have a low incidence of HPV-DNA, and HPV does not seem to have a significant role in the pathogenesis of FOM OSCC. […] OSCCs of different sites have differences in etiology. SCC of FOM appears to be almost entirely cancer caused by the common carcinogens of tobacco and alcohol.
#26
https://www.tobaccoinduceddiseases.org/Oral-squamous-cell-carcinoma-Effect-of-tobacco-and-alcohol-on-cancer-location,189303,0,2.html
In 519 patients, tumors occurred most often in the tongue (51%), gingiva (21%), or floor of the mouth (FOM; 15%). FOM had 26-fold greater odds for a history of smoking and alcohol use than other tumor sites (OR=25.78; 95% CI: 8.0282.95; p […] OSCC of oral cavity sites has notable differences in etiology. FOM seems to be related almost exclusively to conventional smoking and heavy alcohol use. […] The combined use of both increases the risk of OSCC by 15-fold, especially for floor-of-mouth (FOM) cancer. […] The risk of tobacco and alcohol is connected to local exposure. This is attributed to pooling the carcinogens with saliva, which predisposes the thin and non-keratinized mucosa of FOM to repeated exposure to carcinogens. […] The structure of FOM could explain why it is more sensitive to carcinogens. The oral cavity sites differ in tissue composition, molecular marker expression, and epithelial turnover rates. FOM has thin, non-keratinized mucosa, and the carcinogens tend to pool when mixed with saliva, allowing more contact time with noxious substances.
#27
https://www.tobaccoinduceddiseases.org/Oral-squamous-cell-carcinoma-Effect-of-tobacco-and-alcohol-on-cancer-location,189303,0,2.html
In 519 patients, tumors occurred most often in the tongue (51%), gingiva (21%), or floor of the mouth (FOM; 15%). FOM had 26-fold greater odds for a history of smoking and alcohol use than other tumor sites (OR=25.78; 95% CI: 8.0282.95; p […] OSCC of oral cavity sites has notable differences in etiology. FOM seems to be related almost exclusively to conventional smoking and heavy alcohol use. […] The combined use of both increases the risk of OSCC by 15-fold, especially for floor-of-mouth (FOM) cancer. […] The risk of tobacco and alcohol is connected to local exposure. This is attributed to pooling the carcinogens with saliva, which predisposes the thin and non-keratinized mucosa of FOM to repeated exposure to carcinogens. […] The structure of FOM could explain why it is more sensitive to carcinogens. The oral cavity sites differ in tissue composition, molecular marker expression, and epithelial turnover rates. FOM has thin, non-keratinized mucosa, and the carcinogens tend to pool when mixed with saliva, allowing more contact time with noxious substances.
#28
https://www.tobaccoinduceddiseases.org/Oral-squamous-cell-carcinoma-Effect-of-tobacco-and-alcohol-on-cancer-location,189303,0,2.html
Since FOM lacks this barrier, it is more sensitive to carcinogens and the heat of tobacco smoke. […] OSCCs of the non-keratinized lining epithelium of the FOM and buccal mucosa have been linked to tobacco and alcohol consumption, the OSCCs originating from the keratinized masticatory epithelium of the gingiva and hard palate are more commonly seen in women with no risk behavior. […] The differences in the etiology of these cancers remain partly unknown, but examining whether FOM has structural and/or molecular differences from the tongue that could attenuate the effect of these risk factors should be elucidated. […] FOM carcinomas usually also have a low incidence of HPV-DNA, and HPV does not seem to have a significant role in the pathogenesis of FOM OSCC. […] OSCCs of different sites have differences in etiology. SCC of FOM appears to be almost entirely cancer caused by the common carcinogens of tobacco and alcohol.
#29
http://waocp.com/journal/index.php/apjcb/article/view/1221
Oral squamous cell carcinoma (OSCC) is a preventable disease that is primarily caused by environmental factors, with tobacco being the leading culprit. The development of OSCC is directly related to the dose, frequency, and mode of exposure to carcinogens, which are substances that have the potential to cause cancer. […] Tobacco usage is a primary contributor to the development of oral cancer, as it triggers genetic alterations in the buccal cells that can culminate in malignancy. The carcinogenic properties of tobacco are attributed to the chemical compounds present in cigarette smoke and other tobacco products, which instigate mutations in the cellular DNA, thereby increasing the likelihood of cancerous growth in the oral cavity. […] Infection with human papillomavirus (HPV), specifically type 16, is a recognized risk factor and causative agent for oral cancer.
#30
https://www.tobaccoinduceddiseases.org/Oral-squamous-cell-carcinoma-Effect-of-tobacco-and-alcohol-on-cancer-location,189303,0,2.html
Since FOM lacks this barrier, it is more sensitive to carcinogens and the heat of tobacco smoke. […] OSCCs of the non-keratinized lining epithelium of the FOM and buccal mucosa have been linked to tobacco and alcohol consumption, the OSCCs originating from the keratinized masticatory epithelium of the gingiva and hard palate are more commonly seen in women with no risk behavior. […] The differences in the etiology of these cancers remain partly unknown, but examining whether FOM has structural and/or molecular differences from the tongue that could attenuate the effect of these risk factors should be elucidated. […] FOM carcinomas usually also have a low incidence of HPV-DNA, and HPV does not seem to have a significant role in the pathogenesis of FOM OSCC. […] OSCCs of different sites have differences in etiology. SCC of FOM appears to be almost entirely cancer caused by the common carcinogens of tobacco and alcohol.
#31
https://www.tobaccoinduceddiseases.org/Oral-squamous-cell-carcinoma-Effect-of-tobacco-and-alcohol-on-cancer-location,189303,0,2.html
Since FOM lacks this barrier, it is more sensitive to carcinogens and the heat of tobacco smoke. […] OSCCs of the non-keratinized lining epithelium of the FOM and buccal mucosa have been linked to tobacco and alcohol consumption, the OSCCs originating from the keratinized masticatory epithelium of the gingiva and hard palate are more commonly seen in women with no risk behavior. […] The differences in the etiology of these cancers remain partly unknown, but examining whether FOM has structural and/or molecular differences from the tongue that could attenuate the effect of these risk factors should be elucidated. […] FOM carcinomas usually also have a low incidence of HPV-DNA, and HPV does not seem to have a significant role in the pathogenesis of FOM OSCC. […] OSCCs of different sites have differences in etiology. SCC of FOM appears to be almost entirely cancer caused by the common carcinogens of tobacco and alcohol.
#32 Oral Squamous Cell Carcinoma: A Silent Killer
https://ostrowonline.usc.edu/squamous-cell-carcinoma-unveiling-the-faces-of-a-silent-killer-2/
Oral squamous cell carcinoma can be fatal through various mechanisms. The cancers progression, local invasion of nearby organs, and distant metastasis are the primary causes of death. The lesions aggressive growth can rapidly invade and damage surrounding structures, such as the airway, leading to airway blockage, bleeding, and severe infections. Distant metastasis, especially to vital organs like the lungs, significantly affects the diseases survival rates. Patients undergoing resection for OSCC (oral squamous cell carcinoma) are at high risk for cardiovascular and respiratory complications, recognized as significant mortality factors. […] However, the risk of death increases significantly with each additional pack-year of tobacco smoking.
#33 Oral Squamous Cell Carcinoma: A Silent Killer
https://ostrowonline.usc.edu/squamous-cell-carcinoma-unveiling-the-faces-of-a-silent-killer-2/
Oral squamous cell carcinoma can be fatal through various mechanisms. The cancers progression, local invasion of nearby organs, and distant metastasis are the primary causes of death. The lesions aggressive growth can rapidly invade and damage surrounding structures, such as the airway, leading to airway blockage, bleeding, and severe infections. Distant metastasis, especially to vital organs like the lungs, significantly affects the diseases survival rates. Patients undergoing resection for OSCC (oral squamous cell carcinoma) are at high risk for cardiovascular and respiratory complications, recognized as significant mortality factors. […] However, the risk of death increases significantly with each additional pack-year of tobacco smoking.
#34 Oral Squamous Cell Carcinoma: A Silent Killer
https://ostrowonline.usc.edu/squamous-cell-carcinoma-unveiling-the-faces-of-a-silent-killer-2/
Oral squamous cell carcinoma can be fatal through various mechanisms. The cancers progression, local invasion of nearby organs, and distant metastasis are the primary causes of death. The lesions aggressive growth can rapidly invade and damage surrounding structures, such as the airway, leading to airway blockage, bleeding, and severe infections. Distant metastasis, especially to vital organs like the lungs, significantly affects the diseases survival rates. Patients undergoing resection for OSCC (oral squamous cell carcinoma) are at high risk for cardiovascular and respiratory complications, recognized as significant mortality factors. […] However, the risk of death increases significantly with each additional pack-year of tobacco smoking.
#35 Floor of the mouth cancer: Symptoms, treatment and prognosis | CURAPROX
https://curaprox.co.uk/blog/post/interesting-facts-about-floor-of-the-mouth-cancer?srsltid=AfmBOopR8nT9eA5RihokjHNYRIjSDB3lWyRIy_PsIx4bxesw1-pQoObG
About 99 percent of floor of the mouth tumours have an ulcerous form. This means that the tumour invades deep into existing tissue, leaving a „crater”. The tumour grows extremely quickly and is often quite advanced by the time a diagnosis is made. Further, ulcerous tumours tend to develop into metastases. The prognosis for this form of the disease is, therefore, rather negative. […] In only about one per cent of all squamous cell carcinomas of the floor of the mouth does the tumour grow outwards at a gradual rate. This form of progression does not tend to lead to the development of metastases.
#36 Floor of the mouth cancer: Symptoms, treatment and prognosis | CURAPROX
https://curaprox.co.uk/blog/post/interesting-facts-about-floor-of-the-mouth-cancer?srsltid=AfmBOopR8nT9eA5RihokjHNYRIjSDB3lWyRIy_PsIx4bxesw1-pQoObG
About 99 percent of floor of the mouth tumours have an ulcerous form. This means that the tumour invades deep into existing tissue, leaving a „crater”. The tumour grows extremely quickly and is often quite advanced by the time a diagnosis is made. Further, ulcerous tumours tend to develop into metastases. The prognosis for this form of the disease is, therefore, rather negative. […] In only about one per cent of all squamous cell carcinomas of the floor of the mouth does the tumour grow outwards at a gradual rate. This form of progression does not tend to lead to the development of metastases.
#37
https://link.springer.com/article/10.1007/s11604-021-01161-1
In the current study, squamous cell carcinoma of the floor of the mouth lesions which were not detected using MRI suggested a relatively superficial lesion with a pathological DOI3 mm. […] The 8th edition of the AJCC Cancer Staging Manual added a DOI to the criteria for T classification of oral cancer T1 to T4a, because pathological DOI is strongly associated with cervical lymph node metastasis, the most important prognostic factor. […] Therefore, pre-treatment estimation of the DOI is very important clinically, although it is problematic that the standard method for pre-treatment estimation of pathological DOI by radiological evaluation has not been established. […] In floor of the mouth cancer, as in previous reports on tongue cancer, undetectability on MRI is thought to be due to a superficial lesion and thus suggestive of a small DOI (3 mm). […] The DOI of floor of mouth cancer may be an important indicator in determining the combination of local resection and flap reconstruction. […] In the case of squamous cell carcinoma of the floor of the mouth, undetectability on MRI suggests a superficial lesion with a pathological DOI3 mm.
#38
https://link.springer.com/article/10.1007/s11604-021-01161-1
In the current study, squamous cell carcinoma of the floor of the mouth lesions which were not detected using MRI suggested a relatively superficial lesion with a pathological DOI3 mm. […] The 8th edition of the AJCC Cancer Staging Manual added a DOI to the criteria for T classification of oral cancer T1 to T4a, because pathological DOI is strongly associated with cervical lymph node metastasis, the most important prognostic factor. […] Therefore, pre-treatment estimation of the DOI is very important clinically, although it is problematic that the standard method for pre-treatment estimation of pathological DOI by radiological evaluation has not been established. […] In floor of the mouth cancer, as in previous reports on tongue cancer, undetectability on MRI is thought to be due to a superficial lesion and thus suggestive of a small DOI (3 mm). […] The DOI of floor of mouth cancer may be an important indicator in determining the combination of local resection and flap reconstruction. […] In the case of squamous cell carcinoma of the floor of the mouth, undetectability on MRI suggests a superficial lesion with a pathological DOI3 mm.
#39 Floor of Mouth Cancer | Memorial Sloan Kettering Cancer Center
https://www.mskcc.org/cancer-care/types/mouth/types-mouth/floor-mouth
Floor of mouth cancer is a type of head and neck cancer that begins when the cells that make up the floor of the mouth (the horseshoe-shaped area under the tongue) grow out of control and form lesions or tumors. […] Using tobacco products, particularly chewing tobacco, and regularly drinking too much alcohol can increase your chances of developing cancer in the floor of your mouth. […] The most common symptom of floor of mouth cancer is a sore in your mouth that keeps growing larger. Other signs of cancer in the floor of the mouth include: […] Floor of mouth cancer is highly curable when diagnosed early. Treatment often involves surgery performed by a head and neck cancer surgeon. […] The goals in the treatment of floor of mouth cancer are to: […] If the cancer is more advanced, radiation, chemotherapy, or both may be used to shrink the tumor before or after surgery to reduce the risk of the cancer coming back.
#40 Mouth Cancers: Gum, Palate, Inner Cheek & Floor of Mouth
https://www.cancercenter.com/cancer-types/oral-cancer/types/mouth-cancer
Floor of the mouth cancer occurs when cancer cells form in the tissue under the tongue. This type of cancer often appears as a mouth ulcer that doesn’t heal, and it may be confused with a canker sore. […] Other signs of floor of the mouth cancer may include: white or red patch or ulcerative lesion on the floor of the mouth, pain or numbness in the mouth, neck lump.
#41 Mouth Cancers: Gum, Palate, Inner Cheek & Floor of Mouth
https://www.cancercenter.com/cancer-types/oral-cancer/types/mouth-cancer
Floor of the mouth cancer occurs when cancer cells form in the tissue under the tongue. This type of cancer often appears as a mouth ulcer that doesn’t heal, and it may be confused with a canker sore. […] Other signs of floor of the mouth cancer may include: white or red patch or ulcerative lesion on the floor of the mouth, pain or numbness in the mouth, neck lump.
#42 Floor of the mouth cancer: Symptoms, treatment and prognosis | CURAPROX
https://curaprox.us/blog/post/interesting-facts-about-floor-of-the-mouth-cancer?srsltid=AfmBOooXrmQJL-aDEvj-x6hpcYDumOIdEUVwJZ2Bwd13vqyEHgWlxeF0
The prognosis depends significantly on how advanced the cancer is at the time of diagnosis: If the lymph nodes have not yet been affected, the average five-year survival rate is around 70 percent. However, if metastases have formed in the lymph nodes, the survival rate drops to about 20 to 25 percent.
#43 Floor of Mouth Cancer | Memorial Sloan Kettering Cancer Center
https://www.mskcc.org/cancer-care/types/mouth/types-mouth/floor-mouth
Floor of mouth cancer is a type of head and neck cancer that begins when the cells that make up the floor of the mouth (the horseshoe-shaped area under the tongue) grow out of control and form lesions or tumors. […] Using tobacco products, particularly chewing tobacco, and regularly drinking too much alcohol can increase your chances of developing cancer in the floor of your mouth. […] The most common symptom of floor of mouth cancer is a sore in your mouth that keeps growing larger. Other signs of cancer in the floor of the mouth include: […] Floor of mouth cancer is highly curable when diagnosed early. Treatment often involves surgery performed by a head and neck cancer surgeon. […] The goals in the treatment of floor of mouth cancer are to: […] If the cancer is more advanced, radiation, chemotherapy, or both may be used to shrink the tumor before or after surgery to reduce the risk of the cancer coming back.