Materiały źródłowe

• #1 Soft palate cancer – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/soft-palate-cancer/symptoms-causes/syc-20354183

  Soft palate cancer is cancer that starts as a growth of cells on the soft palate. […] Soft palate cancer most often begins in the thin, flat cells that line the inside of the mouth and throat, called squamous cells. When cancer starts in these cells it’s called squamous cell carcinoma. […] Soft palate cancer happens when cells on the soft palate 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 tell the cells to die at a set time. In cancer cells, the 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 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 initiation and development of OPMDs and OSCC share similar risk factors, including smoking, alcohol abuse, betel quid (BQ) chewing, human papillomavirus (HPV) infection, nutritional insufficiency, immune deficiency, and hereditary conditions.

• #3

  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. […] Oral squamous cell carcinoma (OSCC) is a pathological type of oral cancer, accounting for over 90% of oral cancers. […] 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. […] Many studies have shown that tobacco can cause the abnormal expression of p53, GLUT-1, p16, DAPK, MGMT, P13K and other genes in oral epithelium, which is associated with the occurrence of OSCC. […] The p53 cancer suppressor gene is the most universally identified mutated gene in human malignancies.

• #4 Malignant Tumors of the Palate – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564515/

  Palatal SCC pathogenesis is associated with an accumulation of genetic mutations and epigenetic anomalies in signaling pathways that promote uncontrolled cellular proliferation and cancer development. The genetic mutations associated with oral SCC are most often attributed to cigarette smoke, alcohol, and human papillomavirus. Additional factors that may play a role in SCC development include oral microorganisms, vitamin deficiencies, immunosuppression, and environmental pollutants. […] The majority of AdCC tumors contain a recurrent t(6;9) translocation, which fuses the MYB Proto-Oncogene transcription factor (MYB) on chromosome 6q to the Nuclear Factor IB (NFIB) gene on chromosome 9p, resulting in an overexpression of MYB-NFIB fusion oncogene. […] Approximately 50% to 70% of MEC have specific chromosomal translocation t(11;19)(q21:p13) leading to MEC translocated protein 1 (MECT1) and mastermind-like protein 2 (MAML2) gene fusion. Low or intermediate-grade MEC tumors are more likely to display this translocation than high-grade tumors.

• #5 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.

• #6 Risk factors, prevention, diagnosis, and immunotherapy’s involvement in the fight against oral cancer: a comprehensive review

  https://www.explorationpub.com/Journals/em/Article/1001270

  According to research, oral cancers begin as a premalignant progenitor cell line and then undergo a process known as clonal expansion to progress to more advanced stages. As mutations and abnormalities in deoxyribose nucleic acid (DNA) accumulate, clonal proliferation continues until cancer develops into a full-blown disease. […] Two main genetic changes are the inactivation of TSGs and the activation of proto-oncogenes, which play a crucial role in the development of oral cancer. […] Research has linked the development of SCC to a range of premalignant lesions such as leukoplakia, erythroplakia, OLP, and oral submucous fibrosis are prevalent and may develop into malignancy in several ways. […] HPV viral oncoproteins may destroy TSGs instead of altering them. It is believed that the genetic and cellular alterations are induced by the two early gene proteins encoded by HPV 16 and 18, E6 and E7. Cellular division is halted when E6 inactivates or degrades p53. […] The most effective method for treating oral cancer is a thorough neck dissection, and the presence of lymph nodes in the patients body is still a major indicator of prognosis. Recent advances in treating oral cancer have included mAbs directed against the EGFR.

• #6 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. Alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is cytotoxic and results in the production of free radicals and DNA hydroxylated bases; alcohol dehydrogenase type 3 genotypes appear predisposed to oral SCC.

• #7 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. […] 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.

• #8 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. […] Aberrant activation of oncogenic signaling pathways and inactivation of suppressor signaling pathways significantly contribute to the progression of OSCC. […] The dysregulated tumor microenvironment influences OSCC occurrence and progression, including immune suppression, stromal alteration, hypoxia, and an unbalanced oral microbiome.

• #9 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 (cyclin D1, BCRP, Aurora kinase A, COX-2, gene regulator c-Myc, iNOS) and influences the activation of genes involved in cell proliferation, tumor progression, and DNA repair.

• #10 Causes of Oral Cancer – Oral Cancer – Dentalcare

  https://www.dentalcare.com/en-us/ce-courses/ce348/causes-of-oral-cancer

  Two separate lines of research converged to unravel the complex series of events that lead to oral cancer. […] One area has clearly identified site-specific alterations of oncogenes such as EGFR and tumor suppressor genes such as p53. […] The mechanism by which alcohol contributes to oral cancer is not well understood but it probably acts directly on the epithelial cells of the oral mucosa by increasing permeability and through its dehydrating effects. […] The precise oncogenic effects of HSV on the pathogenesis of oral cancers however, have not been established. […] High risk HPV types (HPV16 and 18) have also been linked to some forms of oral epithelial dysplasia outside of the base of tongue and oropharynx.

• #11 Molecular mechanism of inhibitory effects of bovine lactoferrin on the growth of oral squamous cell carcinoma | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191683

  Inhibition of cell cycle progression in cancer cells is one of the main mechanisms by which LF may inhibit cancer growth. Recent studies have shown that LF directly arrested cell cycle in G1/S transition in breast and head and neck cancers both in vitro and in vivo via regulation of cell cycle-associated proteins including Akt, p21, p19, p27, Cdk2, cyclin E, Cdk4, and cyclin D1. […] The mammalian target of rapamycin (mTOR), a serine/threonine kinase, is activated by Akt signaling pathway and sequentially phosphorylates S6 kinase (S6K) to modulate cellular growth. mTOR has recently been considered as an attractive target in cancer therapy. […] Recently, SOCS3 has been shown to deregulate Janus kinase and signal transducer and activator of transcription (JAK2/STAT3) signaling via its interaction with receptor JAK2 through the SH2 domain.

• #12 Unlocking Epigenetics: Breakthrough Insights into Oral Cancer Progression

  https://bioengineer.org/unlocking-epigenetics-breakthrough-insights-into-oral-cancer-progression-and-therapies/

  By orchestrating CDK7 phosphorylation, LSD1 indirectly sustains the activation of Signal Transducer and Activator of Transcription 3 (STAT3), a well-known promoter of oncogenesis and immune evasion. […] The dysregulation of CDK7 in the context of enhanced LSD1 activity thus facilitates persistent STAT3 activation, fostering an environment conducive to epithelial transformation and immunosuppression. […] The validation of LSD1 inhibitors like SP2509 and Seclidemstat as promising agents to reverse early neoplastic changes and boost anti-tumor immunity heralds a new era in precision oncology.

• #13 Targeting epigenetics: New insights into oral cancer progression and treatment

  https://medicalxpress.com/news/2025-05-epigenetics-insights-oral-cancer-treatment.html

  LSD1, an epigenetic regulator, is crucial in oral squamous cell carcinoma (OSCC) progression by modulating pathways such as STAT3 and CDK7. Inhibiting LSD1, genetically or with agents like SP2509 or Seclidemstat, reverses preneoplastic lesions, reduces tumor growth, enhances CD8+ T cell infiltration, and lowers CTLA4, highlighting LSD1 inhibition as a promising early-stage OSCC therapy. […] The study uncovers the pivotal role of LSD1 in the progression of oral cancer. […] The study demonstrates that LSD1, an epigenetic regulator, plays a central role in the development of OSCC by controlling critical signaling pathways such as STAT3 and CDK7. […] This study’s findings underscore the importance of epigenetic regulation in OSCC progression and highlight the therapeutic potential of LSD1 inhibitors in preventing the transition from preneoplastic lesions to malignant tumors.

• #14 Unlocking Epigenetics: Breakthrough Insights into Oral Cancer Progression

  https://bioengineer.org/unlocking-epigenetics-breakthrough-insights-into-oral-cancer-progression-and-therapies/

  Mechanism of LSD1 Inhibition in Reversing OSCC Preneoplasia. Oral squamous cell carcinoma (OSCC) remains a formidable challenge within oncology, owing to its high prevalence and often late-stage diagnosis. […] A groundbreaking study published in the International Journal of Oral Science on April 17, 2025, now illuminates the critical role of lysine-specific demethylase 1 (LSD1) in dictating the fate of OSCC initiation and progression. This research, conducted collaboratively by teams led by Manish Bais at Boston University and colleagues at the University of Florida, unveils precise molecular mechanisms linking LSD1 activity to oncogenic and immunosuppressive pathways that promote tumor development. […] The study reveals that in early-stage OSCC, aberrant upregulation of LSD1 activity sustains oncogenic signaling cascades, notably via altering phosphorylation states of cyclin-dependent kinase 7 (CDK7), a pivotal factor in cell cycle progression and transcriptional regulation.

• #15 Soft Palate Cancer: Causes, Symptoms, and Treatment

  https://www.healthline.com/health/cancer/soft-palate-cancer

  Soft palate cancer is a type of throat cancer that affects your soft palate, which is the muscular area at the roof of your mouth toward your throat. […] It occurs when abnormal cells in the soft palate divide uncontrollably. Soft palate cancer is usually linked to tobacco or alcohol use and, less commonly, infection with the human papillomavirus (HPV). […] Experts think soft palate cancer occurs when chemical carcinogens, like tobacco or alcohol, cause changes (mutations) in genes within the cells of the soft palate. The mutated, cancerous cells then multiply uncontrollably and form tumors. […] Soft palate cancers are linked mainly to tobacco use and heavy alcohol consumption.

• #16 Head and neck cancer | World Cancer Research Fund

  https://www.wcrf.org/preventing-cancer/cancer-types/head-and-neck-cancer/

  Head and neck cancers are caused by damaged cells, which can grow uncontrollably to form a tumour. When you use tobacco or drink alcohol, your mouth and throat are directly exposed to cancer-causing substances (carcinogens). […] Evidence for what causes head and neck cancer comes from large population studies (called epidemiology) and biological studies (where scientists look at cells in a laboratory). […] Smoking (or the use of smokeless tobacco, sometimes called chewing tobacco or snuff) increases the risk of head and neck cancers. […] Drinking alcohol increases the risk of head and neck cancer. […] As much as 90 per cent of mouth cancers worldwide are attributable to tobacco, alcohol or a combination of the 2 together. […] Infection with human papilloma virus (HPV) increases the risk of head and neck cancer. Around 72% of oropharyngeal cancer is linked to high-risk HPV infection.

• #17

  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. […] Oral squamous cell carcinoma (OSCC) is a pathological type of oral cancer, accounting for over 90% of oral cancers. […] 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. […] Many studies have shown that tobacco can cause the abnormal expression of p53, GLUT-1, p16, DAPK, MGMT, P13K and other genes in oral epithelium, which is associated with the occurrence of OSCC. […] The p53 cancer suppressor gene is the most universally identified mutated gene in human malignancies.

• #18 IJCMCR-CR-ID-00210 – International Journal of Clinical Studies & Medical Case Reports

  https://ijclinmedcasereports.com/ijcmcr-cr-id-00210/

  Soft palate cancer is considered a type of throat cancer. […] Patients with squamous cell carcinoma of the palatine complex, frequently have long histories of excessive use of alcohol and tobacco. […] The synergistic effect of these cocarcinogens is well known and explains the high rate of second primary tumors, as well as premalignant erythroplasia frequently seen in patients with carcinoma of the oropharynx. […] In therapy for squamous cell carcinoma of the palatine complex, outcome will be influenced by the size and location of the primary lesion, contiguous spread, and the presence of manifest or occult regional metastasis. […] Oral cancers are usually the result of lifestyle and habits, and soft palate cancer is no different. […] Some of the risky behaviour that can lead to this type of cancer include heavy tobacco and alcohol use (particularly when used together), infection with Human Papillomavirus (HPV), being older than 40, and a poor diet.

• #19 Risk factors, prevention, diagnosis, and immunotherapy’s involvement in the fight against oral cancer: a comprehensive review

  https://www.explorationpub.com/Journals/em/Article/1001270

  From first exposure to risk factors to clinical identification of a lesion, there are many stages in the development of oral cancer. […] Additional research has shown that tobacco smoke extract may activate the epidermal growth factor receptor (EGFR) in a controlled laboratory setting. This activation, in turn, leads to an increase in the production of prostaglandins, such as prostaglandin E2 (PGE2), which might potentially boost EGFR signal transduction even more. Increased cyclin-D1 activity is a downstream process initiated by EGFR activation, and cyclin-D1 overexpression is common in head and neck cancer. […] A different molecular process may be at work in individuals whose tumors contain human papilloma virus (HPV) mRNA, as the frequency of chromosome 3p, 9p, and 17p deletions is much lower in these patients. One possible mechanism of HPV-mediated carcinogenesis is that the viral proteins E6 and E7 deactivate p53 and retinoblastoma (Rb) protein, leading to cell cycle dysregulation.

• #20

  https://step2.medbullets.com/oncology/120411/oropharyngeal-cancer

  malignant growth of tissues (most commonly squamous cell) of the oropharynx, which includes base of tongue, tonsils, soft palate, uvula, and posterior/lateral walls of the pharynx […] continued and repeated exposure to carcinogens leads to malignancy […] associated with HPV type 16 […] expression of E6 and E7 oncoproteins at the host cell, leading to inactivation of tumor suppressor gene p53 and retinoblastoma proteins.

• #21 Potentially Malignant Oral Disorders and Cancer Transformation | Anticancer Research

  https://ar.iiarjournals.org/content/38/6/3223

  The risk of malignant transformation of OSF is 2-8%. […] The risk of malignant transformation in OLP has been controversial for a long time and is estimated to be between 0.4% and 3.7%. […] The majority of patients with DC develop leukoplakia, approximately 87%. […] Dyskeratosis congenita significantly increases the risk of malignant transformation. […] Development of potentially malignant disorders and oral SCC are multistep processes involving genetic changes due to exogenous or indigenous factors. […] Chronic inflammation is a well-known risk factor for malignant disorders. […] Accurate diagnosis and timely treatment may help prevent the transformation of potentially malignant disorders into OSCC.

• #22 Study: Oral Inflammation Promotes Oral Squamous Cell Carcinoma Invasion | Faculty of Dentistry, University of Toronto

  https://www.dentistry.utoronto.ca/news/study-oral-inflammation-promotes-oral-squamous-cell-carcinoma-invasion

  In a first-of-its-kind study, Assistant Professor at U of Ts Faculty of Dentistry, Marco Magalhaes and his colleagues investigate oral inflammation and how it stimulates oral squamous cell carcinoma invasion. […] The objective of this study was to characterize oral squamous cell carcinoma (OSCC) associated inflammation and to determine the molecular mechanisms underlying inflammation-mediated OSCC invasion. […] The authors analyzed how TNFa induces significant changes to the cancer cells leading to increased invasion and the recruitment of more inflammatory cells and ultimately poor disease-free survival. […] We show here that TNF promotes a pro-inflammatory and pro-invasion phenotype leading to the recruitment and activation of inflammatory cells in a paracrine mechanism, said Dr. Magalhaes.

• #23 Study: Oral Inflammation Promotes Oral Squamous Cell Carcinoma Invasion | Faculty of Dentistry, University of Toronto

  https://www.dentistry.utoronto.ca/news/study-oral-inflammation-promotes-oral-squamous-cell-carcinoma-invasion

  The results demonstrate a novel mechanism by which TNF stimulates OSCC invasion. Based on our results, we show that oral inflammation in cancer patients determine a pro-tumor environment that promotes cancer invasion and consequent metastasis said Dr. Magalhaes. […] In combination with our previous findings, we have established a mechanism by which oral cancer modulates oral inflammation leading to worse prognosis and this is dependent on the key inflammatory mediator TNFa.

• #24 THE ROLE OF TUMOR-ASSOCIATED MACROPHAGES IN THE PATHOGENESIS OF ORAL SQUAMOUS CELL CARCINOMA CORRELATED WITH THE CLINICOPATHOLOGICAL PARAMETERS

  https://adjalexu.journals.ekb.eg/article_82702_0.html

  Oral cancer is a major health problem, causing high morbidity and mortality rates. Oral squamous cell carcinoma (OSCC) accounts for 90-95% of all oral malignancies. […] The inflammatory cells and their signals are indispensable participants in the neoplastic process, fostering proliferation, survival, and migration of cancer cells. The macrophages are the most abundant and important stromal cells in the TME, which orchestrate the inflammatory response. They control the cellular proliferation and survival by stimulating the immune cells and by promoting integrated processes of inflammation and tissue repair. […] CD163 was expressed in human OSCC and the TAMs count was significantly correlated with lymph node metastasis and with the tumor differentiation. Higher density was detected in metastatic tumors and in the poorly differentiated OSCC than in the well and moderately differentiated cases. […] CD163 positive TAMs could be a prognostic factor in OSCC cases as TAM density was significantly correlated with the lymph node status and the grade of differentiation of OSCC.

• #25

  https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-a-review-of-carcinogenic-pathways,105844,0,2.html

  The expression of GLUT-1 is upregulated in malignant cells, which suggests increased proliferative activity, energy requirements, aggressive behaviour and poor radiation response. […] 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. […] Immune dysfunction plays an important role in the escape of cancer cells from effector immunological functions, leading to the occurrence, establishment and development of the cancer. […] The immunosuppressive effects may exist in tobacco-related OSCC. […] Tobacco, which is a foreign substance, has been shown to stimulate the body to produce more free radicals that are endogenously produced in various cellular metabolic activities and which play a role in preventing microbial pathogen invasion at low concentrations.

• #26 Oral Cancer Pain Predicts Likelihood of Cancer Spreading

  https://www.nyu.edu/about/news-publications/news/2020/october/oral-cancer-pain-predicts-likelihood-of-cancer-spreading.html

  Oral cancer is more likely to spread in patients experiencing high levels of pain, according to a team of researchers at New York University (NYU) College of Dentistry that found genetic and cellular clues as to why metastatic oral cancers are so painful. […] Given that patients with metastatic oral cancer experience more pain, we thought that a patients level of pain might help predict metastasis. […] This observation suggests that patients with less pain are at low risk of metastasis, and will rarely benefit from a neck dissection. […] Cancer pain is attributed to the release of mediators from cancers that sensitize nerves near the cancer. […] Forty genes were identified that were more highly expressed in painful metastatic cancers, suggesting that they promote metastasis and mediate cancer pain. […] This suggests that exosomes from cancer may be responsible for oral cancer pain. […] The identified genes are targets for therapy aimed at stopping pain and cancer.

• #27 Cancers of the Oral Mucosa: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1075729-overview

  Tobacco is a potent risk factor for oral cancer. An interaction occurs between redox-active metals in saliva and the low-reactive free radicals in cigarette smoke. The result may be that saliva loses its antioxidant capacity and instead becomes a potent pro-oxidant milieu. […] DNA repair genes are clearly involved in the pathogenesis of some rare cancers, such as those that occur in association with xeroderma pigmentosum, but, more recently, evidence of defective DNA repair has also been found to underlie some oral SCCs. […] An immune deficiency state may predispose one to a higher risk of developing oral SCC, especially lip cancer.

• #28 Molecular mechanism of inhibitory effects of bovine lactoferrin on the growth of oral squamous cell carcinoma | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191683

  Our findings indicated that bLF regulates cell proliferation through G1/S cell cycle arrest via modulation of cell cycle-related genes in OSCC but not in normal keratinocyte. […] To further assess the apoptosis-induced growth inhibition of OSCC, HSC3 cells were treated with variable concentration of bLF for 48 h. […] Our data demonstrated that bLF significantly induced apoptosis in HSC3 cells, as observed by PE Annexin V/ 7-AAD staining. […] Based on our observations, bLF-mediated attenuation of p-p65 and p-Akt in HSC3 cells suppressed phosphorylation of mTOR and S6K, induced cell cycle arrest in G1/S, and was involved in apoptotic modulation of OSCC. […] In conclusion, bLF regulates cell cycle, cell proliferation, and apoptosis pathways to reduce cellular growth in OSCC and has minimal effects on normal mucosa.

• #29 Molecular mechanism of inhibitory effects of bovine lactoferrin on the growth of oral squamous cell carcinoma | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191683

  Lactoferrin (LF), a member of the transferrin family, recently has been demonstrated to have anticancer effects on various cancers including oral squamous cell carcinoma (OSCC). However, little is known about the underlying mechanisms of its effects on OSCC. Therefore, we aimed to investigate the mechanism of the suppressive effects of bovine LF (bLF) on the growth of OSCC cells. […] We found that bLF (1, 10, and 100 g/ml) induced activation of p53, a tumor suppressor gene, is associated with the induction of cell cycle arrest in G1/S phase and apoptosis in OSCC. Moreover, bLF downregulated the phosphorylation of Akt and activated suppressor of cytokine signaling 3 (SOCS3), thereby attenuating multiple signaling pathways including mTOR/S6K and JAK/STAT3. […] This is the first report showing that bLF selectively suppresses proliferation through mTOR/S6K and JAK/STAT3 pathways and induction of apoptosis in OSCC.

• #30 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.

• #31 Malignant Tumors of the Palate – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564515/

  Mucosal melanoma arises from precursor melanocytes, which develop from the neural crest cells. The reason for the migration and presence of melanocytes in the mucosa membrane of the oral cavity is not clear. Still, it has been suspected to be an antimicrobial and immunologic function. The pathogenesis of mucosal melanoma is unknown, but it is postulated to be due to genetic mutations with G-Protein Subunit Alpha Q (GNAQ/11) mutations found in 9.5% of patients and overexpression of tyrosin-protein kinase Kit (c-KIT) in over 80% of cases. […] Human herpesvirus 8 (HHV8) is a transforming virus found in several malignancies that can alter the genes of its infected cells. It is theorized that HHV8, along with immunosuppressive cytokines, induce the deterioration of the immune system and proliferation of Kaposi’s sarcoma.

• #32

  https://www.tobaccoinduceddiseases.org/Tobacco-and-oral-squamous-cell-carcinoma-a-review-of-carcinogenic-pathways,105844,0,2.html

  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. […] Further epidemiological and experimental studies are necessary to confirm the interaction between tobacco use and EBV positivity in oral cancer and to reveal potential mechanisms. […] It has been proven that the use of tobacco is associated with the development of OSCC.

• #33

  https://link.springer.com/article/10.1007/s12013-023-01191-8

  Toll-like receptors have been implicated in the development of cancer. […] Certain polymorphisms in toll-like receptor can make a cell more susceptible to develop oral cancer. […] The study revealed that toll-like receptors like TLR7 and TLR5 are found to have a role in suppression of oral cancer while toll-like receptors like TLR4 and TLR2 are found to be associated with the progression of oral cancer. […] Toll-like receptors can turn out as important target molecules in the future in designing therapeutic strategies for oral cancer.

• #34 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.

• #35

  https://talenta.usu.ac.id/ijoep/article/view/11150

  Oral mucosal cancer is a type of cancer that develops from the lining of the oral cavity (mucosa). The pathogenesis of oral mucosal cancer involves various interrelated etiologies such as smoking and alcohol consumption, human papilloma virus (HPV), and patients who have undergone hemopoietic stem cell transplants (stem cell transplants). […] Immunohistochemical examination of the Oral squamous cell carcinoma smear biopsy material which included examination of antibodies in the form of cytokeratin, CDT1, Ki-67, Geminin, Mcm2, -H2A/ histone family member X and Aurora-A, BCL-2, VEGF, p53, p63, p,73, Prb, c-erbB2 or HER2/neu, upregulation of telomerase (human telomerase reverse transcriptase; hTERT), loss of heterozygosity (Chromosome loci 3p, 8p, 9p, 4q, 11q, 13q, 17p), High-risk Human papillomavirus 16/18 (HR-HPV16 and 18), p16, Overexpression of EGFR, c-jun, c-fos, surviving (BIRC5), MMP-9, MMP9, TGF-, COX-1, and-2, and amplification of Cyclins D and E. Thus, paving the way for appropriate therapy.

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