What are the underlying molecular mechanisms that contribute to the development of head and neck cancer?
Best insight from top research papers
Head and neck cancer (HNC) development involves various molecular mechanisms. Areca nut exposure is a high-risk factor in Southeast Asia, with long non-coding RNAs (lncRNAs) like LUCAT1, MIR31HG, and UCA1 playing roles in HNC induced by areca nut . Genomic instability, defective DNA damage repair (DDR), and replication stress are common in HNC, affecting treatment responses . Exosomes, nanosized vesicles, contribute to HNC progression by promoting events like epithelial-to-mesenchymal transition (EMT), metastasis, and drug resistance . Additionally, glycolytic enzyme ENO2 is crucial in HNC, influencing cell proliferation and glycolysis through PKM2 regulation . Understanding these molecular pathways is vital for developing targeted therapies and improving outcomes for individuals with head and neck cancer.
Answers from top 5 papers
More filters
| Papers (5) | Insight |
|---|---|
| Head and neck cancer development involves genomic instability, defective DNA damage repair, and replication stress, highlighting the significance of DNA damage response mechanisms in therapy and survival. | |
| Exosomes play a crucial role in head and neck cancer development by promoting epithelial-to-mesenchymal transition (EMT) through the transfer of specific transcription factors like SNAIL/SLUG, TWIST, and ZEB. | |
| Long non-coding RNAs (lncRNAs) like LUCAT1, MIR31HG, and UCA1 modulate oncogenic mechanisms such as stress response and cellular motility, contributing to areca nut-induced head and neck cancer development. | |
| Genetic aberrations, environmental factors, and Epstein-Barr virus infection cooperate in nasopharyngeal carcinoma tumorigenesis, altering cellular signaling pathways, providing potential druggable targets for therapy. | |
| ENO2 mediates HNSCC progression by stabilizing PKM2, promoting its nuclear translocation, and enhancing glycolytic flux, leading to cell cycle progression. |
Related Questions
Cancer associate gene AND head and neck cancer6 answersResearch into head and neck squamous cell carcinoma (HNSCC) has identified several genes associated with the disease's progression, treatment response, and patient prognosis. The GALNT14 gene, specifically its rs9679162 polymorphism and mRNA expression, has been linked to treatment outcomes in HNSCC, suggesting its potential as a predictive marker for neoadjuvant chemotherapy response. Similarly, the mitotically associated long non-coding RNA (MANCR) has been found to be overexpressed in HNSCC, correlating with poor prognosis and indicating its role in cancer progression. Genetic variations, including single nucleotide polymorphisms (SNPs) in genes such as CXCR2, COMT, PRKDC, TGFb, XRCC1, Cyp2A6, and CTLA4, have been analyzed for their association with HNSCC risk and survival, highlighting the interaction between genetics and lifestyle factors like smoking.
Furthermore, genome-wide association studies (GWAS) have identified novel loci, such as 6p22.1 and 18q22.2, associated with SCCHN risk, emphasizing the importance of immunologic mechanisms in the disease's etiology. The role of HPV in HNSCC has also been underscored, with the MDM2 gene showing significant overexpression in HPV+ HNSCC, affecting p53-target genes and pathways. ADME genes related to drug metabolism have been linked to patient prognosis and immune cell infiltration, suggesting their utility in predicting treatment outcomes.
Genetic variants have also been associated with radiotherapy-induced toxicities, such as mucositis, identified through GWAS in European cohorts of HNC patients. Additionally, SNPs related to acute xerostomia during radiotherapy have been suggested, pointing towards personalized treatment approaches. Lastly, GWAS-identified risk loci have been associated with the progression, efficacy, and toxicity of radiotherapy in HNSCC, further supporting the critical role of genetic background in the disease's therapeutic response. Collectively, these findings underscore the complex interplay of genetic factors in HNSCC, offering avenues for improved prognostication and personalized treatment strategies.
What are the key molecular pathways involved in tumorigenesis?5 answersTumorigenesis involves a complex interplay of molecular pathways. Key pathways implicated in cancer development include the JAK/STAT, NOTCH, PI3K/AKT, MAPK, TGF-beta, NF-B, and Wnt signaling pathways. These pathways undergo significant alterations in cancer, with DNA repair pathways showing positive activation levels and high mutation enrichment, while signaling and cytoskeleton pathways play initiator roles in carcinogenesis. Additionally, the Hippo pathway, particularly involving YAP and TAZ transcriptional coactivators, is crucial in inhibiting organ growth and acting as a tumor suppressor in various tissues, including the liver, skin, and ovaries. Furthermore, in specific cancers like hepatoblastoma in patients with trisomy 18, SMAD4/TGFβ signaling in conjunction with canonical Wnt signaling has been identified as a novel tumorigenic mechanism, highlighting the importance of pathway crosstalk in cancer development.
Which of the kinases genes are involved in the development of oral cancer?5 answersThe development of oral cancer involves various kinase genes. Polo-like kinase 1 (PLK1) has been identified as a crucial gene required for oral squamous cell carcinoma (OSCC) cell proliferation, with elevated expression associated with poor prognosis. Additionally, the receptor tyrosine kinase (RTK) signaling pathway plays a role in OSCC development, with epidermal growth factor receptor (EGFR) showing frequent mutations in OSCC patients. Furthermore, casein kinase 1 epsilon (CK1e) gene polymorphisms have been linked to increased susceptibility to oral squamous cell carcinoma, especially when combined with environmental carcinogens like smoking and betel-quid chewing. These findings highlight the significance of kinases such as PLK1, EGFR, and CK1e in the pathogenesis of oral cancer.
What are the molecular mechanisms underlying the transformation of stem cells into cancer stem cells?5 answersThe transformation of stem cells into cancer stem cells (CSCs) involves various molecular mechanisms. CSCs exhibit self-renewal, differentiation capabilities, and resistance to therapies, contributing to tumor growth and recurrence. RNA modifications like inosine, 5-methylcytosine, and N6-methyladenosine play crucial roles in regulating gene expression during CSC fate transitions. Asymmetric division, where polarity-determining proteins mark the apical side of mother cells, guides the unequal inheritance of fate determinants, maintaining stemness in CSCs. Dysregulation of apoptotic pathways and therapy resistance mechanisms further enhance CSC self-renewal and maintenance, driving tumor initiation and progression. Understanding these mechanisms is vital for developing targeted therapies to eliminate CSCs and improve cancer treatment outcomes.
What are the molecular mechanisms underlying the oncogenesis of gliomas?5 answersThe molecular mechanisms underlying the oncogenesis of gliomas involve various pathways and factors. Histone mutations, such as those found in diffuse midline gliomas (DMGs), are critical tumor initiating events. However, these mutations alone are insufficient to drive gliomagenesis. Other somatic alterations in pathways like TP53, MAPK, and MYC signaling also play a role. In DMGs, the forkhead transcription factor FOXR2 is aberrantly expressed and interacts with ETS transcription factors to mediate oncogenesis. Glioblastoma stem cells (GSCs) contribute to tumor growth, invasion, and resistance to therapy. Dysregulation of critical signaling pathways, including Notch, EGFR, PI3K/Akt, and Wnt, as well as epigenomic changes, drive the oncogenic nature of GSCs. Additionally, long non-coding RNA TCONS_00004099 promotes malignant behaviors in gliomas through its derived miRNA and downstream target PTPRF. These findings provide insights into the complex molecular mechanisms underlying glioma oncogenesis.
What is the Molecular mechanism of breast cancer?5 answersBreast cancer is a complex pathology characterized by the uncontrolled proliferation and growth of cells in the breast tissue. The molecular mechanisms underlying breast cancer involve genetic and environmental risk factors, as well as changes in signaling mechanisms mediated by estrogen and estrogen receptors. Abnormal methylation of tumor suppressor genes and miRNAs, regulated by DNMTs, can promote tumorigenesis and drug resistance in breast cancer. BC cells undergo adaptive mutations, rearrange chromosomes, and repress tumor suppressor genes while inducing oncogene activities, leading to aggressive and heterogeneous cancer cells. Drug resistance in breast cancer is driven by various mechanisms, including the activation of signaling pathways, upregulation of drug efflux pumps, emergence of cancer stem cells, and genetic and epigenetic changes. The initiation and progression of breast cancer involve a multi-step process, with epithelial-mesenchymal transition playing a crucial role in facilitating metastasis.