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Head & Neck Cancer


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Head & Neck Cancer

Head and neck squamous cell carcinoma (HNSCC) arises in the oral cavity, oropharynx, larynx or hypopharynx, and is the sixth leading cancer by incidence worldwide. Head and neck cancers include cancers of the upper aero digestive tract (including the oral cavity, oropharynx, nasopharynx, hypopharynx, and larynx), the paranasal sinuses, and the salivary glands. Cancers at different sites have different courses and variable histopathological types, although squamous cell carcinoma is the most common so far. The anatomical sites affected are important for functions such as speech, taste, smell, and swallowing, so the cancers and their treatments may have considerable functional sequelae with subsequent impairment of quality of life.

Cancer arises through the accumulation of genetic and epigenetic changes in genes acting in cancer associated signaling pathways, causing the acquisition of cancer-related phenotypes that have been well summarized by Hanahan and Weinberg, including limitless replicative potential, self-sufficiency in growth signals, insensitivity to anti-growth signals, ability to evade apoptosis, invasion and metastasis, and angiogenesis. Recently, a plethora of studies have been published on the identification of candidate cancer genes in HNSCC.

One of the key cellular functions that is often, if not always, changed in cancer cells to overcome senescence and to obtain limitless replicative potential is the regulation of the cell cycle. Crucial genes involved in the regulation of the cell cycle that are targeted by mutations in HNSCC, or alternatively by HPV oncogenes, are those encoding proteins in the p53 and RB pathways. Somatic mutations in TP53 are found in 60–80% of HNSCC cases, and overexpression of a dominant-negative mutant of p53, in conjunction with ectopic expression of telomerase reverse transcriptase (TERT, the catalytic subunit of telomerase), as well as overexpression of cyclin D1, or a p16INK4A-insensitive cyclin-dependent kinase 4 (CDK4) mutant, causes immortalization of cultured mucosal keratinocytes in vitro. Lately, these initial studies on primary epithelial cells were extended using a conditionally immortalized model of oral keratinocytes in vitro. An extended lifespan was conferred on oral keratinocytes by inactivation of p53, either by knockdown of TP53 with short hairpin RNA (shRNA), by expression of dominant-negative mutant p53R172H or by expression of the HPV16 oncoprotein E6.

One of the most studied groups of receptor tyrosine kinases is the Erbb family. After ligand binding or other activating interactions, the four Erbb receptors form homodimers or heterodimers, and initiate a signaling cascade. EGFR seems to be crucial in squamous cells and signals through the PI3K-PTEN-AKT, Ras-MAPK, and phospholipase C pathways. Most interestingly, EGF-bound EGFR is also able to translocate to the nucleus and it functions as a transcription factor or co-activator of other transcription factors, such as signal transducer and activator of transcription (STAT) proteins. Ectopic expression of EGFR has been implicated in the transformation of oral keratinocytes in vitro. The introduction of anti-EGFR therapy is the first of the novel biological treatment modalities to find its way to the clinic. Effective methods to select anti-EGFR-sensitive tumors are urgently awaited. Not all HNSCCs are addicted to EGFR, and more insight is required about the effect of treatment and the involvement of altered signaling pathways. Targeted therapy will increasingly demand more predictive biomarkers besides HPV, EGFR and the mutation status of TP53. It is likely that these markers need to be combined with conventional staging, tobacco use and other clinical factors for optimal personalized treatment.

Creative Biogene, as a leading biotechnology company, is able to offer various head and neck cancer pathway related products including stable cell lines, viral particles and clones for your pathogenesis study and drug discovery projects.

References:

  1. C. René Leemans, et al. The molecular biology of head and neck cancer. Nature Reviews Cancer.
  2. Ferris, R. L. Immunology and Immunotherapy of Head and Neck Cancer. Journal of Clinical Oncology, 2015:JCO.2015.61.1509.
  3. Bose P, at al. Head and neck cancer: from anatomy to biology. International Journal of Cancer, 2013, 133(9):2013-2023.
  4. Mehanna H, et al. Head and neck cancer—Part 1: Epidemiology, presentation, and prevention. BMJ: British Medical Journal, 2010, 341(7774):663-666.

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