By Henning Bier
The improvement of head and neck melanoma is a multistep method during which genetic in addition to epigenetic adjustments intrude with the usual features of proto-oncogenes and tumor suppressor genes. moreover, carcinogenesis is promoted via the impairment of mechanisms answerable for the upkeep of genetic balance. the buildup of an important occasions reminiscent of evasion of apoptosis, loss of senescence, deregulated proliferation, invasion and metastasis, in addition to neoangiogenesis finally determines the malignant phenotype. The sixteen articles of this quantity span from advances within the knowing of underlying molecular pathways (conditional mouse version, folate task, DNA fix, genomic heterogeneity, p53 relations, human papillomavirus), to preclinical and scientific stories investigating strength novel healing goals.
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Extra info for Current research in head and neck cancer: molecular pathways, novel therapeutic targets, and prognostic factors
Nunn J, Scholes AG, Liloglou T, Nagini S, Jones AS, Vaughan ED, Gosney JR, Rogers S, Fear S, Field JK: Fractional allele loss indicates distinct genetic populations in the development of squamous cell carcinoma of the head and neck (SCCHN). Carcinogenesis 1999;20:2219–2228. Bazan V, Zanna I, Migliavacca M, Sanz-Casla MT, Maestro ML, Corsale S, Macaluso M, Dardanoni G, Restivo S, Quintela PL, Bernaldez R, Salerno S, Morello V, Tomasino RM, Gebbia N, Russo A: Prognostic significance of p16INK4a alterations and 9p21 loss of heterozygosity in locally advanced laryngeal squamous cell carcinoma.
Cancer Epidemiol Biomarkers Prev 1998;7:465–468. Matullo G, Palli D, Peluso M, Guarrera A, Carturan S, Polidoro S, Munnia A, Krogh V, Masala G, Berrino F, Panico S, Tumino R, Vineis P: Combination of DNA repair gene single nucleotide polymorphisms and increased levels of DNA adducts in a population-based study. Cancer Epidemiol Biomarkers Prev 2003;12:674–677. Goode EL, Ulrich CM, Potter JD: Polymorphisms in DNA repair genes and associations with cancer risk. Cancer Epidemiol Biomarkers Prev 2002;11:1513–1530.
Tumor specimens that contained no sufficient DNA for CGH analysis (No. 21-P, 7-M and 5-P) were amplified by degenerate-oligonucleotideprimed polymerase chain reaction . Comparative Genomic Hybridization CGH analysis was performed as described previously . Briefly, tumor DNA and genomic DNA of a healthy male donor (reference DNA) were labeled by standard nick translation procedures. Biotinylated tumor DNA and digoxigenin-labeled reference DNA were precipitated in the presence of Cot-1 DNA (Roche Diagnostics) and hybridized to metaphase spreads from a healthy male donor.
Current research in head and neck cancer: molecular pathways, novel therapeutic targets, and prognostic factors by Henning Bier