By Henning Bier
The improvement of head and neck melanoma is a multistep strategy within which genetic in addition to epigenetic adjustments intrude with the common features of proto-oncogenes and tumor suppressor genes. furthermore, carcinogenesis is promoted by means of the impairment of mechanisms accountable for the upkeep of genetic balance. the buildup of the most 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 realizing of underlying molecular pathways (conditional mouse version, folate task, DNA fix, genomic heterogeneity, p53 kin, human papillomavirus), to preclinical and medical reports investigating strength novel healing ambitions.
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Extra info for Current research in head and neck cancer: molecular pathways, novel therapeutic targets, and prognostic factors
To understand the impact of DNA repair genes in the estimation of genetic risk and in the development of laryngeal cancer we attempted to study the distribution of 3 polymorphic DNA repair genes. To choose the most representative genes it was decided to focus on XPD, XRCC1 and XRCC3. The chosen genes take part in the 3 major mechanisms of DNA repair involved in the removal of DNA lesions induced by tobacco smoke carcinogens, namely nucleotide excision repair (XPD), base excision repair (XRCC1) and recombination repair Gajecka/Rydzanicz/Jaskuta-Sztul/Wierzbicka/Szyfter/Szyfter 34 (XRCC3), but a cross-participation is not excluded .
Contributed equally to this work and should be considered as first author. Primary and advanced head and neck squamous cell carcinomas (HNSCCs) are characterized by complex karyotypes with multiple chromosome aberrations and cytogenetically different subclones [1–3]. This intratumoral heterogeneity can be explained by selective growth advantage of certain cells with slightly varying karyotypes (related subclones) reflecting ongoing clonal evolution [4, 5]. Furthermore, prolonged exposure to carcinogenic agents such as tobacco can lead to the development of multiple synchronous or metachronous tumors with karyotypically unrelated subclones due to the hypothesis of ‘field cancerization’ .
Cancer Res 1996;56:4103–4107. Cheng L, Eicher SA, Guo Z, Hong WK, Spitz MR, Wei Q: Reduced DNA repair capacity in head and neck cancer patients. 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.