Oncogene genetic alteration

Levy L, Renard CA, Wei Y, Buendia MA (2002). Genetic alterations and oncogenic pathways in hepatocellnlar carcinoma. Ann N YAcad Sci 003 21 36. 

Figure 21.19 Development of a secondary carcinoma from a normal epithelium by effects of activated genes, i.e. oncogenes, and inactive tumour suppressor genes. It is somatic mutations in four or five genes in a given cell plus hypomethylation changes in histones and chromatin stracture that are involved. It is the accumulation of these genetic alterations, not the sequence, that determines the progression to a tumour cell.

As in cancer predisposing syndromes, these genetic alterations are sometimes carried in the germline. Among human tumours, heritable mutations are an exception. Most alterations are acquired in somatic life in the form of chromosomal translocations, deletions, inversions, amplifications or point mutations. Certain oncogenic viruses play important roles in a few human tumours. Examples are human papilloma-virus in cervical cancer and skin tumours, Ep-stein-Barr virus in nasopharyngeal carcinoma and Burkitt s lymphoma, and human T-cell leukaemia viruses (e.g. HTLV-I, HTLV-II) in T-cell leukaemia. 

Sheppard RD, Samant SA, Rosenberg M, Silver LM, Cole MD. Transgenic N-myc mouse model for indolent B cell lymphoma Tumor characterization and analysis of genetic alterations in spontaneous and retrovirally accelerated tumors. Oncogene 1998 17 2073-85. 

Genetic Alterations in Oncogenes and Tumor Suppressor Genes 1167... 

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