Author/Editor		Rott, Tomaž; Podpečnik, Darja; Stražišar, Mojca; Glavač, Damjan; Terčelj-Zorman, Marjeta; Eržen, Janez
Title		Molecular basis of lung cancer histogenesis
Translated title		Molekularna osnova histogeneze pljučnega raka
Type		članek
Source		In: Luzar B, Poljak M, Glavač D, et al, editors. Molekularna diagnostika v medicini. Zbornik 15. spominsko srečanje akademika Janeza Milčinskega, 36. memorialni sestanek profesorja Janeza Plečnika, 1. srečanje Slovenskega društva za humano genetiko z mednarodno udeležbo; 2005 30 nov - 2 dec; Ljubljana. Ljubljana: Medicinska fakulteta,
Publication year		2005
Volume		str. 167-76
Language		eng
Abstract		The carcinogenesis of lung cancer is a multi-step process similar to those found in other organic systems. Accumulation of genetic changes is associated with histological-phenotypic changes, from normal tissue through precancerouslesions (metaplasia,dysplasia), to iniraepithelial and invasive cancer. Carcinogenesis is essentially a disease of cell cycle. In normal cell, molecular mechanisms of the cell cycle are balanced and self-controlled. The dominant growth-promoting oncogenes, the recessive growth-inhibiting tumour-suppressor genes, genes that regulate programmed cell death (apoptosis), genes involved in DNA repair, and telomerase are the most important molecular systems implicated in carcinogenesis. Exogenous factors can cause gradual accumulation of their molecular changes, with consecutive activation of dominant proto-oncogenes (e.g. KRAS, HRAS, MYC) and silencing of recessive tumour-suppressor genes, which are involved in growth suppression and promotion of apoptosis (e.g. P53, RB, BAX). Cells with mutations in oncogenes and tumour-suppressor genes multiply without any restriction and express phenotypic changes from precancerous lesions to invasive carcinoma, corresponding to the amount of molecular changes.
Descriptors		LUNG NEOPLASMS GENOTYPE PHENOTYPE TELOMERASE GENES, P53