The role of ras gene expression and transforming growth factor α production in the etiology and progression of rodent and human breast cancer

摘要: Cancer represents a spectrum of different diseases that generally arise through series multiple yet discrete steps include initiation, promotion, transformation, progression, and metastasis [1]. Genetic alterations to specific host cellular genes or sets are associated with some all these stages [1–3]. Damage DNA can result in somatic changes due the action chemical carcinogens, mutagens, viruses, radiation. A large body evidence suggests certain endogenous regulatory likely targets for insult from exogenous environmental agents. These proto-oncogenes have been implicated control proliferation and/or differentation [3–7]. Activation processes such as point mutation, amplification, rearrangement, insertional mutagenesis, chromosomal translocation, overexpression lead neoplastic transformation vitro tumorigenicity vivo [3,5,7]. Approximately 35–40 identified date be stratified cases into families based on their structure function [3, 7]. gene were originally detected dominantly transforming genome acutely retroviruses transduced captured [3,4,7]. transfection assays also demonstrated presence other additional groups activated obtained number rodent tumors small fraction primary human capable immortalized fibroblasts, NIH-3T3 cells, [8–15]. In addition this group genes, there exists second major tumor suppressor antioncogenes, which give rise after allelic deletion inactivation [16–18]. recessive Rb—1 (retinoblastoma) gene, code nuclear phosphoproteins negatively regulate cell growth potential interact subsequently inactivated by oncogene proteins, SV40T antigen protein Adenovirus E1A [19–22].