作者: Takehiko Sasazuki , Senji Shirasawa
DOI: 10.1007/978-1-59259-313-2_12
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摘要: It is now widely accepted that cancer results from an accumulation of genetic alterations, including subtle sequence changes, alterations in chromosome number, chromosomal translocation, and gene amplifications (1). These result a gain function oncogenes loss tumor suppressor genes, leading to uncontrolled growth, differentiation, apoptosis. The number mutations required for develop human populations age-dependent, seven or eight acquired cell are commonly occurring solid tumors before overt malignancy becomes evident (2). ectopic expression the telomerase catalytic subunit, combination with two oncogenes, simian virus 40 large T oncogenic allele Ha-ras, lead direct tumorigenic conversion normal cells (3). Therefore, there succession each which conferring one another type growth advantages, transformation into malignant tissue (4). Cancer genotypes manifestation six essential physiology collectively dictate through various mechanistic strategies: self-sufficiency signals, insensitivity growth-inhibitory evasion apoptosis, limitless replicative potential, sustained angiogenesis, invasion metastasis This classification needed better understanding molecular mechanisms involved tumorigenesis designing appopriate therapy.