摘要: The concept that cancer is a multi-step process caused by genetically- and epigenetically-determined abnormal gene function now well established. Gain-of-function or loss-of-function changes affect number of genes control cellular processes such as cell cycle, apoptosis differentiation consequently behave oncogenes tumor suppressors, respectively. It also established several genetic hits are required to trigger transformation malignant progression cancer, in which the altered functions each oncogene suppressor contribute, coordinated way, compose complex network phenotypic traits [1, 2]. Elucidating how diversity generated during tumorigenic events an unanswered question. Although tremendous advances knowledge have occurred recent years, there still no clear understanding this field.
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