肿瘤发生的潜在分子基础(1)

肿瘤发生是一个多步骤过程.绝大多数人肿瘤由产生了系列相继变化的单一细胞形成.这些变化导致细胞有丝分裂信号或生长控制的细微异常,逐步赋予细胞赘生的特性,直至细胞形成恶性肿瘤.防御肿瘤发生的一个重要机能是诱导细胞死亡,这种机能持续不断地清除机体内多余的,受损的或变异的细胞.对肿瘤细胞增殖优势的分子机理的认识,揭示了许多肿瘤细胞如何应答异常有丝分裂信号的内在现象,而蛋白磷酸激酶是介导这些信号通路的主体.天然细胞或病毒蛋白能作为细胞死亡效应子发挥作用,尤其有意义的是,有些细胞和病毒蛋白具有肿瘤特异性细胞死亡效应,可望发展成为新的抗肿瘤治疗制剂.

Underlying Molecular Mechanisms of Tumorigenesis(1)--Unbalance between Proliferation and Cell Death

Cancer formation is a multi-step process. Most, if not all, human tumors develop through sequential genetic alterations in a single cell. These alterations cause subtle aberrations in mitogenic signaling or growth control, confer increasingly neoplastic characteristics on cells, and culminate in cells that are able to form malignant tumors. An important mechanism to prevent tumor-igenesis is the induction of cell death that takes place continuously in many tissues of our body to remove unwanted, damaged or aberrant cells. Understanding the molecular mechanisms underlying the proliferative advantage of cancer cells has revealed many insights into how tumor cells respond to the altered mitogenic signaling, which predominantly involve protein kinases. Natural cellular or viral proteins may function as death effectors. Of particular interest, some of these cause tumor-specific cell death, which makes possible the development of novel anti-cancer therapeutic agents. Here, unbalance between proliferation and cell death underlying tumorigenesis (part 1) will be discussed. The effectors of survival and death underlying tumorigenesis will be discribed in part 2.