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凋亡增加可促进肿瘤的生长和转移
引用本文:郑平菊,师建国,王瑞安.凋亡增加可促进肿瘤的生长和转移[J].第四军医大学学报,2014(2):14-19.
作者姓名:郑平菊  师建国  王瑞安
作者单位:[1]长安医院肿瘤部,陕西西安710018 [2]第四军医大学西京医院病理科,陕西西安710032 [3]第四军医大学基础医学院病理学与病理生理学教研室,陕西西安710032
基金项目:国家自然科学基金(30971535)
摘    要:长期以来,细胞凋亡与肿瘤的发生和发展关系受到了广泛的关注和研究。Hanahan和Weinberg提出的肿瘤的特征一文.将“逃避凋亡”作为肿瘤的特征之一,被广泛引用,基本上是科学界的“共识”。但这一“共识”就像哥白尼之前人们认为太阳围着地球转的“共识”一样,并不一定正确。实际上,恰与事实相反——肿瘤中的凋亡要远较其相对应的正常组织多,肿瘤细胞的寿命也比正常细胞短。我们认为.正是由于细胞凋亡的增多.才导致肿瘤细胞不得不持续地增殖,并使GO期细胞减少,组织分化差;为求得更好的生存环境,肿瘤细胞才转移到其他器官。因而,过多的细胞死亡是肿瘤恶性增殖和转移的根源。

关 键 词:肿瘤  细胞凋亡  增殖  转移  生物相对论  分子适应  细胞周期

Increased apoptosis stimulates tumor growth and metastasis
ZHENG Ping-Ju,SHI Jtan-Guo,WANG Rui-An.Increased apoptosis stimulates tumor growth and metastasis[J].Journal of the Fourth Military Medical University,2014(2):14-19.
Authors:ZHENG Ping-Ju  SHI Jtan-Guo  WANG Rui-An
Institution:1.Department of Medical Oncology, Chang'an Hospital, Xi'an 710018, China; 2.Department of Pathology, Xijing Hospital, 3.Department of Pathology and Pathophysiology, Fourth Military Medical University, Xi'an 710032, China)
Abstract:The relationship between apoptosis and tumorigenesis has long been in the spotlight of cancer research. Hanahan and Weinberg, in their famous paper of "the hallmarks of cancer", regarded "evasion of apoptosis" as one of the six hallmarks they summarized. The paper has been widely cited, and the "resistance to apoptosis'" became a consensus in the scientific community. However, a consensus does not necessarily mean truth, as people had the consensus that sun moved around the earth before Copernicus. In fact, cancer tissues show much more apoptosis than corresponding normal tissues, and cancer cells live shorter than normal cells. We hold the point that it is the increased apoptosis that pushes cancer cells to proliferate ceaselessly and thus reduce the proportion of GO cells, which further leads to poor tissue construction and differentiation. For better survival, the cancer cells move to new places. Therefore, increased cell death is the origin of malignancy.
Keywords:cancer  apoptosis  proliferation  metastasis  biorelativity  molecular adaptation  cell cycle
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