【优选】肿瘤分子生物学细胞永生化与肿瘤发生PPT资料

3、实验显示，端粒酶活性的获得（从大量进入危象的细胞群中自主产生的变异细胞）足以使细胞逃逸危象，其产生的子代细胞能够 无限制生长（永生化）。
●GdnehnTEeRrTaetnizoymnesis onoft inctreinsllicsally cytotoxic 端f粒o酶r全m酶i其n他g亚a单t位u（m包括ohrT(Rb-端) 粒酶相关RNA分子）在危象前的细胞均适量储存。
二、癌基因与抑癌基因
癌基因－控制细胞生长和分裂的正常基因的一种突变形式 抑癌基因－正常细胞增殖过程中的负调控因子
三、肿瘤的发生是基因突变逐渐积累的结果
Normal cell populations register the number of cell generations
C. eleganceThe lineage of all 959 somatic cells in the adult body( could be) has been traced to their founder and can be depicted as a pedigree
Loss of proliferative capacity with age
Senescent cells--
When the cells enter into senescence, they cease proliferating but remain viable, “Fried egg appearance” is the morphological feature because of the enlarged cytoplasm. Metabolically, senescent cells characteristically express the senescence-associated, acidic β-galactosidase enzyme, which can be detected by supplying them with substrate that turns blue upon cleavage by this enzyme
肿瘤概念
Cancer is a genetic disease, arising from an accumulation of mutations that promote clonal selection of cells with increasingly aggressive behavior. The vast majority of mutations in cancer are somatic and are found only in an individual's cancer cells. However, about 1% of all cancers arise in individuals with an unmistakable hereditary cancer syndrome. These individuals carry a particular germline mutation in every cell of their body. Science Vol. 278. no. 5340, pp.
Cancer cells need to become immortal in order to form cancer
Generations of cells forming a tumor(a)
1cm3=109 cell, life-threatening tumor 103cm3 ≈ 1012 cell, 103 ≈210 , hence 1012 ≈240 cycles Cell PD 60 1018cell ≈109cm3 ≈106kg
1043 – 1050, 7 November 1997
肿瘤是机体在各种致瘤因素的作用下，局部组织的细胞在 基因水平上失去对其生长的正常调控，导致克隆性异常增生而 形成的新生物（病理学－卫生部统编教材第五版2001） 。
癌细胞的基本特征
1、细胞生长与增殖失去控制 2、具有浸润性和扩散性 3、细胞间相互作用改变 4、蛋白表达谱系或蛋白活性改变 5、mRNA转录谱系改变 6、体外培养的恶性转化细胞的特征
Brca1 mutant which is involved in maintaining genomic integrity
CanCceerllispaogpeunleatitciodinsesatshe,aatriasirneg from an accumulation of mutations that promote clonal selection of cells with increasingly aggerevsosilvveinbgehtaovwiora. rd the d危ivin象sieo的no时cpyl相cales、)i以t形ic后态记s变t录a化细t提e胞示a连n其d续触传发代机的制功是能独性立计于数衰装老置的， 启动危象的分子装置确实是 细胞谱系从胚胎早期（进入 growth-and●tdhnosheTEtRhTaet nazryemeailsrenaotdinytrinsically cytotoxic Genneeoraptiolanss toicf ceelxlspfoerrmieinngcaetumor(a) 端s粒u酶b是st端an粒ti重al建a的tt关rit键ion during Prevaecnhtiocneolflcgriseisnbeyraextiporenssion of telomerase
1960 Leonard Hayflik’s work by counting the number of times that population of cells had doubled . When the cells enter into senescence ,
they could remain viable but nonproliferating for as long as a year
发育生物学：关注的是不同细胞谱系中的细胞个体如何从 其周围获取信息，使其进入特定的分化程序， 而不关注与 肿瘤发生最相关的问题，
有无特定的 控制系统 决定一个生物体特定的细胞谱系一 生中能够传多少代？一个细胞系谱的分支 是否能够无限制 生定，有限的？