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本帖最后由 细胞海洋 于 2010-5-5 18:25 编辑
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李锦军,顾健人*
6 |5 h( W; M4 `" F(上海交通大学上海市肿瘤研究所癌基因及相关基因国家重点实验室,上海200032)+ x8 q, ?9 N/ T* ]& j V+ a
摘 要:关于肿瘤发生及发展的机制人们已探索多年,但由于肿瘤病因本身的复杂性、研究技术和知
0 F1 x+ u$ ]$ B7 V/ o" `9 u+ X识积累不足等各种原因,研究进展缓慢。近些年来,癌干细胞的发现、确认和特性研究为肿瘤发病! U! }& z! n; ]; i
机制的揭示,乃至新型高效治疗策略的制定提出了新线索。许多研究成果显示,癌干细胞因具有自我3 n1 ]4 z; D8 L- q$ A+ `
更新和潜在的强增殖能力,在肿瘤发生发展、复发转移中均发挥着很重要的作用;肿瘤化疗的失败与% B! O3 h; Z; k/ t' [! X+ g
肿瘤组织中癌干细胞的耐药性可能存在密切关系。本文就癌干细胞在这方面的研究进展及存在的问题作7 R& }2 p( j2 Q2 L F; [5 i
一综述。
4 c% y: q+ \1 B6 B+ p6 x关键词:干细胞;癌干细胞;自我更新;耐药性;肿瘤发生
1 r# b$ I- |2 _; f3 b中图分类号:R730.21; R730.231 文献标识码:A
* \6 Q( K6 d) E- J# |' ]! \) j; qRecent progress in research on cancer stem cells
+ P5 g" p L! l" A" mLI Jin-Jun, GU Jian-Ren*. i3 ~/ x+ L6 k/ a8 ^
(State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute,3 H( `$ b# u/ ]
Shanghai Jiaotong University, Shanghai 200032, China)
* b9 y3 `$ V% H! E! X' ^9 b6 _Abstract: Mechanism of carcinogenecity and cancer progression has been explored for decades, however it is
- l1 A3 O& r% q4 a1 Ystill unclear because of the complexity of carcinogenesis progress, the limited techniques, and lack of8 `9 B9 @& l3 |, ~; @
knowledgements. Recently, cancer stem cells from several types of tumors were isolated, identified and preliminarily
% y6 t4 o u! @9 q$ @characterized, which might provide a novel clue for explanation of tumorigenesis and establishment of( ?6 b5 H! k9 r- ^) K9 A$ [
novel strategy of effective chemotherapy. Many reports have suggested that cancer stem cells possessed the6 _( L' O' H J( A# w4 Y4 E
properties of self-renewal, strong potentials of proliferation, which might play important roles in progression,+ _8 a9 ]' L$ ^. T# U) w
recurrence and metastasis of cancer. Meanwhile, chemotherapeutic failure may be associated with the drug
1 m3 J! x: e& ?+ Presistance of cancer stem cells. This review described the recent progress in cancer stem cell research as well as
. N9 `8 l s0 K* Dmany problems that remained to be solved.
4 L: c# Y6 {$ K5 ~Key words: stem cell; cancer stem cell; self-renewal; drug resistance; tumorigenesis3 I: U+ c* k1 Q- \9 f2 F! S9 F
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