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- 请大家谈谈对肿瘤干细胞的认识
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最近在看肿瘤干细胞方面的文章，也在丁香园里面看到这方面的讨论还是比较激烈的，想在此处也开个话题，大家共同关注一下。欢迎各位多多发表自己的看法。
肿瘤干细胞（Cancer stem cell/Tumor stem cell）是具有自我更新能力，通过对称和不对称两种分裂形式产生新的肿瘤干细胞和具有无限增殖能力并分化成不同表型细胞群的细胞。肿瘤干细胞是决定肿瘤发生和转移的肿瘤细胞群体，在恶性肿瘤的发生和发展中发挥重要作用，是肿瘤治疗的靶细胞。1994年Lapidot 等首次通过特异细胞表面标志分离出了人急性粒细胞白血病干细胞，其表型为CD34+/CD38-，该发现为肿瘤干细胞的存在提供了实验依据。
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wangzhen_01 离线
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本帖最后由 于 2007-05-08 23:14:00 编辑
后来的研究进一步证实：在乳腺癌（CD44+CD24-/lowLin-）和脑肿瘤（CD133+）中也存在肿瘤干细胞。
Lapidot, T., C. Sirard, et al. (1994). "A cell initiating human acute myeloid leukaemia after transplantation into SCID mice." Nature 367(6464): 645-8.
Al-Hajj, M., M. S. Wicha, et al. (2003). "Prospective identification of tumorigenic breast cancer cells." Proc Natl Acad Sci U S A 100(7): 3983-8.
Singh, S. K., I. D. Clarke, et al. (2003). "Identification of a cancer stem cell in human brain tumors." Cancer Res 63(18): 5821-8.
肿瘤干细胞是否与肿瘤转移、复发和转移有关呢？研究表明，在明显局部发生的乳腺癌中有30％存在骨的微转移；而在手术后，50％的骨微转移乳腺癌中，10年的随访并未见到乳腺癌的复发和转移。这是否提示肿瘤干细胞就是paget所谓的致命的“种子”呢？肿瘤干细胞是否跟肿瘤的休眠有关系呢？
Braun, S., F. D. Vogl, et al. (2005). "A pooled analysis of bone marrow micrometastasis in breast cancer." N Engl J Med 353(8): 793-802.
随便扔个砖头进来，希望“抛砖引玉”，^_^。
- 吾表兄，年四十余。始从文，连考三年而不中。遂习武，练武场上发一矢，中鼓吏，逐之出。改学医，自撰一良方，服之，卒。
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WRONG TARGET. Traditional cancer therapies (top) kill rapidly dividing tumor cells (red) but may spare stem cells (blue) that can give rise to a new tumor. In theory, killing cancer stem cells (bottom) should halt a tumor's growth and perhaps even lead to its disappearance.
传统的肿瘤治疗仅仅是杀死快速分裂的肿瘤细胞，如果我们针对肿瘤干细胞进行化疗应该会使肿瘤的生长停滞，甚至会使肿瘤消失。
- 吾表兄，年四十余。始从文，连考三年而不中。遂习武，练武场上发一矢，中鼓吏，逐之出。改学医，自撰一良方，服之，卒。
我最近申请的一个课题就是关于肿瘤干细胞标志物的。在前几年使用肿瘤干细胞一词比较多，现在多用癌干细胞一词。近年来肿瘤干细胞的发现、确认和特性研究为肿瘤发病机制的揭示，乃至新型高效治疗策略的制定提供了新的线索。肿瘤干细胞学说，认为肿瘤生长是肿瘤组织中极少量具有特殊细胞表面标志的肿瘤干细胞增殖的结果。研究证据表明，大多数肿瘤如脑瘤、乳腺癌 、前列腺癌、消化道肿瘤等中均存在癌干细胞。肿瘤干细胞因具有自我更新和潜在的强增殖能力，在肿瘤发生发展、复发转移中发挥着很重要的作用。有人认为肿瘤干细胞自我更新的特性是造成肿瘤复发、转移及预后不良的主要原因。因此研究肿瘤干细胞特异性的生物学特点，对肿瘤的发生、发展和转归的理论以及肿瘤的诊断、预防和治疗均有重要意义。
- 空想家
发一个新看到的文章，对这方面比较感兴趣，欢迎大家讨论哦不过只有摘要哦
A Perivascular Niche for Brain Tumor Stem Cells
Summary
Cancers are believed to arise from cancer stem cells (CSCs), but it is not known if these cells remain dependent upon the niche microenvironments that regulate normal stem cells. We show that endothelial cells interact closely with self-renewing brain tumor cells and secrete factors that maintain these cells in a stem cell-like state. Increasing the number of endothelial cells or blood vessels in orthotopic brain tumor xenografts expanded the fraction of self-renewing cells and accelerated the initiation and growth of tumors. Conversely, depletion of blood vessels from xenografts ablated self-renewing cells from tumors and arrested tumor growth. We propose that brain CSCs are maintained within vascular niches that are important targets for therapeutic approaches. CANCERCELL Volume 11, Issue 1, January 2007, Pages 69-82
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本帖最后由 于 2007-06-07 21:15:00 编辑
| 以下是引用zoujane 在2007-5-15 21:59:00的发言：我最近申请的一个课题就是关于肿瘤干细胞标志物的。在前几年使用肿瘤干细胞一词比较多，现在多用癌干细胞一词。近年来肿瘤干细胞的发现、确认和特性研究为肿瘤发病机制的揭示，乃至新型高效治疗策略的制定提供了新的线索。肿瘤干细胞学说，认为肿瘤生长是肿瘤组织中极少量具有特殊细胞表面标志的肿瘤干细胞增殖的结果。研究证据表明，大多数肿瘤如脑瘤、乳腺癌 、前列腺癌、消化道肿瘤等中均存在癌干细胞。肿瘤干细胞因具有自我更新和潜在的强增殖能力，在肿瘤发生发展、复发转移中发挥着很重要的作用。有人认为肿瘤干细胞自我更新的特性是造成肿瘤复发、转移及预后不良的主要原因。因此研究肿瘤干细胞特异性的生物学特点，对肿瘤的发生、发展和转归的理论以及肿瘤的诊断、预防和治疗均有重要意义。 |
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本帖最后由 于 2007-06-08 20:05:00 编辑
偶最近也看了挺多这方面的文章！挺感兴趣的！PTEN-deficient intestinal stem cells initiate intestinal polyposis
Xi C He, Tong Yin, Justin C Grindley, Qiang Tian, Toshiro Sato, WAndy Tao, Raminarao Dirisina,Kimberly S Porter-Westpfahl, Mark Hembree, Teri Johnson, Leanne M Wiedemann, Terrence A Barrett, Leroy Hood, Hong Wu & Linheng Li
Intestinal polyposis, a precancerous neoplasia, results primarily from an abnormal increase in the number of crypts, which contain intestinal stem cells (ISCs). In mice, widespread deletion of the tumor suppressor Phosphatase and tensin homolog (PTEN) generates hamartomatous intestinal polyps with epithelial and stromal involvement. Using this model, we have established the relationship between stem cells and polyp and tumor formation. PTEN helps govern the proliferation rate and number of ISCs and loss of PTEN results in an excess of ISCs. In PTEN-deficient mice, excess ISCs initiate de novo crypt formation and crypt fission, recapitulating crypt production in fetal and neonatal intestine. The PTEN-Akt pathway probably governs stem cell activation by helping control nuclear localization of the Wnt pathway effector b-catenin. Akt phosphorylates b-catenin at Ser552, resulting in a nuclear-localized form in ISCs. Our observations show that intestinal polyposis is initiated by PTEN-deficient ISCs that undergo excessive proliferation driven by Akt activation and nuclear localization of b-catenin.
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I read the information above. Many people are interested in cancer stem cells. Here I will talk about my experience in cancer stem cell research.
1. Cancer cells can arise normal stem/proginitor cells and different differentatiated cells after mutation. The cells that can give rise to the daughter cells and can differentiated into mature cells are called to stem cells. They posses the potential ability or self-renewal and differentiation. You know the cancer cells can proliferate, but are absence of differentiation potential. So the initiated cells are called to stem-like cells or cancer stem cells or tumor stem cells, not real stem cells.
2. Cancer can arise from the mutation of normal stem cells and progenitor cells, and the dedifferentiated cells from differentiated cells (terminal cells, matural cells). Currently no specific markers are used to identify stem cells, no makers also to cancer stem cells. The question is that if you use some markers to identify the cancer stem cells, the population are differentiated cells, not stem cells.
3. Currently, some publications suggested that cancer stem cells are strong ability to resistant to drug, radiation therapy. There are the causes of the cancer ocurrence or mestatasis.
4. some publications suggested cancer stem cells possess the potential ability of invasion, extension and metastasis
