能否攻克肿瘤现在似乎肿瘤干细胞是希望！！！

 !

 向这个方向努力

 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

 Tumor Stem Cell是今后的研究方向。

 

 很有意思

 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.

 血液干细胞有人去分离并已经用于治疗，实体瘤难度大。共聚焦的原理你读读看，在这里不合适使用。

 各位前辈有没有成功分离肿瘤干细胞的经验？可否介绍一二？

 dream 老师谢谢您的留言，目前我的实验还只停留在初步设计阶段，初步设想是从实体瘤中分离，也看了相关的好多报道，知道分离的难度很大，请问dream老师是否看到过应用激光显微切割技术分离肿瘤干细胞的，我只看到一篇综述中提到过这个方法，没有看到具体应用的。

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。

等您的课题做好了，就给我们做一次讲座吧。

A Perivascular Niche for Brain Tumor Stem Cells  CANCERCELL Volume 11, Issue 1, January 2007, Pages 69-82

我看了，还可以，如果你愿意翻译一些在这里供大家学习就好了，我把全文发到你的信箱了。

 免疫磁珠分离肿瘤有转移病人血液中cancer cell是没有问题，你可以用下面几家公司的产品。

 你研究的是实体瘤还是白血病？实体瘤的问题是：在你收集的血液样品中，肿瘤干细胞的比例是非常小的，1－2个估计就很不错了，所以目前我读的文献中，还没有看到有人报道从血液中分离出实体瘤肿瘤干细胞。

 各位前辈，请问有没有用过免疫磁珠分离肿瘤干细胞的？效果如何呢？

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