肿瘤干细胞研究进展

干细胞是一类具有自我更新能力和多向分化潜能的原始细胞，干细胞的自我更新调节通路异常与肿瘤形成密切相关。恶性肿瘤的进行性生长、转移和复发与干细胞的基本特性相似，推测在肿瘤组织中存在少数能驱使肿瘤形成与发展的肿瘤干细胞。随着近年来正常干细胞研究的飞速发展，肿瘤干细胞的研究取得了令人鼓舞的成果，急性髓细胞白血病、乳腺癌及脑瘤中的肿瘤干细胞已相继得到分离和鉴定。现对近年来肿瘤干细胞的研究进展作简要综述。     

肿瘤干细胞研究进展

干细胞是一类具有自我更新能力和多向分化潜能的原始细胞,干细胞的自我更新调节通路异常与肿瘤形成密切相关。恶性肿瘤的进行性生长、转移和复发与千细胞的基本特性相似, 推测在肿瘤组织中存在少数能驱使肿瘤形成与发展的肿瘤干细胞。随着近年来正常干细胞研究的飞速发展,肿瘤干细胞的研究取得了令人鼓舞的成果,急性髓细胞白血病、乳腺癌及脑瘤中的肿瘤干细胞已相继得到分离和鉴定。现对近年来肿瘤干细胞的研究进展作简要综述。     

肿瘤干细胞研究进展

肿瘤研究的基本问题之一是哪些肿瘤细胞能够无限生长.传统理论认为肿瘤生长是所有肿瘤细胞一起增殖的结果.最近通过对造血系肿瘤的研究发现肿瘤细胞的生长繁殖和干细胞之间有许多惊人的相似之处,提出了肿瘤干细胞学说,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.研究证明人类急性髓性白血病(AML)中的肿瘤干细胞存在于CD34 /CD38亚群中,而人乳腺癌中的肿瘤干细胞属于ESA CD44 CD24-/low亚群.肿瘤干细胞概念的提出,提供了靶向性或选择性杀伤肿瘤干细胞从而根治肿瘤和防止肿瘤复发和转移的可能性.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.     

肿瘤干细胞的研究进展

肿瘤干细胞是存在于肿瘤中的一小部分具有干细胞性质的细胞群,具有高度的致瘤性和耐药性。同正常干细胞一样,肿瘤干细胞具有无限的自我更新和多向分化的潜能,使肿瘤在体内不断扩大或形成新的肿瘤,导致肿瘤复发和转移。肿瘤干细胞的研究有助于认识和理解肿瘤发生发展的机制,指导肿瘤的临床治疗。     

肿瘤干细胞研究进展

利用特异性的细胞表面标记分子已经从各类肿瘤组织中分离到了肿瘤干细胞,包括骨髓瘤、肺癌、结肠癌、前列腺癌和胰腺癌.但存在细胞表面标记分子专属性差以及异种移植问题.从临床应用角度来看,将肿瘤干细胞作为肿瘤治疗的靶点,寻找肿瘤干细胞与肿瘤发生的密切关系,选择性地杀伤肿瘤干细胞,为临床根治肿瘤和防止肿瘤复发与转移提供了新的思路.     

肿瘤干细胞研究进展

近年提出的肿瘤干细胞（TSC）学说认为肿瘤组织中存在极少量具有干细胞性质的癌细胞亚群,具有多向分化潜能和无限增殖及自我更新能力,是肿瘤发生、发展、侵袭、转移、复发及耐药的决定性因素。目前已在部分肿瘤分离鉴定出TSC的存在。TSC学说的提出将为最终根治肿瘤提供新靶点。     

肿瘤干细胞研究进展

肿瘤是由功能异质性的细胞群体组成的。有研究认为肿瘤起源于干细胞，是一种千细胞疾病。只有小部分肿瘤干细胞才有成瘤及维持恶性显型的作用。由此可推论：肿瘤治疗的关键应是针对肿瘤干细胞的治疗。肿瘤干细胞研究对肿瘤发生发展机制的阐明、治疗新靶点的发现等将产生深远影响。     

肿瘤干细胞研究进展

目的:了解近年来肿瘤千细胞的研究进展.方法:应用检索Pubmed数据库检索系统,以肿瘤、干细胞、肿瘤干细胞为关键词,检索1979-01-2008-12的相关文献,共检索到英文文献2 760条.纳入标准:1)肿瘤干细胞的表面标志、耐药机制、信号传导通路;2)肿瘤干细胞来源;3)肿瘤干细胞与肿瘤临床诊治的联系.根据纳入标准,最后精选33篇文献进行分析综述.结果:肿瘤干细胞能够自我更新和分化,具有特异的表面分子标志,对放化疗不敏感.肿瘤干细胞存在Wnt、Notch、Hedgehog、Bmi-1等调节细胞自我更新信号通路异常.肿瘤干细胞是维持肿瘤生长、复发和转移的根源,已经成为抗肿瘤研究的靶细胞.结论:肿瘤干细胞研究进展迅速,深入研究肿瘤干细胞的特性,对恶性肿瘤的诊断,治疗和预后评估具有重要意义.肿瘤干细胞理论将改变目前肿瘤的诊治模式.     

肿瘤干细胞的研究进展

肿瘤干细胞(cancer stem cell)是存在于肿瘤组织中的一小部分具有干细胞性质的细胞群体.近年来,越来越多的学者认为肿瘤干细胞的残存是恶性肿瘤复发的根源.随着研究的深入,肿瘤干细胞的靶向治疗为恶性肿瘤的治疗带来了新的希望.     

甲状腺肿瘤干细胞研究进展

肿瘤干细胞已经成为肿瘤发病机制的研究热点,并且已经在很多肿瘤中发现并分离出了肿瘤干细胞.甲状腺肿瘤干细胞模型也已经被提出,越来越多的实验研究支持甲状腺肿瘤干细胞的存在,并认为他们可能来源于甲状腺干细胞.本文综述了目前甲状腺干细胞和甲状腺肿瘤干细胞的研究进展.     

肿瘤干细胞标志物与胃癌关系的研究进展

肿瘤干细胞（cancer stem cell,CSCs）是理论认为肿瘤中存在一小部分细胞具有自我更新和多向分化的潜能,具有特异性表面标志的细胞.目前已经从乳腺癌、结直肠癌、皮肤癌等多种恶性肿瘤中鉴定分离出了各自的肿瘤干细胞标志物.本文就与胃癌相关的干细胞标志物进行综述.     

Implications of Stem Cells and Cancer Stem Cells for Understanding Fomation and Therapy of Cancer

Most cancers are heterogeneous with respect to proliferation and differentiation. There is increasing evidence suggesting that only a minority of cancer cells, tumorigenic or tumor initiating cells, possess the capacity to proliferate extensively and form new hematopoietic cancer or solid tumors. Tumor initiating cells share characteristics required for normal stem cells. The dysregulation of self-renewal and proliferation of stem cells is a likely requirement for cancer development. This review formulates a model for the origin of cancer stem cells and regulating self-renewal which influences the way we study and treat cancer.     

肿瘤干细胞与肿瘤的诊断、转归和预后的关系

肿瘤干细胞（cancerstemcells,CSCs）是近年来干细胞研究和肿瘤研究的热点之一,它具有强大的自我更新和致瘤能力以及不断分化的潜能。目前研究发现肿瘤治疗后易复发、预后差、具有强耐药性与肿瘤中存在肿瘤干细胞有密切的关系。且肿瘤干细胞学说认为,肿瘤很可能是肿瘤干细胞产生的,并且已有学者和专家在造血系统肿瘤和多种实体瘤中分离并鉴定出肿瘤干细胞。对肿瘤干细胞、肿瘤干细胞与肿瘤的发生、发展、诊断、治疗及预后之间的关系作一综述。     

肿瘤干细胞及其耐药性的研究进展

传统理论认为肿瘤生长是所有肿瘤细胞一起增殖的结果,因而治疗方法主要是针对肿瘤组织内的大多数细胞,其结果是常有复发和转移,使治疗失败。随着肿瘤干细胞(cancer stem cells,CSCs)在不同肿瘤组织中被成功分离及其功能研究的深入,传统的肿瘤治疗方式面临着巨大的挑战。同时为深入探讨肿瘤的发生、发展及评价预后等提供了新的理论依据,也为肿瘤的治疗带来了新的思路。因此,只有杀灭CSCs,才能达到根治肿瘤的目的。本文就CSCs与其耐药性作一综述。     

肿瘤干细胞与肿瘤的诊断、转归和预后的关系

肿瘤干细胞(cancer stem cells,CSCs)是近年来干细胞研究和肿瘤研究的热点之一,它具有强大的自我更新和致瘤能力以及不断分化的潜能。目前研究发现肿瘤治疗后易复发、预后差、具有强耐药性与肿瘤中存在肿瘤干细胞有密切的关系。且肿瘤干细胞学说认为,肿瘤很可能是肿瘤干细胞产生的,并且已有学者和专家在造血系统肿瘤和多种实体瘤中分离并鉴定出肿瘤干细胞。对肿瘤干细胞、肿瘤干细胞与肿瘤的发生、发展、诊断、治疗及预后之间的关系作一综述。     

Lung cancer stem cells: Progress and prospects

Epithelial stem cells are critical for tissue generation during development and for repair following injury. In both gestational and postnatal stages, the highly branched and compartmentalized organization of the lung is maintained by multiple, resident stem/progenitor cell populations that are responsible for the homeostatic maintenance and injury repair of pulmonary epithelium. Though lung epithelial injury in the absence of oncogenic mutation is more commonly expressed as chronic lung disease, lung cancer is the most common form of death worldwide and poses a highly significant risk to human health. Cancer is defined by the cell of origin, responsible for initiating the disease. The Cancer Stem Cell Hypothesis proposes that cancer stem cells, identified by stem-like properties of self-renewal and generation of differentiated progeny, are responsible for propagating growth and spread of the disease. In lung cancer, it is hypothesized that cancer stem cells derive from several possible cell sources. The stem cell-like resistance to injury and proliferative potentials of bronchioalveolar stem cells (BASCs) and alveolar epithelial type II cells (AEC2), as well as cells that express the cancer stem cell marker glycoprotein prominin-1 (CD133) or markers for side populations make them potential reservoirs of lung cancer stem cells. The abnormal activation of pathways that normally regulate embryonic lung development, as well as adult tissue maintenance and injury repair, including the Wnt, Hedgehog (Hh) and Notch pathways, has also been identified in lung tumor cells. It is postulated that therapies for lung cancer that specifically target stem cell signaling pathways utilized by lung cancer stem cells could be beneficial in combating this disease.     

Neoplastic human embryonic stem cells as a model of radiation resistance of human cancer stem cells

Studies have implicated that a small sub-population of cells within a tumour, termed cancer stem cells (CSCs), have an enhanced capacity for tumour formation in multiple cancers and may be responsible for recurrence of the disease after treatment, including radiation. Although comparisons have been made between CSCs and bulk-tumour, the more important comparison with respect to therapy is between tumour-sustaining CSC versus normal stem cells that maintain the healthy tissue. However, the absence of normal known counterparts for many CSCs has made it difficult to compare the radiation responses of CSCs with the normal stem cells required for post-radiotherapy tissue regeneration and the maintenance of tissue homeostasis. Here we demonstrate that transformed human embryonic stem cells (t-hESCs), showing features of neoplastic progression produce tumours resistant to radiation relative to their normal counterpart upon injection into immune compromised mice. We reveal that t-hESCs have a reduced capacity for radiation induced cell death via apoptosis and exhibit altered cell cycle arrest relative to hESCs in vitro. t-hESCs have an increased expression of BclXL in comparison to their normal counterparts and re-sensitization of t-hESCs to radiation upon addition of BH3-only mimetic ABT737, suggesting that overexpression of BclXL underpins t-hESC radiation insensitivity. Using this novel discovery platform to investigate radiation resistance in human CSCs, our study indicates that chemotherapy targeting Bcl2-family members may prove to be an adjuvant to radiotherapy capable of targeting CSCs.     

上皮间质转化和肿瘤干细胞

最近,两个新的概念出现在肿瘤生物学中：上皮间质转化（epitheilal-mesenchymal transition,EMT）和肿瘤干细胞（cancer stem cells,CSCs）。EMT不仅赋予细胞迁移和侵袭特征,还可使肿瘤细胞获得自我更新能力而具有干细胞的特性,从而促进CSCs的产生。本文讨论EMT和CSCs之间的联系、EMT获得干细胞特征促进CSCs产生、EMT是形成CSCs的重要环节及二者在干细胞巢中的转化,并分析影响EMT和CSCs的因素。研究EMT在肿瘤发生中的作用,与CSCs理论相融合,从而可能发现新的肿瘤靶向治疗。