Rajasekhar Vinagolu K, Dalerba Piero, Passegué Emmanuelle, Lagasse Eric, Najbauer Joseph
Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, Rockefeller Research Laboratories, New York, New York 10021, USA.
Stem Cells. 2008 Jan;26(1):292-8. doi: 10.1634/stemcells.2007-0647. Epub 2007 Oct 25.
This report presents highlights of discussions that focused on the biology of cancer stem cells as conducted at the fifth Annual Meeting of the International Society for Stem Cell Research, held in Cairns, Australia, June 17-20, 2007. The function of adult stem cells is believed to depend on their niches, that is, the microenvironment in which these stem cells reside. A similar concept applies to understanding the development of cancer, as it is becoming increasingly clear that only a small subset of cancer cell populations is capable of initiating/sustaining tumor formation. These tumorigenic cells, commonly referred to as cancer stem cells, also appear to reside in particular niches, and they bear the known, albeit dysfunctional, stem cell characteristics of self-renewal and differentiation. Dysregulation of stem cell niches is thought to contribute to tumorigenesis by affecting the complex network of signaling interactions that occur between stem cells and their neighboring cells, thus imbalancing the physiological controls on self-renewal and differentiation processes. This hypothesis was widely explored at the conference to shed new light on the mechanisms of tumor origin and progression and to unveil novel antitumor therapeutic approaches.
本报告介绍了2007年6月17日至20日在澳大利亚凯恩斯举行的国际干细胞研究学会第五届年会上,针对癌症干细胞生物学展开的讨论要点。成体干细胞的功能被认为取决于其生态位,即这些干细胞所处的微环境。类似的概念也适用于理解癌症的发展,因为越来越明显的是,只有一小部分癌细胞群体能够启动/维持肿瘤形成。这些具有致瘤性的细胞,通常被称为癌症干细胞,似乎也存在于特定的生态位中,并且它们具有已知的、尽管功能失调的自我更新和分化的干细胞特征。干细胞生态位的失调被认为通过影响干细胞与其相邻细胞之间发生的复杂信号相互作用网络,从而破坏自我更新和分化过程的生理控制,进而导致肿瘤发生。会议广泛探讨了这一假说,以阐明肿瘤起源和进展的机制,并揭示新的抗肿瘤治疗方法。