据12月19日的《科学》杂志报道说，在研究致命的白血病细胞在小鼠中是如何对循环系统进行攻击之后，他们已经找到了癌症细胞所支使的一种特别的蛋白质。这种蛋白质有可能成为一种治疗该种癌症的良好的标靶。
Angela Colmone及其同僚为了发现这一秘密对罹患白血病的活体小鼠进行了实时成像检测，并对白血病细胞是如何破坏健康的造血始祖细胞（HPCs）的功能（HPCs负责终身为机体提供健康的血细胞）进行了研究。研究人员观察到，白血病细胞通过挖掘进入小鼠的骨髓中，并在那里制造出一个能吸引 HPCs的“龛位”。这些恶性的龛位比小鼠的自然的龛位更能吸引 HPCs的注意力，从而使得血流中的 HPCs的数目减少，因此破坏了 HPC的正常功能。研究人员接着观察到，通过中和白血病细胞中的一种叫做干细胞因子的特殊蛋白，这样， HPCs就不再会跌入这一陷阱，因而避开了这些恶性的龛位。他们的这些发现仍然需要在人体中获得证实。但是这一对白血病细胞的新的观点提示可以有一种阻断 HPCs进入这些癌性陷阱的方法，因而有助于确保机体生产健康的血细胞。（生物谷Bioon.com）
生物谷推荐原始出处：
Science 19 December 2008: DOI: 10.1126/science.1164390
Leukemic Cells Create Bone Marrow Niches That Disrupt the Behavior of Normal Hematopoietic Progenitor Cells
Angela Colmone, Maria Amorim, Andrea L. Pontier, Sheng Wang, Elizabeth Jablonski, Dorothy A. Sipkins*
The host tissue microenvironment influences malignant cell proliferation and metastasis, but little is known about how tumor-induced changes in the microenvironment affect benign cellular ecosystems. Applying dynamic in vivo imaging to a mouse model, we show that leukemic cell growth disrupts normal hematopoietic progenitor cell (HPC) bone marrow niches and creates abnormal microenvironments that sequester transplanted human CD34+ (HPC-enriched) cells. CD34+ cells in leukemic mice declined in number over time and failed to mobilize into the peripheral circulation in response to cytokine stimulation. Neutralization of stem cell factor (SCF) secreted by leukemic cells inhibited CD34+ cell migration into malignant niches, normalized CD34+ cell numbers, and restored CD34+ cell mobilization in leukemic mice. These data suggest that the tumor microenvironment causes HPC dysfunction by usurping normal HPC niches and that therapeutic inhibition of HPC interaction with tumor niches may help maintain normal progenitor cell function in the setting of malignancy.
Department of Medicine, Section of Hematology/Oncology, The University of Chicago, 5841 South Maryland Avenue MC 2115, Chicago, IL 60637, USA.
