Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Division of Hematology-Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Division of Hematology-Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA; Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Cancer Cell. 2014 Mar 17;25(3):261-3. doi: 10.1016/j.ccr.2014.03.001.
In this issue of Cancer Cell, Cao and colleagues identify an FGF4/Jagged1-driven crosstalk between tumor cells and their vascular niche that activates Notch signaling, sustaining the aggressiveness of certain mouse and human B cell lymphomas. These findings identify new therapeutic opportunities to target pathogenic angiocrine functions in cancer.
在本期《癌细胞》杂志中，曹等研究人员发现了肿瘤细胞与其血管龛之间由 FGF4/Jagged1 驱动的串扰，该串扰激活了 Notch 信号通路，维持了某些小鼠和人类 B 细胞淋巴瘤的侵袭性。这些发现为靶向癌症中致病性血管生成功能提供了新的治疗机会。
