Bierie Brian, Moses Harold L
Department of Cancer Biology and Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, 691 Preston Building, Nashville, TN 37232, USA.
Cell. 2005 Dec 16;123(6):985-7. doi: 10.1016/j.cell.2005.11.029.
In this issue of Cell, Hill et al. (2005) demonstrate in a mouse model of prostate cancer that the tumor cells can initiate and promote expansion of stromal fibroblasts that lack the tumor-suppressor protein p53 through a paracrine mechanism. This results in selection of highly proliferative fibroblasts associated with the carcinoma that further promote tumor progression.
在本期《细胞》杂志中,希尔等人(2005年)在前列腺癌小鼠模型中证明,肿瘤细胞可通过旁分泌机制启动并促进缺乏肿瘤抑制蛋白p53的基质成纤维细胞的扩增。这导致选择出与癌相关的高度增殖性成纤维细胞,进而促进肿瘤进展。