Under pressure: stromal fibroblasts change their ways.
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.
Bierie
Brian
B
Department of Cancer Biology and Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, 691 Preston Building, Nashville, TN 37232, USA.
Moses
Harold L
HL
D000818:Animals; D003238:Connective Tissue / Q000473:pathology; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology*; D005347:Fibroblasts / Q000473:pathology*; D008297:Male; D051379:Mice; D008954:Models, Biological; D009154:Mutation / Q000235:genetics*; D019899:Paracrine Communication; D011471:Prostatic Neoplasms / Q000235:genetics / Q000473:pathology; D017154:Stromal Cells / Q000473:pathology*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
D016159:Tumor Suppressor Protein p53