Journal
CANCER CELL
Volume 13, Issue 5, Pages 394-406Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2008.03.007
Keywords
-
Categories
Funding
- NCI NIH HHS [R01 CA094074-01A1, R37 CA064786, R01 CA116235-01A1, P50 CA089393-040004, R01 CA094074-05, P50 CA089393, R01 CA116235, P50 CA089393-070014, P50 CA089393-020004, R01 CA094074-02, R01 CA116235-03, P50 CA089393-090014, P50 CA089393-080014, CA116235, P50 CA089393-060014, R01 CA094074-04, CA94074, P50 CA089393-010004, R01 CA094074-03, R01 CA064786, CA89393, R01 CA094074, P50 CA089393-050004, P50 CA089393-030004, R01 CA116235-02, CA64786] Funding Source: Medline
Ask authors/readers for more resources
The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGF beta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available