ArticlePloS one2015
Krt6a-positive mammary epithelial progenitors are not at increased vulnerability to tumorigenesis initiated by ErbB2.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Advances in Immunocompetent Mouse and Rat Models.Cold Spring Harbor perspectives in medicine · 2024Review
- In Vivo Gene Delivery into Mouse Mammary Epithelial Cells Through Mammary Intraductal Injection.Journal of visualized experiments : JoVE · 2023Article
- Intraductal Injection of Lentivirus Vectors for Stably Introducing Genes into Rat Mammary Epithelial Cells in Vivo.Journal of mammary gland biology and neoplasia · 2020Article
- Alteration of tumor-associated macrophage subtypes mediated by KRT6A in pancreatic ductal adenocarcinoma.Aging · 2020Article
- Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes.Cancer research · 2019Article
- Hyperprolactinemia-inducing antipsychotics increase breast cancer risk by activating JAK-STAT5 in precancerous lesions.Breast cancer research : BCR · 2018Article
- Article
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Authors and funding
6 authors.
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Abstract
While most breast cancers are thought to arise from the luminal layer of the breast tissue, it remains unclear which specific cells in the luminal layer are the cells of origin of breast cancer. We have previously reported that WAP-positive luminal epithelial cells are at increased susceptibility to tumor initiation by ErbB2 compared to the bulk population, while the mammary cells with canonical Wnt signaling activity fail to evolve into tumors upon ErbB2 activation. Here, we used retrovirus to introduce ErbB2 into the Krt6a-positive mammary progenitor subset of the luminal epithelium and, for comparison, into the mammary luminal epithelium indiscriminately. Tumors developed from both groups of cells with a similar latency. These data indicate that the Krt6a-positive subset of mammary epithelial cells can be induced to form cancer by ErbB2 but it is not more susceptible to tumorigenesis initiated by ErbB2 than the bulk population of the luminal epithelium.
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