Year: 2007
Type: dissertation
Abstract: Phosphatase and Tensin homolog deleted on chromosome 10 (Pten), an antagonist of Phosphotidylinositol-3 Kinase (PI3K) signaling, is one of the most commonly inactivated tumour suppressor genes in human cancers. However, its role in breast cancer is not well understood. Here I have used a conditional knock-out mouse model in which Pten was specifically disrupted in the mammary gland to study the effect of the PI3K/Pten pathway on the mammary stem cell compartment and tumour-initiating cells. The loss of Pten in mammary epithelium gave rise to mixed population tumours containing myoepithelial and luminal epithelial cells and lead to an expansion of stem cell population. PtenDeltaf/f mammary tumours exhibited nuclear accumulation of cyclin D2 and beta-catenin and contained keratin 6 positive cell population. Comparative analysis of Pten Deltaf/f mammary tumours suggested that like MMTV-Wnt1, loss of Pten in the mammary gland induces tumours by targeting the stem cell/early progenitor cell population.
Source: TSpace (University of Toronto)
Author: Lehal, Rajwinder Singh
Language: English
Topic: Cancer Cells and Metastasis
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W7132951235