Characterizing the HER2/neu Status and Metastatic Potential of Breast Cancer Stem/Progenitor Cells

摘要: Treatment resistance, long latency, and high recurrence rates suggest that breast cancers arise from defective stem cells. Within cancers, subpopulations of cells will demonstrate differences in stem/progenitor potential, HER2/neu amplification, gene expression. Related be found normal tissue. ER-/PR-/HER2/neu + breast cancer were flow-sorted into subpopulations: (A) CD49f+ CD24−, (B) CD49f+CD24+, (C) CD49f (D) CD49f−CD24+. Gel matrix cell invasion, fluorescence situ hybridization (FISH) qRT-PCR expression measured all groups. Cells sorted groups implanted rat brains. Resultant tumors analyzed by immunohistochemistry (IHC) FISH. Normal tissue was examined IHC. Tumor development varied among (25–75%), but highest group A. mostly CD49f−CD24−, with variable fractions other Tumors showed fewer chromosome 17 per than inoculates. Group A exhibited copy number near amplification. Cell invasion 61% higher unsorted 34–42% compared controls. Sorted significantly different development, proliferation, associated genes. In tissue, identified CD14+ CK19− basal epithelial layers mammary glands; these 95% CD24+ and 60% CD44+. Breast populations differ tumor-initiating potential are not solely responsible for metastasis. Cancer less polyploid general may amplified. cell-like present.