Abstract
Abstract Cancer stem cells (CSCs) are now recognized as pivotal entity in the development and progression of breast cancer. The CSCs are believed to be responsible for recurrence/relapse of cancer because of their ability to resist chemotherapeutic drugs. The present drugs in the clinics predominantly target the highly proliferating cells sparing the slow dividing and resistant cells. If the drugs targeting the cancer stem cells evolve, there is a possibility of eradication of cancer. In this direction it is imperative to understand the fundamental difference between the cancer stem cells and the non cancer stem cells. Hence, a basic understanding of genes expressed in CSCs vs non-CSCs needs to be explored. A large number of high throughput and extensive Micro array studies have been carried out to understand the normal and various breast cancer subtypes however, the RNA profiles does not necessarily match the protein profile, Therefore determination of protein levels is the key to identify the novel targets for cancer stem cells. To address this issue and to identify meaningful targets for breast cancer we have characterized breast cancer stem cells from primary cultures of Her2/Neu transgenic mice. We identified the altered proteins through LC-MS/MS using an LTQ-orbitrap mass spectrometer and confirmed those results using quantitative RT-PCR. We further performed insilico analysis, using microarray datasets, for identification of group of genes, which in combination can provide prognostic importance. We identified PTMA, S100A4, S100A6, TNXRD1, COX-1, COX-2 and FTH1 as a group of genes, which in combination were significantly associated with poor clinical outcome of breast cancer patients. Among these genes FTH1 was identified as a novel protein associated with prognosis of breast cancer, which is overexpressed in enriched breast CSCs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5347. doi:1538-7445.AM2012-5347
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