Cancer Stem Cells--Perspectives on Current Status and Future Directions: AACR Workshop on Cancer Stem Cells

Stanford University School of Medicine, Stanford, California, USA.
Cancer Research (Impact Factor: 9.33). 11/2006; 66(19):9339-44. DOI: 10.1158/0008-5472.CAN-06-3126
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    • "CSCs are suggested to be highly treatment-resistant, aggressive and responsible for local and/or distant tumor relapses [25] [40] [42]. Detailed evaluation of CSC protein profiles can therefore have a deep clinical impact. "
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    ABSTRACT: The majority of tumor-related deaths are due to metastasis. Despite the clinical importance of understanding metastasis, we lack knowledge of the molecular mechanisms underlying tumor cell spreading and cell survival far from the primary tumor. Elucidating the molecular characteristics of highly metastatic carcinoma cells would help identify biomarkers or therapeutic targets relevant to predicting or combatting metastasis, and for this the phenotype of metastatic cells could be much more important than their genotype. Hence, proteomic approaches have wide potential utility. This review discusses possibilities of analyzing metastasis-specific protein patterns in a range of sample types, including in vitro and in vivo cancer models, and tissues and biological fluids from patients. Proteome approaches can identify proteins involved in regulating the metastatic capacities of tumors. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    PROTEOMICS - CLINICAL APPLICATIONS 04/2015; DOI:10.1002/prca.201400128 · 2.96 Impact Factor
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    • "The immunostaining results were semi-quantitatively measured and using the results of the statistical analysis a significant correlation between the number of S100A4-positive cells and the histopathological grade of the tumour. It has been widely hypothesised recently that this cellular diversity or heterogeneity within the tumour could be a result of small population of cancer stem cells or cancerinitiating cells (CICs) [44] [45] [46] [47]. If, following further validation, the findings were found to hold true and the aggressiveness of the cancer along with the chances of detecting positive lymph nodes earlier could be tested through the immunoassay staining for presence of S100A4 protein, the assay could be translated to a more automated method of staining evaluation , e.g. "
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    ABSTRACT: MS-based proteomic methods were utilised for the first time in the discovery of novel penile cancer biomarkers. MALDI MS imaging was used to obtain the in situ biomolecular MS profile of squamous cell carcinoma of the penis which was then compared to benign epithelial MS profiles. Spectra from cancerous and benign tissue areas were examined to identify MS peaks that best distinguished normal epithelial cells from invasive squamous epithelial cells, providing crucial evidence to suggest S100A4 to be differentially expressed. Verification by immunohistochemistry resulted in positive staining for S100A4 in a sub-population of invasive but not benign epithelial cells.
    EuPA Open Proteomics 02/2015; 27. DOI:10.1016/j.euprot.2015.02.001
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    • "These specific processes are carried out by a minor population of cells, cancer stem cells (CSCs), which are programmed to preferentially metastasize to specific organs based on their gene expression patterns [11]. These cells have the ability to generate tumors after implantation into animal hosts, and to self-renew and give rise to non-stem cells [12], showing a dynamic equilibrium between CSCs and non-CSCs that could be shifted in one direction or another by contextual signals within the tumor microenvironment [13]. It is important to highlight that, while CSCs can differentiate into non-CSCs, the reverse process must also be considered [13]. "
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    ABSTRACT: The molecular mechanisms of tumor metastasis remain largely unknown and undefined. A recent model suggests that a minor population of cells (cancer stem cells) is programmed to preferentially metastasize to specific organs based on their gene expression patterns. These cells have the ability to generate tumors after implantation into animal hosts, to self-renew and give rise to non-stem cells. In this paper I hypothesize that epigenetic mechanisms could play an important role in tumor metastasis through the reorganization of the bivalent chromatin marks in cancer stem cells in three phases: 1) the reprogramming of epigenetic marks in differentiation master regulator genes responsible for the differentiation to one particular lineage 2) the resolution of these bivalent chromatin marks forces cells to develop the necessary mechanisms to migrate to a new niche and 3) the epigenetic activation of the tissue-specific genes associated with the specific target organ and, simultaneously, the repression of genes associated with alternative developmental pathways.
    Iranian Journal of Medical Hypotheses and Ideas 01/2015; 9(1). DOI:10.1016/j.jmhi.2015.01.001
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