Stem Cells: The Real Culprits in Cancer?

University of Michigan, Ann Arbor, USA.
Scientific American (Impact Factor: 1.07). 08/2006; 295(1):52-9. DOI: 10.1038/scientificamerican0706-52
Source: PubMed


A dark side of stem cells—their potential to turn malignant—is at the root of a handful of cancers and may be the cause of many more. Eliminating the disease could depend on tracking down and destroying these elusive killer cells

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    • "Collectively, these initial studies provide strong evidence for clonal evolution (Campbell and Polyak 2007; Navin and Hicks 2010; Greaves and Maley 2012) in many primary tumors and hematological malignancies. These data challenge the strict cancer stem cell model (Clarke and Becker 2006; Shipitsin and Polyak 2008; Tomasson 2009) by showing that the majority of tumor cells have continued lineages and are capable of continued proliferation and clonal expansion. Furthermore, the phylogenetic trees from these studies show strong evidence of a common set of founder mutations in every cancer patient, suggesting that most solid tumors evolve from a single somatic cell in the normal tissue. "
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    ABSTRACT: Single-cell sequencing (SCS) is a powerful new tool for investigating evolution and diversity in cancer and understanding the role of rare cells in tumor progression. These methods have begun to unravel key questions in cancer biology that have been difficult to address with bulk tumor measurements. Over the past five years, there has been extraordinary progress in technological developments and research applications, but these efforts represent only the tip of the iceberg. In the coming years, SCS will greatly improve our understanding of invasion, metastasis, and therapy resistance during cancer progression. These tools will also have direct translational applications in the clinic, in areas such as early detection, noninvasive monitoring, and guiding targeted therapy. In this perspective, I discuss the progress that has been made and the myriad of unexplored applications that still lie ahead in cancer research and medicine.
    Preview · Article · Oct 2015 · Genome Research
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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.
    Full-text · Article · Feb 2015 · EuPA Open Proteomics
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    • "Further on, metastasis process occurs that according to clonal theory involve invasion and angiogenesis , migration and arrest in the capillary beds of distant organs. lls are based on this theory [6]. According to this model, tumour is induced after multiple mutations occur in a random single cell, conferring it a selective growth advantage over adjacent normal cells [3]. "
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    ABSTRACT: Despite the abundance of attention that cancer has attracted, it continues to constitute one of the deadliest scourges of the modern era. Tumour heterogeneity greatly contributes to the ineffectiveness of current therapies and hampers the study and treatment of cancer. There are two models accounting for tumour heterogeneity and propagation, namely clonal evolution model and cancer stem cell model. In particular, cancer stem theory has attracted much attention lately, as these cells with self-renewal and differentiation abilities are responsible for the initiation of tumour development, growth, and its ability to metastasize and reoccur, and provide a reasonable explanation for poor prognosis for patients in advanced stages of solid tumours. Advances in technologies such as proteomics open new avenues in metastasis research by specifically revealing complex protein networks involved in tumour progression, which should facilitate early diagnosis and provide the basis for designing more effective treatment strategies.
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