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By Chengzhuo Gao, Robert E. Hollingsworth, Elaine M. Hurt (auth.), Lesley A Mathews, Stephanie M Cabarcas, Elaine M. Hurt (eds.)

ISBN-10: 9400745893

ISBN-13: 9789400745896

ISBN-10: 9400745907

ISBN-13: 9789400745902

The life of ‘cancer stem cells’ (CSCs) has been an issue of heated debate for the previous few years in the box of melanoma biology. Their non-stop characterization in a number of strong tumors has result in an abundance of proof assisting their life. CSCs are believed to be answerable for resistance opposed to traditional therapy regimes of chemotherapy and radiation, eventually, resulting in metastasis and sufferer death. to aid relief clinicians, pharmaceutical businesses and educational labs investigating tips on how to larger kill those hugely competitive cells we've got summarized the DNA fix mechanism(s) and their function within the upkeep and rules of either general and melanoma stem cells. Our e-book represents a complete research into the powerful DNA fix mechanisms of CSCs and what we have to comprehend which will advance extra complicated cures to remove them from sufferers. presently, there aren't any different released works solely on DNA fix and melanoma Stem Cells. moreover, our e-book presents a entire assessment of CSC isolation and characterization from a number of strong tumor types.

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Extra resources for DNA Repair of Cancer Stem Cells

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The only CSC marker that was found to be correlated with radiation-resistance was ALDH1. These results highlight differences in individual CSC markers that might be relevant in a context-dependent manner, although the involvement of CSCs and radio-resistance is becoming clearer. Another report has also identified elevated ALDH levels in breast cancer CSCs and it was found to be responsible for radiation resistance [61]. The other factors that have been linked with radio-resistance of CSCs are nicotinamide N-methyltransferase expression [62], maternal embryonic leucine zipper kinases [63] and STAT3 signaling [64].

Also, as suggested below, stem cell markers are known to induce the expression of ABC transporters, which might also explain the increased activity of these transporters in the side populations. Studies of hepatocellular carcinoma proposed that the cells dual positive for CD133 and CD44 represent CSCs [39]. As expected, CD133(+)/CD44(+) cells were observed to be more resistant to chemotherapeutic agents and the up-regulation of ABC transporters ABCB1, ABCC1 and ABCG2 was believed to be the mechanism of drug resistance in these CSCs.

Cell Res 18(1):148–161 22. Shimizu M, Gruz P, Kamiya H et al (2003) Erroneous incorporation of oxidized DNA precursors by Y-family DNA polymerases. EMBO Rep 4(3):269–273 23. McClendon AK, Osheroff N (2007) DNA topoisomerase II, genotoxicity, and cancer. Mutat Res 623(1–2):83–97 24. Pourquier P, Pommier Y (2001) Topoisomerase I-mediated DNA damage. Adv Cancer Res 80:189–216 25. Bridges BA (2005) Error-prone DNA repair and translesion synthesis: focus on the replication fork. DNA Repair (Amst) 4(5):618–619, 634 26.

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DNA Repair of Cancer Stem Cells by Chengzhuo Gao, Robert E. Hollingsworth, Elaine M. Hurt (auth.), Lesley A Mathews, Stephanie M Cabarcas, Elaine M. Hurt (eds.)

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