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Chemotherapeutic Resistance: Surviving Stressful Situations

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dc.contributor.author Gilbert, Luke Andrew
dc.contributor.author Hemann, Michael
dc.date.accessioned 2012-10-05T18:26:06Z
dc.date.available 2012-10-05T18:26:06Z
dc.date.issued 2011-07
dc.date.submitted 2011-04
dc.identifier.uri http://hdl.handle.net/1721.1/73659
dc.description.abstract Chemotherapeutic regimens involve the systemic administration of genotoxic compounds that induce cancer cell death via well-established DNA damage response signaling networks. Less understood is how the treatment of other cell types within the tumor microenvironment affects the therapeutic response. Here we discuss recent work that shows that tumor-adjacent cells can respond to genotoxic stress by activating a paracrine secretory program. Although this secretory response serves to protect progenitor cells and promote tissue regeneration in conditions of cellular stress, it can also be coopted by tumor cells to survive frontline chemotherapy. Thus, local prosurvival signaling may present a fundamental barrier to tumor clearance by genotoxic agents, suggesting that effective treatments need to target both cancer cells and the tumor microenvironment. Cancer Res; 71(15); 5062–6. en_US
dc.description.sponsorship National Institutes of Health (U.S.) (RO1 CA128803) en_US
dc.description.sponsorship Massachusetts Institute of Technology. Ludwig Center for Molecular Oncology (Ludwig Graduate Fellowship) en_US
dc.language.iso en_US
dc.publisher American Association for Cancer Research en_US
dc.relation.isversionof http://dx.doi.org/10.1158/0008-5472.can-11-0277 en_US
dc.rights Creative Commons Attribution-Noncommercial-Share Alike 3.0 en_US
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/3.0/ en_US
dc.source PMC en_US
dc.title Chemotherapeutic Resistance: Surviving Stressful Situations en_US
dc.type Article en_US
dc.identifier.citation Gilbert, L. A., and M. T. Hemann. “Chemotherapeutic Resistance: Surviving Stressful Situations.” Cancer Research 71.15 (2011): 5062–5066. Web. en_US
dc.contributor.department David H. Koch Institute for Integrative Cancer Research at MIT en_US
dc.contributor.department Massachusetts Institute of Technology. Department of Biology en_US
dc.contributor.mitauthor Gilbert, Luke Andrew
dc.contributor.mitauthor Hemann, Michael
dc.relation.journal Cancer Research en_US
dc.identifier.mitlicense OPEN_ACCESS_POLICY en_US
dc.eprint.version Author's final manuscript en_US
dc.type.uri http://purl.org/eprint/type/JournalArticle en_US
eprint.status http://purl.org/eprint/status/PeerReviewed en_US
dspace.orderedauthors Gilbert, L. A.; Hemann, M. T. en


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