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dc.contributor.authorBonavita, Eduardo
dc.contributor.authorPelly, Victoria S
dc.contributor.authorZelenay, Santiago
dc.date.accessioned2018-01-14T18:40:09Z
dc.date.available2018-01-14T18:40:09Z
dc.date.issued2018-01-02
dc.identifier.citationResolving the dark side of therapy-driven cancer cell death. 2018, 215(1): 9-11 J Exp Meden
dc.identifier.issn1540-9538
dc.identifier.pmid29263217
dc.identifier.doi10.1084/jem.20172044
dc.identifier.urihttp://hdl.handle.net/10541/620775
dc.description.abstractIn this issue of JEM, Sulciner et al. (https://doi.org/10.1084/jem.20170681) provide evidence that therapy-induced cancer cell death can, paradoxically, stimulate and accelerate the growth of surviving malignant cells by fueling tumor-promoting inflammation. Resolvins, a class of lipid mediators, counteract this effect, representing an attractive target for therapeutic intervention.
dc.language.isoenen
dc.rightsArchived with thanks to The Journal of experimental medicineen
dc.titleResolving the dark side of therapy-driven cancer cell death.en
dc.typeArticleen
dc.contributor.departmentCancer Inflammation and Immunity Group, CRUK Manchester Institute, The University of Manchester, Manchester, England, UKen
dc.identifier.journalThe Journal of Experimental Medicineen
refterms.dateFOA2018-12-17T15:11:33Z
html.description.abstractIn this issue of JEM, Sulciner et al. (https://doi.org/10.1084/jem.20170681) provide evidence that therapy-induced cancer cell death can, paradoxically, stimulate and accelerate the growth of surviving malignant cells by fueling tumor-promoting inflammation. Resolvins, a class of lipid mediators, counteract this effect, representing an attractive target for therapeutic intervention.


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