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dc.contributor.authorRickelt, Steffen
dc.contributor.authorHynes, Richard O
dc.date.accessioned2018-10-30T15:20:06Z
dc.date.available2018-10-30T15:20:06Z
dc.date.issued2017-12
dc.identifier.issn0036-8075
dc.identifier.issn1095-9203
dc.identifier.urihttp://hdl.handle.net/1721.1/118804
dc.description.abstractBone has a well-established role in advanced cancer. It provides a supportive microenvironment for the growth of metastatic cells that escape the primary tumor, which ultimately leads to loss of bone mass. Engblom et al. show that bone may also contribute to early-stage tumorigenesis through a mechanism that leads to an increase in bone mass (see the Perspective by Zhang and Lyden). In mouse models of lung adenocarcinoma, primary tumor cells remotely activated bone-resident cells called osteoblasts, which have a bone-building function. The activated osteoblasts in turn triggered production of a certain type of neutrophil that infiltrates the primary tumor and promotes its growth. Patients with early-stage lung cancer were also found to have an increase in bone density, consistent with the findings in mice.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant U54-CA163109)en_US
dc.description.sponsorshipHoward Hughes Medical Instituteen_US
dc.description.sponsorshipMassachusetts Institute of Technology. Ludwig Center for Molecular Oncology (Postdoctoral Fellowship)en_US
dc.language.isoen_US
dc.publisherAmerican Association for the Advancement of Science (AAAS)en_US
dc.relation.isversionofhttp://dx.doi.org/10.1126/science.aal5081en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alikeen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/en_US
dc.sourceProf. Hynes via Courtney Crummetten_US
dc.titleOsteoblasts remotely supply lung tumors with cancer-promoting SiglecFen_US
dc.typeArticleen_US
dc.identifier.citationEngblom, Camilla, et al. “Osteoblasts Remotely Supply Lung Tumors with Cancer-Promoting SiglecF High Neutrophils.” Science, vol. 358, no. 6367, Dec. 2017, p. eaal5081.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentKoch Institute for Integrative Cancer Research at MITen_US
dc.contributor.approverHynes Richarden_US
dc.contributor.mitauthorRickelt, Steffen
dc.contributor.mitauthorHynes, Richard O
dc.relation.journalScienceen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsEngblom, Camilla; Pfirschke, Christina; Zilionis, Rapolas; Da Silva Martins, Janaina; Bos, Stijn A.; Courties, Gabriel; Rickelt, Steffen; Severe, Nicolas; Baryawno, Ninib; Faget, Julien; Savova, Virginia; Zemmour, David; Kline, Jaclyn; Siwicki, Marie; Garris, Christopher; Pucci, Ferdinando; Liao, Hsin-Wei; Lin, Yi-Jang; Newton, Andita; Yaghi, Omar K.; Iwamoto, Yoshiko; Tricot, Benoit; Wojtkiewicz, Gregory R.; Nahrendorf, Matthias; Cortez-Retamozo, Virna; Meylan, Etienne; Hynes, Richard O.; Demay, Marie; Klein, Allon; Bredella, Miriam A.; Scadden, David T.; Weissleder, Ralph; Pittet, Mikael J.en_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-5224-7764
dc.identifier.orcidhttps://orcid.org/0000-0001-7603-8396
mit.licenseOPEN_ACCESS_POLICYen_US


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