Journal
CELL REPORTS
Volume 17, Issue 7, Pages 1764-1772Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2016.10.031
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Funding
- Samana Cay MGH Research Scholar Fund
- NIH [R21-CA190344, P50-CA86355, R01-AI084880, U54-CA126515, U54-CA163109, F31-CA196035]
- European Molecular Biology Organization (EMBO) [ALTF 1535-2011]
- Massachusetts General Hospital Executive Committee On Research (ECOR) Funds for Medical Discovery Fellowship
- Deutsche Forschungsgemeinschaft [PF809/1-1, RI2408/1-1]
- Metastasis/Cancer Research Postdoc fellowship from MIT Ludwig Center for Molecular Oncology Research
- Boehringer Ingelheim Funds
- Howard Hughes Medical Institute
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Co-option of host components by solid tumors facilitates cancer progression and can occur in both local tumor microenvironments and remote locations. At present, the signals involved in long-distance communication remain insufficiently understood. Here, we identify platelet factor 4 (PF4, CXCL4) as an endocrine factor whose overexpression in tumors correlates with decreased overall patient survival. Furthermore, engineered PF4 over-production in a Kras-driven lung adenocarcinoma genetic mouse model expanded megakaryopoiesis in bone marrow, augmented platelet accumulation in lungs, and accelerated de novo adenocarcinogenesis. Additionally, anti-platelet treatment controlled mouse lung cancer progression, further suggesting that platelets can modulate the tumor microenvironment to accelerate tumor outgrowth. These findings support PF4 as a cancer-enhancing endocrine signal that controls discrete aspects of bone marrow hematopoiesis and tumor microenvironment and that should be considered as a molecular target in anticancer therapy.
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