Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 128, Issue 1, Pages 16-25Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI93554
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Funding
- NIH [R01 CA105155, R01 HL127283, R01 HL132585, R21 AR060978]
- Cancer Prevention Research Institute of Texas Multi-investigator Research [RP120713, RP160652]
- Jeane F. Shelby Scholarship Fund
- NATIONAL CANCER INSTITUTE [R01CA105155, P50CA070907] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL132585, R01HL127283] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R21AR060978] Funding Source: NIH RePORTER
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Intratumoral fibrosis results from the deposition of a cross-linked collagen matrix by cancer-associated fibroblasts (CAFs). This type of fibrosis has been shown to exert mechanical forces and create a biochemical milieu that, together, shape intratumoral immunity and influence tumor cell metastatic behavior. In this Review, we present recent evidence that CAFs and tumor cells are regulated by provisional matrix molecules, that metastasis results from a change in the type of stromal collagen cross-link, and that fibrosis and inflammation perpetuate each other through proteolytic and chemotactic mediators released into the tumor stroma. We also discuss aspects of the emerging biology that have potential therapeutic value.
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