期刊
PHYSIOLOGICAL GENOMICS
卷 46, 期 7, 页码 223-244出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiolgenomics.00158.2013
关键词
wound healing; regeneration; fibrosis; cancer; tumor stroma; myofibroblasts; tumor- or cancer-associated fibroblasts; desmoplasia; epithelial-to-mesenchymal transition
资金
- Commonwealth of Pennsylvania
- FCCC's Keystone Program in Personalized Kidney Cancer Therapy
- Nodal Temple-FCCC Award
- Bucks County Board of Associates
- National Cancer Institute [CA-113451, CA-06927]
The wound healing, chronic fibrosis, and cancer progression triad. Physiol Genomics 46: 223-244,2014. First published February 11, 2014; doi:10.1152/physiolgenomics.00158.2013.- For decades tumors have been recognized as wounds that do not heal. Besides the commonalities that tumors and wounded tissues share, the process of wound healing also portrays similar characteristics with chronic fibrosis. In this review, we suggest a tight interrelationship, which is governed as a concurrence of cellular and microenvironmental reactivity among wound healing, chronic fibrosis, and cancer development/ progression (i.e., the WHFC triad). It is clear that the same cell types, as well as soluble and matrix elements that drive wound healing (including regeneration) via distinct signaling pathways, also fuel chronic fibrosis and tumor progression. Hence, here we review the relationship between fibrosis and cancer through the lens of wound healing.
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