Journal
CANCER CELL
Volume 4, Issue 4, Pages 291-299Publisher
CELL PRESS
DOI: 10.1016/S1535-6108(03)00245-9
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Funding
- NCRR NIH HHS [RR000171] Funding Source: Medline
- NIAID NIH HHS [AI001773] Funding Source: Medline
- NIAMS NIH HHS [AR48246] Funding Source: Medline
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Id genes regulate tumor angiogenesis and loss of Id1 inhibits tumor xenograft growth in mice. Here we evaluate the role of Id1 in a more clinically relevant tumor model system using a two-step chemical carcinogenesis protocol. Remarkably, we find that Id1(-/-) mice are more susceptible to skin tumorigenesis compared to their wild-type counterparts. Cutaneous neoplasms in Id1(-/-) mice show increased proliferation without alterations in tumor angiogenesis; however, Id1(-/-) mice possess 50% fewer cutaneous gammadelta T cells than their wild-type counterparts due to an intrinsic migration defect associated with loss of expression of the chemokine receptor, CXCR4. We suggest that there are important differences between the mechanisms of angiogenesis in transplanted and autochthonous tumors and that these findings will have significant implications for the potential utility of antiangiogenic therapies in cancer.
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