Effect of p53 status on tumor response to antiangiogenic therapy - PubMed (original) (raw)
. 2002 Feb 22;295(5559):1526-8.
doi: 10.1126/science.1068327.
Affiliations
- PMID: 11859195
- DOI: 10.1126/science.1068327
Effect of p53 status on tumor response to antiangiogenic therapy
Joanne L Yu et al. Science. 2002.
Abstract
The p53 tumor suppressor gene is inactivated in the majority of human cancers. Tumor cells deficient in p53 display a diminished rate of apoptosis under hypoxic conditions, a circumstance that might reduce their reliance on vascular supply, and hence their responsiveness to antiangiogenic therapy. Here, we report that mice bearing tumors derived from p53(-/-) HCT116 human colorectal cancer cells were less responsive to antiangiogenic combination therapy than mice bearing isogenic p53(+/+) tumors. Thus, although antiangiogenic therapy targets genetically stable endothelial cells in the tumor vasculature, genetic alterations that decrease the vascular dependence of tumor cells can influence the therapeutic response of tumors to this therapy.
Comment in
- Cancer research. Obstacle for promising cancer therapy.
Marx J. Marx J. Science. 2002 Feb 22;295(5559):1444. doi: 10.1126/science.295.5559.1444a. Science. 2002. PMID: 11859164 No abstract available. - Antiangiogenic therapy and p53.
Hammond EM, Giaccia AJ. Hammond EM, et al. Science. 2002 Jul 26;297(5581):471; discussion 471. doi: 10.1126/science.297.5581.471a. Science. 2002. PMID: 12142499 No abstract available. - Antiangiogenic therapy and p53.
Browder T, Folkman J, Hahnfeldt P, Heymach J, Hlatky L, Kieran M, Rogers MS. Browder T, et al. Science. 2002 Jul 26;297(5581):471; discussion 471. Science. 2002. PMID: 12143876 No abstract available.
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