The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Effect of p53 Status on Tumor Response to Antiangiogenic Therapy
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.
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Cites
Requirement for p53 and p21 to Sustain G 2 Arrest After DNA Damage
Bunz, F., Dutriaux, A., Lengauer, C., Waldman, T., Zhou, S., Brown, J. P., Sedivy, J. M., Kinzler, K. W., & Vogelstein, B. (1998) · Science · doi:10.1126/science.282.5393.1497 · Cited by 2,803
Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
Graeber, T. G., Osmanian, C., Jacks, T., Housman, D. E., Koch, C. J., Lowe, S. W., & Giaccia, A. J. (1996) · Nature · doi:10.1038/379088a0 · Cited by 2,300
Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance
Boehm, T., Folkman, J., Browder, T., & O'Reilly, M. S. (1997) · Nature · doi:10.1038/37126 · Cited by 1,683
Cited by
Tumorigenesis and the angiogenic switch
Bergers, G., & Benjamin, L. E. (2003) · Nature reviews. Cancer · doi:10.1038/nrc1093 · Cited by 3,559
Modes of resistance to anti-angiogenic therapy
Bergers, G., & Hanahan, D. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2442 · Cited by 2,953
Angiogenesis as a therapeutic target
Ferrara, N., & Kerbel, R. S. (2005) · Nature · doi:10.1038/nature04483 · Cited by 2,653
Self-citationCasanovas, O., Hicklin, D. J., Bergers, G., & Hanahan, D. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.09.005 · Cited by 1,621
Self-citationHypoxia promotes invasive growth by transcriptional activation of the met protooncogene
Pennacchietti, S., Michieli, P., Galluzzo, M., Mazzone, M., Giordano, S., & Comoglio, P. M. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00085-0 · Cited by 1,311
Metadata
- Authors
- Yu, J. L., Rak, J. W., Coomber, B. L., Hicklin, D. J., & Kerbel, R. S.
- Venue
- Science
- Published
- 2002-02-22
- Volume
- 295
- Issue
- 5559
- Pages
- 1526-1528
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2080237506
- Cited by
- 426
- References
- 3
- FWCI
- 15.01
- Type
- journal article
- Language
- en
- Open access
- closed
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- Yu, J. L., Rak, J. W., Coomber, B. L., Hicklin, D. J., & Kerbel, R. S. (2002). Effect of p53 Status on Tumor Response to Antiangiogenic Therapy. Science. https://doi.org/10.1126/science.1068327
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