The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Mutant p53-dependent growth suppression distinguishes PRIMA-1 from known anticancer drugs: a statistical analysis of information in the National Cancer Institute database
Abstract
We recently identified PRIMA-1 as a low molecular weight compound that restores tumor suppressor function to mutant p53 proteins and has anti-tumor activity in vivo (1). Here we report the statistical analysis of the effect of PRIMA-1 on a panel of human tumor cell lines using information available in a database at the Developmental Therapeutics Program of the National Cancer Institute (NCI). We extracted growth inhibition profiles for PRIMA-1 and 44 known anticancer agents, p53 status of cell lines, population doubling time, and level of p53 protein expression from the NCI database. The data were analyzed by linear regression, Wilcoxon matched pairs test, and cluster analysis. In a subset of human cell lines derived from colon, ovarian, renal, and non-small cell lung cancer and melanoma, the level of mutant p53 expression correlated with cell population doubling time, r = -0.53, P = 0.018. The GI(50) values for PRIMA-1 correlated with levels of mutant p53, r = -0.75, P = 0.0002. PRIMA-1 showed a statistically significant preference at P = 0.04 for growth inhibition of tumor cell lines expressing mutant p53 as compared with lines expressing wild-type p53. In contrast, none of several known anticancer drugs showed such preference. PRIMA-1 inhibited the growth of cell lines derived from various human tumor types in a mutant p53-dependent manner. This distinguishes PRIMA-1 from known anticancer drugs and supports the idea that PRIMA-1 can serve as a lead for the development of novel therapeutic compounds.
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Cites
Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound
Bykov, V. J. N., Issaeva, N., Shilov, A., Hultcrantz, M., Pugacheva, E., Chumakov, P., Bergman, J., Wiman, K. G., & Selivanova, G. (2002) · Nature Medicine · doi:10.1038/nm0302-282 · Cited by 1,067
Self-citationDisruption of p53 in human cancer cells alters the responses to therapeutic agents.
Bunz, F., Hwang, P. M., Torrance, C., Waldman, T., Zhang, Y., Dillehay, L., Williams, J., Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6863 · Cited by 1,044
Cited by
Targeting mutant p53 for efficient cancer therapy
Bykov, V. J. N., Eriksson, S. E., Bianchi, J., & Wiman, K. G. (2018) · Nature Reviews Cancer · doi:10.1038/nrc.2017.109 · Cited by 889
Self-citationPRIMA-1 reactivates mutant p53 by covalent binding to the core domain
Lambert, J. M. R., Gorzov, P., Veprintsev, D. B., Söderqvist, M., Segerbäck, D., Bergman, J., Fersht, A. R., Hainaut, P., Wiman, K. G., & Bykov, V. J. N. (2009) · Cancer Cell · doi:10.1016/j.ccr.2009.03.003 · Cited by 592
Self-citationMustafa, M., Ahmad, R., Tantry, I. Q., Ahmad, W., Siddiqui, S., Alam, M., Abbas, K., Moinuddin, Hassan, M. I., Habib, S., et al. (2024) · Cells · doi:10.3390/cells13221838 · Cited by 595
Lehmann, S., Bykov, V. J. N., Ali, D., Andrén, O., Cherif, H., Tidefelt, U., Uggla, B., Yachnin, J., Juliusson, G., Moshfegh, A., et al. (2012) · Journal of Clinical Oncology · doi:10.1200/jco.2011.40.7783 · Cited by 406
Self-citationAPR-246 reactivates mutant p53 by targeting cysteines 124 and 277
Zhang, Q., Bykov, V. J. N., Wiman, K. G., & Zawacka-Pankau, J. (2018) · Cell Death & Disease · doi:10.1038/s41419-018-0463-7 · Cited by 261
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Metadata
- Authors
- Bykov, V. J. N.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-12-01
- Volume
- 23
- Issue
- 12
- Pages
- 2011-2018
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- OpenAlex
- W1996649572
- Cited by
- 172
- References
- 2
- FWCI
- 2.33
- Type
- journal article
- Language
- en
- Open access
- closed
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- Bykov, V. J. N. (2002). Mutant p53-dependent growth suppression distinguishes PRIMA-1 from known anticancer drugs: a statistical analysis of information in the National Cancer Institute database. Carcinogenesis. https://doi.org/10.1093/carcin/23.12.2011
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