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Mikhail V. Blagosklonny

Medicine Branch

National Cancer Institute

NIH, Bethesda

MD 20892

USA

[email]@box-m.nih.gov

Name/email consistency: high

 
 
 
 
 
 
 

Affiliations

  • Medicine Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA. 1998 - 2002
  • National Cancer Institute-Medicine Branch, Building 10, Room 12N226, 10 Center Drive, USA. 2002
  • Department of Experimental Therapeutics, NCI, National Institutes of Health, Bethesda, USA. 1998

References

  1. P53: an ubiquitous target of anticancer drugs. Blagosklonny, M.V. Int. J. Cancer (2002) [Pubmed]
  2. Basic cell cycle and cancer research: is harmony impossible?. Blagosklonny, M.V. Cell. Cycle (2002) [Pubmed]
  3. Inhibition of transcription results in accumulation of Wt p53 followed by delayed outburst of p53-inducible proteins: p53 as a sensor of transcriptional integrity. Blagosklonny, M.V., Demidenko, Z.N., Fojo, T. Cell. Cycle (2002) [Pubmed]
  4. Resistance to growth inhibitory and apoptotic effects of phorbol ester and UCN-01 in aggressive cancer cell lines. Blagosklonny, M.V., Dixon, S.C., Robey, R., Figg, W.D. Int. J. Oncol. (2001) [Pubmed]
  5. Inhibition of HIF-1- and wild-type p53-stimulated transcription by codon Arg175 p53 mutants with selective loss of functions. Blagosklonny, M.V., Giannakakou, P., Romanova, L.Y., Ryan, K.M., Vousden, K.H., Fojo, T. Carcinogenesis (2001) [Pubmed]
  6. Exploiting cancer cell cycling for selective protection of normal cells. Blagosklonny, M.V., Pardee, A.B. Cancer Res. (2001) [Pubmed]
  7. Hypoxia-inducible factor: Achilles' heel of antiangiogenic cancer therapy (review). Blagosklonny, M.V. Int. J. Oncol. (2001) [Pubmed]
  8. How carcinogens (or telomere dysfunction) induce genetic instability: associated-selection model. Blagosklonny, M.V. FEBS Lett. (2001) [Pubmed]
  9. Pretreatment with DNA-damaging agents permits selective killing of checkpoint-deficient cells by microtubule-active drugs. Blagosklonny, M.V., Robey, R., Bates, S., Fojo, T. J. Clin. Invest. (2000) [Pubmed]
  10. Loss of cell cycle control allows selective microtubule-active drug-induced Bcl-2 phosphorylation and cytotoxicity in autonomous cancer cells. Blagosklonny, M.V., Bishop, P.C., Robey, R., Fojo, T., Bates, S.E. Cancer Res. (2000) [Pubmed]
  11. p53 from complexity to simplicity: mutant p53 stabilization, gain-of-function, and dominant-negative effect. Blagosklonny, M.V. FASEB J. (2000) [Pubmed]
  12. A node between proliferation, apoptosis, and growth arrest. Blagosklonny, M.V. Bioessays (1999) [Pubmed]
  13. Molecular effects of paclitaxel: myths and reality (a critical review). Blagosklonny, M.V., Fojo, T. Int. J. Cancer (1999) [Pubmed]
  14. Acute overexpression of wt p53 facilitates anticancer drug-induced death of cancer and normal cells. Blagosklonny, M.V., El-Deiry, W.S. Int. J. Cancer (1998) [Pubmed]
  15. Like p53, the proliferation-associated protein p120 accumulates in human cancer cells following exposure to anticancer drugs. Blagosklonny, M.V., Iglesias, A., Zhan, Z., Fojo, T. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
  16. p53 inhibits hypoxia-inducible factor-stimulated transcription. Blagosklonny, M.V., An, W.G., Romanova, L.Y., Trepel, J., Fojo, T., Neckers, L. J. Biol. Chem. (1998) [Pubmed]
  17. The mitogen-activated protein kinase pathway mediates growth arrest or E1A-dependent apoptosis in SKBR3 human breast cancer cells. Blagosklonny, M.V. Int. J. Cancer (1998) [Pubmed]
 
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