ESP Biography



SOPHIA CHERNIKOVA, Cancer Biology Scientist at Stanford University




Major: Radiation Oncology

College/Employer: Stanford

Year of Graduation: Not available.

Picture of Sophia Chernikova

Brief Biographical Sketch:

EDUCATION
Ph.D. in Cell & Molecular Radiation Biology (1998)
Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO

M.S. in Applied Mathematics & Physics, qualification of Engineer-Physicist, Honor Diploma (1990)
Moscow Institute of Physics and Technology, Moscow, Russia

PROFESSIONAL EXPERIENCE
Senior Research Scientist
Stanford University School of Medicine, Department of Radiation Oncology (Laboratory of Dr. J.M. Brown), Stanford, CA
Projects 2005 - present
• Role of neovasculogenesis in the post-irradiation tumor regrowth
• Chromatin remodeling in radiation response and genomic instability
• Finding small-molecule inhibitors of homologous recombination for tumor therapy
• Mechanism of action of new hypoxia-activated cytotoxins
• Homologous recombination pathway as a main pathway for repair of damage induced by a hypoxic cytotoxin tirapazamine

Postdoctoral Research Fellow
Lawrence Berkeley National Laboratory, Department of Cell and Molecular Biology (Laboratory of Dr. P. K. Cooper), Berkeley, CA
Projects 1999 -2004
• Identifiication of interacting partners for the nucleotide excision repair protein XPG (defective in xeroderma pigmentosum and Cockayne syndromes)
• Characterization of the interaction of XPG with DNA-dependent protein kinase DNA-PK and WRN (Werner’s syndrome) proteins
• Identification of kinases involved in XPG phosphorylation

Ph.D. Student
Colorado State University, Department of Environmental and Radiological Health Sciences (Laboratory of Dr. M. M. Elkind), Fort Collins, CO
Projects 1993 -1998
• Cell-cycle dependence of low-dose radiation-induced mutation and neoplastic transformation in normal and DNA-PK compromised cells
• Role for DNA-PK in radiation sensitization by a PI3K inhibitor, wortmannin
• Cell cycle dependence of wortmannin effect on radiation sensitivity and mutation induction

TEACHING INTERESTS
Cell and Molecular Biology, Cancer Biology, Human Biology, DNA Repair, Radiation Biology, Cancer Prevention, Genetics, Biochemistry of Health and Disease, Environmental Carcinogenesis/Mutagenesis and Toxicology, Nutrition for Health

PUBLICATIONS
Chernikova SB, Razorenova OV, Higgins JP, Sishc BJ, Nicolau M, Dorth JA, Chernikova DA, Kwok S, Brooks JD, Bailey SM, Game JC, Brown JM. Deficiency in mammalian histone H2B ubiquitin ligase Bre1 (Rnf20/Rnf40) leads to replication stress and chromosomal instability. Cancer Res. 2012 Feb 21. [Epub ahead of print]
Chernikova SB, Game JC, Brown JM. Inhibiting homologous recombination for cancer therapy. Cancer Biol Ther. 2012 Jan 15;13(2):61-8
Trego KS, Chernikova SB, Davalos AR, Perry JJ, Finger LD, Ng C, Tsai MS, Yannone SM, Tainer JA, Campisi J, Cooper PK. The DNA repair endonuclease XPG interacts directly and functionally with the WRN helicase defective in Werner syndrome. Cell Cycle, 2011, 10(12):1998-2007.
Razorenova O.V., Finger E., Colavitti R., Chernikova S.B., Boiko A.D., Chan C., Krieg A.J., Bedogni B., LaGory E., Weissman I.L., Broome-Powell M., Giaccia A.J. VHL loss in renal cell carcinoma leads to HIF-dependent upregulation of CUB domain-containing protein 1 to stimulate PKCδ-driven migration. Proc Natl Acad Sci USA, 2011, 108(5):1931-6.
Chernikova S.B., Dorth J.A., Razorenova O.V., Game J.C., Brown J.M. Deficiency in Bre1 impairs homologous recombination repair and cell cycle checkpoint response to radiation damage in mammalian cells. Radiat Res, 2010, Vol. 174, No. 5: 558-565.
Gu Y., Patterson A.V., Atwell G.J., Chernikova S.B., Brown J.M., Thompson L.M., Wilson W.R. Roles of DNA repair and reductase activity in the cytotoxicity of the hypoxia-activated dinitrobenzamide mustard PR-104A, Mol Cancer Ther 2009; 8(6)
Game J.C., Chernikova S.B., The role of RAD6 in recombinational repair, checkpoints and meiosis via histone modification. DNA Repair, 2009; 8(4):470-82.
Evans J.W.,* Chernikova S.B. * (* equal contribution) , Kachnic L., Banath J.P., Sordet O., Delahoussaye Y.M., Treszezamsky A., Chon B., Feng Z., Pommier Y., Olive P.L., Powell S.N., and Brown J.M. Homologous recombination is the principal pathway for the repair of DNA damage induced by tirapazamine. Cancer Research, 2008; 68(1), 257-65
Chernikova, S.B., Lindquist, K.L., and Elkind, M.M. Cell cycle-dependent effects of wortmannin on radiation survival and mutation. Radiation Research 2001; 155 (6): 826-831.
Chernikova, S.B., Wells, R.L., and Elkind, M.M. Wortmannin sensitizes mammalian cells to radiation by inhibiting the DNA-dependent protein kinase-mediated rejoining of double-strand breaks. Radiation Research 1999; 151(2): 159-66.
Gotlib VI, Serebrianyi AM, Chernikova SB, Kudriashova OV, Pelevina II. A comparison of the patterns of delayed cell death after exposure to genotoxic agents. Tsitologiia, 1996; 38(9): 974-82.
Chernikova, S.B., Gotlib, V.Y., and Pelevina, I.I. Effect of low-dose ionizing radiation on radiosensitivity to the next irradiation. Radiobiologia 1993; 33(4): 537-41.
Krutova, T.V., Chernikova, S.B., Konradov, A.A., Burlakova, E.B. The effect of methylnitrosourea in low doses on the stationary cell population. Experiment and model. Izvestiya Academii Nauk, Rossiya (News of the Russian Academy of Sciences), Biological Series, N 4, 511-518 (1992).



Past Classes

  (Clicking a class title will bring you to the course's section of the corresponding course catalog)

B2510: WE ARE WHAT WE EAT. in Splash! Fall 2012 (Nov. 03 - 04, 2012)
We will explore the evolution of an old saying in relationship to modern chronic disease, touching upon the role of a healthy lifestyle in prevention and cure of various chronic diseases including cancer.


B2153: Cancer… Do we know enough about it to fight it successfully? in Splash! Spring 2012 (Apr. 21 - 22, 2012)
I will overview the mechanisms of cancer development, and specifically, the body’s defense and detection mechanisms against neoplastic transformation and tumor growth. We will talk about the nature of the disease, predisposing factors, conventional treatments, and the role of a “healthy lifestyle” in preventing and fighting the disease.