Andrei V. Gudkov, PhD, DSci, a pre-eminent cancer researcher was appointed Senior Vice President for Basic Research; Chair of the Department of Cell Stress Biology, and a member of the senior leadership team for National Cancer Institute (NCI) Cancer Center Support Grant at Roswell Park Cancer Institute (RPCI) in 2007. He is responsible for building on the basic and translational research strengths of the Cell Stress Biology program in DNA damage and repair, photodynamic therapy, thermal and hypoxic stress and immune modulation. As Senior Vice President, he will assist the President & CEO in developing and implementing strategic plans for new scientific programs and enhance collaborations in research programs with regional and national academic centers as well as with industry.
Dr. Gudkov comes to Roswell Park from the Lerner Research Institute, Cleveland Clinic Foundation where he served as chair of the Department of Molecular Genetics and professor of biochemistry at Case Western University. He earned his doctoral degree in Experimental Oncology at the Cancer Research Center, USSR and a Doctorate of Science (D.Sci) in Molecular Biology at the Moscow State University, USSR. He has authored or co-authored 135 scientific articles and holds 27 patents.
Area of general research interest: Drug discovery approaches, gene discovery, molecular targets for cancer treatment
Identifying and Targeting Cancer-Related Genes
My laboratory is engaged in a broad research program involving several distinct but highly integrated branches of study. We are identifying new disease-associated genes and deciphering molecular mechanisms of activity of their products as potential targets for therapeutic modulation by small molecules or peptides. Our focus is on developing and applying new technologies for functional gene discovery, which will lead to designing new therapeutic approaches to cancer treatment.
Novel Gene Discovery Approaches
Our laboratory uses the Genetic Suppressor Element (GSE) methodology, which can identify genes that are responsible for recessive phenotypes and are thus undetectable by a direct positive selection of expression libraries. The key element of this technique is creation of libraries of randomly fragmented cDNAs that are screened for biologically active GSEs encoding either inhibitory antisense RNA or dominant-negative truncated mini-proteins.
The GSE approach can generate gene repressors from known genes and can identify unknown genes, the suppression of which is associated with certain selectable phenotypic alteration. With GSE, we can isolate genes involved in negative growth regulation and those acting as tumor suppressor, drug sensitivity or pro-apoptotic genes. The GSE approach has revealed new genes controlling drug-mediated cell killing. Specifically, we identified kinesin motor protein as a mediator of cell sensitivity to genotoxic stress through a new mechanism involving the “bystander” effect in drug-treated cell populations.
Our program is aimed at identifying factors determining this new type of cell stress response. A new candidate tumor suppressor gene (TSG), ING1, was also isolated by the GSE technique. ING1 encodes several evolutionary conserved proteins involved in regulation of cell growth, presumably by mediating cooperation between the p53 pathway and the histone deacetylation complex. The phenotype of Ing1-deficient knockout mice has confirmed the tumor suppressor function of this gene. One branch of our gene discovery program is devoted to isolating new viral anti-apoptotic genes as potential leads to new cellular mechanisms controlling programmed cell death. Three anti-apoptotic proteins have been identified among polypeptides encoded by poliovirus; the molecular mechanisms of activity of one of them causes resistance to tumor necrosis factor (TNF) by eliminating the TNF receptor from the cell surface. This finding presents a new mechanism of virus control of cell death. Our program is being expanded to analyze other parasites and their targets in the host apoptotic machinery.
Recently, we have developed a new functional genetic methodology, the Selection-Subtraction Approach (SSA), which allows a direct functional selection of growth-suppressive or killing clones from expression libraries. We consider the SSA our major tool for gene discovery and are applying it to isolate novel cancer-related genes for future drug targeting.
Role of p53 in Cancer
Our p53 studies are focused on the mechanism and role of this TSG in how normal tissues respond to genotoxic stresses associated with cancer treatment. Our previous studies have shown tissue specificity of p53-mediated apoptosis and its major role in determining the radiation sensitivity of mammals. We defined p53 as a determinant of cancer treatment side effects; the new therapeutic concept—targeting p53 for therapeutic suppression—was justified by isolating a small molecule p53 inhibitor that rescues mice from lethal doses of gamma irradiation.
Analysis of an animal model of chemotherapy-induced hair loss (alopecia) has indicated that p53 plays a major role in this common side effect, thus opening another area for clinical application of p53 inhibitors.
Mechanisms of tissue specificity of the p53 response are being addressed by cDNA microarray-based analysis of tissue-specific p53 responsive genes. This direction of studies is linked to identification of new tumor markers among the genes that are under the negative control of p53, a mechanism we have shown to be a possible underlying cause of elevated prostate-specific antigen expression.
The role of p53-dependent apoptosis and growth arrest and the interaction of p53 with other signaling pathways (TNF, Fas, heat shock, etc.) in determining its tumor suppressor function is being analyzed in several model systems. The impact of distinct p53 function (i.e., control of growth arrest or apoptosis) in its tumor suppressor activity is under investigation. We showed that control of radiosensitivity of tissues by p53 in vivo does not involve the p21/waf1 p53-responsive CDK inhibitor. Induction of apoptosis was found to be dispensable for p53-mediated control of genomic stability; moreover, suppression of p53-dependent apoptosis by Bcl-2 delays tumor progression by eliminating selective advantages for genetically unstable p53-deficient cells.
Having already defined ING1, Bloom syndrome and SUMO proteins as p53 interactors, we are continuing the search for cellular modulators of p53 expression and function among p53-interacting proteins; several additional candidates are under study.
Drug Discovery Program
Our drug discovery program involves searching for new p53 inhibitors and testing their potential therapeutic applications for reducing cancer treatment side effects and possibly other pathologies involving p53-inducing stresses. It is based on creation of new cell-based readout systems and high-throughput screening of chemicals with the desired biological properties.
We are also isolating a new class of small molecules acting as modulators of multi-drug transporters that can greatly change the pattern of cross-resistance, including the ability to enhance their activity against certain compounds. The molecular mechanisms of activity of newly isolated compounds are being addressed, as are therapeutic fields for their practical applications.
- Elena Feinstein, M.D., Ph.D. (Quark Biotech, Inc., Nes Ziona, Israel)
- Peter Chumakov, MD, Ph.D. (Lerner Research Institute, CCF)
- Michelle Haber, Ph.D. & Murray Norris, Ph.D. (Children's Cancer Institute of Australia, Sydney)
- Raymond Tubbs, MD (Pathology, CCF)
- Mikhail Nikiforov, Ph.D. (University of Michigan)
- Mark Whitnall, Ph.D. (Armed Forces Radiobiology Research Institute)
- Boris Naroditsky, Ph.D. (Gamaleya Institute of Microbiology, Russia)
- Bruce Blazar, MD (University of Minnesota)
- Joseph DiDonato, Ph.D. (Lerner Research Institute, CCF)
- George R. Stark, Ph.D. (Lerner Research Institute, CCF)
- Eric Klein, MD (CCF)
- Oskar W. Rokhlin, Ph.D. (University of Iowa)
Demidenko ZN, Korotchkina LG, Gudkov AV, Blagosklonny MV. Paradoxical suppression of cellular senescence by p53. Proceedings of the National Academy of Sciences of the United States of America 2010; 107(21):9660-9664
Kelly RM, Hollander GA, Gudkov AV, Komarova EA, Scott HS, Osborn MJ, Stefanski HE, Mueller SN, Taylor PA, Goren EM, Blazar BR. Short-term inhibition of p53 combined with keratinocyte growth factor improves thymic epithelial cell recovery and enhances T-cell reconstitution after murine bone marrow transplantation. Blood 2010; 115(5):1088-1097
Leonova KI, Shneyder J, Antoch MP, Toshkov IA, Novototskaya LR, Komarov PG, Komarova EA, Gudkov AV. A small molecule inhibitor of p53 stimulates amplification of hematopoietic stem cells but does not promote tumor development in mice. Cell cycle (Georgetown, Tex.) 2010; 9(7):1434-1443
Lu T, Jackson MW, Wang B, Yang M, Chance MR, Miyagi M, Gudkov AV, Stark GR. Regulation of NF-kappaB by NSD1/FBXL11-dependent reversible lysine methylation of p65. Proceedings of the National Academy of Sciences of the United States of America 2010; 107(1):46-51
Gasparian AV, Neznanov N, Jha S, Galkin O, Moran JJ, Gudkov AV, Gurova KV, Komar AA. Inhibition of encephalomyocarditis virus and poliovirus replication by quinacrine: implications for the design and discovery of novel antiviral drugs. Journal of virology 2010; 84(18):9390-9397
Gudkov AV, Komarova EA. Pathologies associated with the p53 response.Cold Spring Harbor perspectives in biology 2010; 2(7):a001180
Gudkov AV, Komarova EA. Radioprotection: smart games with death. Journal of clinical investigation 2010; 120(7):2270-2273
Gurova K, Gudkov AV. Targeting transcriptional regulators for simultaneous modulation of p53 and NF-kappa B in cancer treatment. Proceedings of the American Association for Cancer Research Annual Meeting 2010; 51:1418
Korotchkina LG, Leontieva OV, Bukreeva EI, Demidenko ZN, Gudkov AV, Blagosklonny MV. The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway. Aging 2010; 2(6):344-352
Blagosklonny MV, Kenyon C, Kroemer G, Longo V, Nussenzweig A, Osiewacz HD, Peeper DS, Rando TA, Rudolph KL, Sassone-Corsi P, Serrano M, Sharpless NE, Skulachev VP, Tilly JL, Tower J, Verdin E, Karlseder J, Helfand SL, Hekimi S, Campisi J, Sinclair DA, Bartke A, Blasco MA, Bonner WM, Bohr VA, Brosh RM, Brunet A, DePinho RA, Donehower LA, Finch CE, Finkel T, Gorospe M, Gudkov AV, Hall MN, Vijg J. Impact papers on aging in 2009.Aging 2010; 2(3):111-121
Leontieva OV , Gudkov AV , Blagosklonny MV. Weak p53 permits senescence during cell cycle arrest. Cell cycle (Georgetown, Tex.) 2010; 9(21):4323-4327
Tukhvatulin AI , Logunov DY , Shcherbinin DN , Shmarov MM , Naroditsky BS ,Gudkov AV , Gintsburg AL. Toll-like receptors and their adapter molecules.Biochemistry (Moscow) 2010; 75(9):1098-1114
Burkhart CA, Gudkov AV, Norris MD, Marshall GM, Sartorelli AC, Gurova KV, Komarov PG, Isachenko N, Purmal A, Smith J, Flemming C, Xue C, Prokvolit A, Pajic M, Murray J, Watt F, Haber M. Small-molecule multidrug resistance-associated protein 1 inhibitor reversan increases the therapeutic index of chemotherapy in mouse models of neuroblastoma. Cancer research 2009;69(16):6573-6580
Guo C, Gasparian AV, Zhuang Z, Bosykh DA, Komar AA, Gudkov AV, Gurova KV. 9-Aminoacridine-based anticancer drugs target the PI3K/AKT/mTOR, NF-kappaB and p53 pathways. Oncogene 2009; 28(8):1151-1161
Korotchkina LG, Demidenko ZN, Gudkov AV, Blagosklonny MV. Cellular quiescence caused by the Mdm2 inhibitor nutlin-3A. Cell cycle (Georgetown, Tex.) 2009; 8(22):3777-3781
Logunov DY, Scheblyakov DV, Zubkova OV, Shmarov MM, Rakovskaya IV, Gintsburg AL, Gudkov AV, Naroditskii BS. Lipid-associated membrane lipopeptides of M. arginini activate NF-κB by interacting with TLR2/1, TLR2/6, and TLR2/CD14. Molecular genetics, microbiology and virology 2009;24(2):72-75
Lu T, Jackson MW, Singhi AD, Kandel ES, Yang M, Zhang Y, Gudkov AV, Stark GR. Validation-based insertional mutagenesis identifies lysine demethylase FBXL11 as a negative regulator of NFkappaB. Proceedings of the National Academy of Sciences of the United States of America 2009;106(38):16339-16344
Narizhneva NV, Tararova ND, Ryabokon P, Shyshynova I, Prokvolit A, Komarov PG, Purmal AA, Gudkov AV, Gurova KV. Small molecule screening reveals a transcription-independent pro-survival function of androgen receptor in castration-resistant prostate cancer. Cell cycle (Georgetown, Tex.) 2009;8(24):4155-4167
Neznanov N, Fairchild RL, Almasan A, Banerjee AK, Gasparian AV, Gurova KV, Komarov AP, Neznanova L, Gorbachev AV, Gudkov AV. Anti-malaria drug blocks proteotoxic stress response: anti-cancer implications. Cell cycle (Georgetown, Tex.) 2009; 8(23):3960-3970
Pospelova TV, Demidenko ZN, Bukreeva EI, Pospelov VA, Gudkov AV, Blagosklonny MV. Pseudo-DNA damage response in senescent cells. Cell cycle (Georgetown, Tex.) 2009; 8(24):4112-4118
Neznanov N , Komarov AP , Neznanova L , Stanhope-Baker P , Gudkov AV.Proteotoxic stress targeted therapy (PSTT): induction of protein misfolding enhances the antitumor effect of the proteasome inhibitor bortezomib.Oncotarget 2011; 2(3):209-221
Glybochko P, Gudkov A, Naroditsky B, Shmarov M, Logunov D, Vinarova N, Barykova Y, Fiev D, Vinarov AZ, Ginzburg A. Does the possible role of mycoplasma infection in prostate cancer pathogenesis exist? . European urology supplements 2011; 10(2):204
Lee MH, Jothi M, Gudkov AV, Mal AK. Histone Methyltransferase KMT1A Restrains Entry of Alveolar Rhabdomyosarcoma Cells into a Myogenic Differentiated State. Cancer research 2011; 71(11):3921-3931
Burdelya LG, Feinstein E, Didonato JA, Osterman AL, Fort FL, Kurnasov OV, Gupta D, Gleiberman AS, Strom E, Tallant TC, Krivokrysenko VI, Gudkov AV.An agonist of toll-like receptor 5 has radioprotective activity in mouse and primate models. Science (New York, N.Y.) 2008; 320(5873):226-230
Gudkov AV, Gleiberman A. In regard to Schuller et Al. (Int J Radiat Oncol Biol Phys 2007;68:205-210). International journal of radiation oncology, biology, physics 2008; 70(3):800-801; author reply 802-3
Komarov AP, Rokhlin OW, Yu CA, Gudkov AV. Functional genetic screening reveals the role of mitochondrial cytochrome b as a mediator of FAS-induced apoptosis. Proceedings of the National Academy of Sciences of the United States of America 2008; 105(38):14453-14458
Kravchenko JE, Feinstein E, Gudkov AV, Kovriga I, Frolova EI, Strom E, Kochetkov DV, Agapova LS, Komarov PG, Ilyinskaya GV, Chumakov PM.Small-molecule RETRA suppresses mutant p53-bearing cancer cells through a p73-dependent salvage pathway. Proceedings of the National Academy of Sciences of the United States of America 2008; 105(17):6302-6307
Logunov DY, Ginzburg AL, Naroditsky BS, Burdelya LG, Tararova ND, Gurova KV, Rakovskaya IV, Shmarov MM, Zubkova OV, Scheblyakov DV, Gudkov AV.Mycoplasma infection suppresses p53, activates NF-kappaB and cooperates with oncogenic Ras in rodent fibroblast transformation. Oncogene 2008;27(33):4521-4531
Neznanov N, Dragunsky EM, Chumakov KM, Neznanova L, Wek RC, Gudkov AV, Banerjee AK. Different effect of proteasome inhibition on vesicular stomatitis virus and poliovirus replication. PloS one 2008; 3(4):e1887
Neznanov N, Kondratova A, Chumakov KM, Neznanova L, Kondratov R, Banerjee AK, Gudkov AV. Quercetinase pirin makes poliovirus replication resistant to flavonoid quercetin. DNA and cell biology 2008; 27(4):191-198
Shcheblyakov DV, Logunov DY, Zubkova OV, Shmarov MM, Rakovskaya IV, Naroditskii BS, Gintsburg AL, Gudkov AV. Mycoplasma infection with M. Arginini results in NF-κB constitutive activation and inhibition of apoptosis in cells expressing toll-like receptors TLR2/6. Molecular genetics, microbiology and virology 2008; 23(4):163-167
Tararova ND, Narizhneva N, Krivokrisenko V, Gudkov AV, Gurova KV. Prostate cancer cells tolerate a narrow range of androgen receptor expression and activity. Prostate 2007; 67(16):1801-1815
Xue C, Haber M, Flemming C, Marshall GM, Lock RB, MacKenzie KL, Gurova KV, Norris MD, Gudkov AV. P53 Determines Multidrug Sensitivity of Childhood Neuroblastoma. Cancer research 2007; 67(21):10351-10360
Alferov Z, Bukhtiyarov V, Dvurechensky A, Kvardakov V, Son E, Gudkov A, Nemanich R, Satish K, Zhang X, Zvyagin A, Kalyuzhny S, Kazaryan K, Khokhlov A, Fortov V, Deev S, Aseev A, Bagaev S, Gintsburg A, Grigoryev A, Kovalchuk M, Lunin V, Parmon V, Petrov R, Skryabin K, Tkachuk V, Zhavoronkov S. Preface. Journal of physics. Conference series 2011;291(1):11001
Gasparian AV, Gudkov AV, Komar AA, Veith J, Koman IE, Sviridov S, Safina A, Pal S, Guryanova OA, Commane M, Bosykh DA, Saranadasa M, Pal M, Brodsky L, Purmal AA, Burkhart CA, Gurova KV. Curaxins: anticancer compounds that simultaneously suppress NF-kappaB and activate p53 by targeting FACT. Science translational medicine 2011; 3(95):95ra74
Gudkov AV, Gurova KV, Komarova EA. Inflammation and p53: A Tale of Two Stresses. Genes and cancer 2011; 2(4):503-516
Barykova YA, Logunov DY, Shmarov MM, Vinarov AZ, Fiev DN, Vinarova NA, Rakovskaya IV, Baker PS, Shyshynova I, Stephenson AJ, Klein EA, Naroditsky BS, Gintsburg AL, Gudkov AV. Association of Mycoplasma hominis infection with prostate cancer. Oncotarget 2011; 2(4):289-297
Lu T, Jackson MW, Singhi AD, Kandel E, Wang BL, Yang MJ, Zhang Y, Chance M, Miyagi M, Gudkov AV, Stark GR. Promoter insertion reveals lysine demethylase FBXL11 as a negative regulator of NF-kappa B. Cytokine 2008;43(3):326
Lu T, Jackson MW, Singhi AD, Kandel E, Yang M, Gudkov AV, Stark GR. Using lentiviral-based promoter insertional mutagenesis to identify negative regulators of nuclear factor kappa B. Cytokine 2007; 39(1):92
Lu T, Jackson MW, Wang BL, Yang MJ, Chance MR, Miyagi M, Gudkov AV, Stark GR. Regulation of NF kappa B by NSD1/FBXL11-dependent reversible lysine methylation of p65. Cytokine 2009; 48(1-2):19-20
Saito NG, Woods DA, Gurova KV, Gudkov AV. Radiation sensitization by a small molecule that simultaneously suppresses NF-kappa B and activates p53.Proceedings of the American Association for Cancer Research Annual Meeting2008; 49:1002
Barykova IuA, Shmarov MM, Logunov DIu, Verkhovskaia LV, Aliaev IuG, Fiev DN, Vinarov AZ, Vinarova NA, Rakovskaia IV, Naroditskii BS, Gudkov AV, Gintsburg AL. Identification of Mycoplasma in patients with suspected prostate cancer. Zhurnal mikrobiologii, epidemiologii, i immunobiologii 2010; (4):81-85
Gorbachev AV, Gasparian AV, Gurova KV, Gudkov AV, Fairchild RL.Quinacrine inhibits the epidermal dendritic cell migration initiating T cell-mediated skin inflammation. European journal of immunology 2007;37(8):2257-2267
Gudkov AV, Komarova EA. Dangerous habits of a security guard: the two faces of p53 as a drug target. Human molecular genetics 2007; 16(R1):R67-R72
Mao H, Thakur CS, Chattopadhyay S, Silverman RH, Gudkov A, Banerjee AK.Inhibition of human parainfluenza virus type 3 infection by novel small molecules. Antiviral research 2008; 77(2):83-94
Rossi SW, Jeker LT, Ueno T, Kuse S, Keller MP, Zuklys S, Gudkov AV, Takahama Y, Krenger W, Blazar BR, Hollander GA. Keratinocyte growth factor (KGF) enhances postnatal T-cell development via enhancements in proliferation and function of thymic epithelial cells. Blood 2007; 109(9):3803-3811
Thakur CS, Jha BK, Dong B, Das Gupta J, Silverman KM, Mao H, Sawai H, Nakamura AO, Banerjee AK, Gudkov A, Silverman RH. Small-molecule activators of RNase L with broad-spectrum antiviral activity. Proceedings of the National Academy of Sciences of the United States of America 2007;104(23):9585-9590
Wang H, Mannava S, Grachtchouk V, Zhuang D, Soengas MS, Gudkov AV, Prochownik EV, Nikiforov MA. c-Myc depletion inhibits proliferation of human tumor cells at various stages of the cell cycle. Oncogene 2008; 27(13):1905-1915
Fukuzawa N, Petro M, Baldwin III WM, Gudkov AV, Fairchild RL. A TLR5 agonist inhibits acute renal ischemic failure. Journal of immunology (Baltimore, Md. : 1950) 2011; 187(7):3831-3839
Leontieva OV, Demidenko ZN, Gudkov AV, Blagosklonny MV. Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin. PloS one 2011; 6(10):e26126
Logunov DI, Shchebliakov DV, Zubkova OV, Shmarov MM, Rakovskaia IV, Gintsburg LA, Gudkov AV, Naroditskii BS. Lipid-associated membrane lipopeptides of M. arginini activate NF-kB by interacting with TLR2/1, TLR2/6, and TLR2/CD14. Molekuliarnaia genetika, mikrobiologiia i virusologiia 2009; (2)(2):25-28
Shchebliakov DV, Logunov DI, Zubkova OV, Shmarov MM, Rakovskaia IV, Naroditskii BS, Gintsburg AL, Gudkov AV. Mycoplasma M. arginini infection induces constitutive activation of NF-kappaB and inhibits apoptosis in cells expressing toll-like receptors TLR2/6. Molekuliarnaia genetika, mikrobiologiia i virusologiia 2008; (4)(4):6-10
Hu Y, Spengler ML, Kuropatwinski KK, Comas-Soberats M, Jackson M, Chernov MV, Gleiberman AS, Fedtsova N, Rustum YM, Gudkov AV, Antoch MP. Selenium is a modulator of circadian clock that protects mice from the toxicity of a chemotherapeutic drug via upregulation of the core clock protein, BMAL1. Oncotarget 2011; 2(12):1279-1290
Jegede O, Khodyakova A, Chernov M, Weber J, Menendez-Arias L, Gudkov A, Quinones-Mateu ME. Identification of low-molecular weight inhibitors of HIV-1 reverse transcriptase using a cell-based high-throughput screening system.Antiviral research 2011; 91(2):94-98
Yoon S-I, Kurnasov O, Natarajan V, Hong M, Gudkov AV, Osterman AL, Wilson IA. Structural basis of TLR5-flagellin recognition and signaling. Science (New York, N.Y.) 2012; 335(6070):859-864
Alex Chenchik, Diehl P, Tedesco D, Bonneau K, Makhanov M, Frangou CG, Sun P, Gudkov A. Identification of potential cancer drug targets in prostate, blood, and breast cancer cells using HT RNAi screening with pooled shRNA libraries. Proceedings of the American Association for Cancer Research Annual Meeting 2011; 52:Abstract #1648
Xue C, Cheung L, Norris MD, Haber M, Burkhart C, Fedtsova N, Gudkov A, Makarov SS. Small molecule that simultaneously inhibits Myc oncoprotein and activates HIF1A. Proceedings of the American Association for Cancer Research Annual Meeting 2011; 52:Abstract #617
Burdelya LG, Gleiberman AS, Toshkov I, Aygun-Sunar S, Bapardekar M, Manderscheid-Kern P, Bellnier D, Krivokrysenko VI, Feinstein E, Gudkov AV.Toll-like receptor 5 agonist protects mice from dermatitis and oral mucositis caused by local radiation: implications for head-and-neck cancer radiotherapy.International journal of radiation oncology, biology, physics 2012; 83(1):228-234
Shakhov AN, Singh VK, Bone F, Cheney A, Kononov Y, Krasnov P, Bratanova-Toshkova TK, Shakhova VV, Young J, Weil MM, Panoskaltsis-Mortari A, Orschell CM, Baker PS, Gudkov A, Feinstein E. Prevention and mitigation of acute radiation syndrome in mice by synthetic lipopeptide agonists of Toll-like receptor 2 (TLR2). PloS one 2012; 7(3):e33044
Singh VK, Ducey EJ, Fatanmi OO, Singh PK, Brown DS, Purmal A, Shakhova VV, Gudkov AV, Feinstein E, Shakhov A. CBLB613: A TLR 2/6 agonist, natural lipopeptide of mycoplasma arginini, as a novel radiation countermeasure.Radiation research 2012; 177(5):628-642
Koman IE, Commane M, Paszkiewicz G, Hoonjan B, Pal S, Safina A, Toshkov I, Purmal AA, Wang D, Liu S, Morrison C, Gudkov AV, Gurova KV. Targeting FACT complex suppresses mammary tumorigenesis in Her2/neu transgenic mice. Cancer prevention research (Philadelphia, Pa.) 2012; 5(8):1025-1035
Leontieva OV, Natarajan V, Demidenko ZN, Burdelya LG, Gudkov AV, Blagosklonny MV. Hypoxia suppresses conversion from proliferative arrest to cellular senescence. Proceedings of the National Academy of Sciences of the United States of America 2012; 109(33):13314-13318
Spengler ML, Kuropatwinski KK, Comas M, Gasparian AV, Fedtsova N, Gleiberman AS, Gitlin II, Artemicheva NM, Deluca KA, Gudkov AV, Antoch MP.Core circadian protein CLOCK is a positive regulator of NF-kappaB-mediated transcription. Proceedings of the National Academy of Sciences of the United States of America 2012; 109(37):E2457-E2465