My interests over the years have focussed on the proteins and mechanisms involved in the coordination and regulation of Base Excision Repair.
Grigory Dianov was recently made Emeritus Professor in the Department of Oncology following his retirement in May 2018 after 50 years undertaking research on DNA repair protein biochemistry, mechanisms of DNA repair and base excision repair regulation. He carries on his research at the Novosibirsk State University and Institute of Cytology and Genetics in Novosibirsk, Russia and continues to offer advice to members of the CRUK/MRC Oxford Institute for Radiation Oncology and the Department of Oncology.
Professor Grigory Dianov was the Head of Biochemistry at the CRUK/MRC Oxford Institute for Radiation Oncology within the Department of Oncology until May 2018.
He obtained his Doctor of Biological Sciences degree from the Institute of Cytology and Genetics, Siberian Department of the Russian Academy of Sciences at the age of 36 to become the youngest Doctor of Biological Sciences in the country. The same year Grigory was awarded Lenin’s Komsomol Prize, the highest Russian award for young scientists. He continued to work at the Institute of Cytology and Genetics as a Professor and Head of the Laboratory of Molecular Mechanisms of Mutagenesis until 1990. Dr Dianov moved to England and from 1990 - 1993 worked as a Senior Fellow at the Imperial Cancer Research Fund (London) with Dr. Tomas Lindahl (2015 Nobel Prize in Chemistry for DNA Repair mechanisms), where he worked on the basic mechanisms of DNA repair and genome stability. One of Grigory’s papers published jointly with Dr. Lindahl was cited in the Nobel Prize Committee’s justification for the Nobel Prize. In 1993 Grigory moved to the United States where he continue his work on DNA repair as a visiting Professor at the Southwestern Medical Center, Dallas with Dr. Errol Friedberg, a legendary figure in DNA repair field and later as a Senior Fellow with Dr. Vilhelm Bohr (National Institute on Ageing, NIH, Baltimore) where he investigated the role of DNA repair in ageing. In 2000, Dr Dianov moved back to England to become Head of the Biochemistry Group at the Medical Research Council and in 2007 he became Head of Biochemistry at the University of Oxford. Grigory is a member of Editorial Board of several international journals and a frequent reviewer for the Grants Council of the Russian Federation Government, Member of Reviewers Board for the European Research Council, the French National Research Agency, Grant reviewer for Medical Research Council, Cancer Research UK and many international journals.
Chen X, Legrand AJ, Cunniffe S, Hume S, Poletto M, Vaz B, Ramadan K, Yao D, Dianov GL. Interplay between base excision repair protein XRCC1 and ALDH2 predicts overall survival in lung and liver cancer patients. Cell Oncol . 2018 Aug 7. doi: 10.1007/s13402-018-0390-8. [Epub ahead of print] PubMed PMID:30088263.
Legrand AJ, Poletto M, Pankova D, Clementi E, Moore J, Castro-Giner F, Ryan AJ, O'Neill E, Markkanen E, Dianov GL. Persistent DNA strand breaks induce a CAF-like phenotype in normal fibroblasts. Oncotarget. 2018, 9:13666-13681.
Papaspyropoulos A, Bradley L, Thapa A, Leung CY, Toskas K, Koennig D, Pefani DE, Raso C, Grou C, Hamilton G, Vlahov N, Grawenda A, Haider S, Chauhan J, Buti L, Kanapin A, Lu X, Buffa F, Dianov G, von Kriegsheim A, Matallanas D, Samsonova A, Zernicka-Goetz M, O'Neill E. RASSF1A uncouples Wnt from Hippo signalling and promotes YAP mediated differentiation via p73. Nat Commun. 2018, 9:424.
Fletcher SC, Grou CP, Legrand AJ, Chen X, Soderstrom K, Poletto M, Dianov GL. Sp1 phosphorylation by ATM downregulates BER and promotes cell elimination in response to persistent DNA damage. Nucleic Acids Res. 2018, 46:1834–1846
Fischer R, Legrand AJ, Dianov GL Modulation of proteostasis counteracts oxidative stress and affects DNA base excision repair capacity in ATM-deficient cells. Poletto M, Yang D, Fletcher SC, Vendrell I. Nucleic Acids Res. 2017,45:10042-10055.
Poletto M, Legrand AJ, Fletcher SC and Dianov GL. p53 coordinates base excision repair to prevent genomic instability.,. Nucleic Acids Research, 2016, 44:3165-3175
Inhibiting WEE1 selectively kills histone H3K36me3-deficient cancers by dNTP starvation. Pfister SX, Markkanen E, Jiang Y, Sarkar S, Woodcock M, Orlando G, Mavrommati I, Pai CC, Zalmas LP, Drobnitzky N, Dianov GL, Verrill C, Macaulay VM, Ying S, La Thangue NB, D’Angiolella V, Ryan A and Humphrey TC. Cancer Cell, 2015, 28:557-568
Khoronenkova SV, Dianov GL. ATM prevents DSB formation by coordinating SSB repair and cell cycle progression. Proc Natl Acad Sci U S A. 2015, 112:3997-4002