Dr. Natalia Issaeva
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Academic Career Length
25Years (2002-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications1 November 2006 in Nature
Journal Article
JBJiri Bartek
Jiri BartekNRNousin Rezaei
Nousin Rezaei
MLMichalis Liontos
Michalis LiontosPKPanagiotis Karakaidos
Panagiotis Karakaidos
Dimitris KletsasVGVassilis G. Gorgoulis
Vassilis G. Gorgoulis
+19
1 March 2002 in Nature Medicine
Journal Article
VBVladimir J.N. Bykov
Vladimir J.N. BykovNatalia IssaevaASAlexandre Shilov
Alexandre Shilov
MHMonica Hultcrantz
Monica Hultcrantz
EPElena Pugacheva
Elena PugachevaGSGalina Selivanova
Galina Selivanova +3
1 February 2010 in Molecular Cell
Journal Article
EPEva Petermann
Eva PetermannMOManuel Luís Orta
Manuel Luís OrtaNatalia IssaevaNSNiklas Schultz
Niklas Schultz
THThomas Helleday
Thomas HelledayFaithful DNA replication is essential to all life. Hydroxyurea (HU) depletes the cells of dNTPs, which initially results in stalled replication forks that, after prolonged treatment, collapse into DSBs. Here, we report that stalled replication forks are efficiently restarted in a RAD51-dependent process that does not trigger homologous recombination (HR). The XRCC3 protein, which is required for RAD51 foci formation, is also required for replication restart of HU-stalled forks, suggesting that RAD51-mediated strand invasion supports fork restart. In contrast, replication forks collapsed by prolonged replication blocks do not restart, and global replication is rescued by new origin firing. We find that RAD51-dependent HR is triggered for repair of collapsed replication forks, without apparent restart. In conclusion, our data suggest that restart of stalled replication forks and HR repair of collapsed replication forks require two distinct RAD51-mediated pathways.
21 November 2004 in Nature Medicine
Journal Article
Natalia IssaevaPBPrzemyslaw Bozko
Przemyslaw Bozko
MEMartin Enge
Martin EngeMPMarina Protopopova
Marina Protopopova
LVLisette G G C Verhoef
Lisette G G C Verhoef
GSGalina Selivanova
Galina Selivanova +2
In tumors that retain wild-type p53, its tumor-suppressor function is often impaired as a result of the deregulation of HDM-2, which binds to p53 and targets it for proteasomal degradation. We have screened a chemical library and identified a small molecule named RITA (reactivation of p53 and induction of tumor cell apoptosis), which bound to p53 and induced its accumulation in tumor cells. RITA prevented p53–HDM-2 interaction in vitro and in vivo and affected p53 interaction with several negative regulators. RITA induced expression of p53 target genes and massive apoptosis in various tumor cells lines expressing wild-type p53. RITA suppressed the growth of human fibroblasts and lymphoblasts only upon oncogene expression and showed substantial p53-dependent antitumor effect in vivo. RITA may serve as a lead compound for the development of an anticancer drug that targets tumors with wild-type p53.
23 July 2009 in The EMBO Journal
Journal Article
HBHelen E Bryant
Helen E Bryant
EPEva Petermann
Eva PetermannNSNiklas Schultz
Niklas Schultz
AJAnn‐Sofie Jemth
Ann‐Sofie JemthOLOlga Loseva
Olga Loseva
THThomas Helleday
Thomas Helleday +4
EMBO Press is an editorially independent publishing platform for the development of EMBO scientific publications.
13 October 2014 in Proceedings of the National Academy of Sciences
Journal Article
MPMichael Parfenov
Michael Parfenov
CPChandra Sekhar Pedamallu
Chandra Sekhar Pedamallu
NGNils Gehlenborg
Nils GehlenborgSFSamuel S. Freeman
Samuel S. FreemanLDLudmila Danilova
Ludmila Danilova
ZZZhixiang Zuo
Zhixiang Zuo +31
Significance: A significant proportion of head and neck cancer is driven by human papillomavirus (HPV) infection, and the expression of viral oncogenes is involved in the development of these tumors. However, the role of HPV integration in primary tumors beyond increasing the expression of viral oncoproteins is not understood. Here, we describe how HPV integration impacts the host genome by amplification of oncogenes and disruption of tumor suppressors as well as driving inter- and intrachromosomal rearrangements. Tumors that do and do not have HPV integrants display distinct gene expression profiles and DNA methylation patterns, which further support the view that the mechanisms by which tumors with integrated and nonintegrated HPV arise are distinct.
About Me
Professor Natalia Issaeva, PhD currently is an Assistant Professor at the Department of Otolaryngology/Head and Neck Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. She earned a Ph.D. in Cell and Tumor Biology at the Karolinska Institutet, Stockholm, Sweden, in 2005 before completing a Postdoctoral Associate at the Department of Genetics, Microbiology and Toxicology (GMT), Stockholm University, from 2006 to 2009 and at the Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA, from 2009 to 2010. She has been awarded funding for "Exploring mechanisms of therapeutic demethylation effects in HPV-associated head and neck cancer", "Observational study to validate circulating HPV DNA and prognostic genomic biomarkers for diagnosis and treatment of HPV-associated OPSCC", and " Dissecting NF-kB pathway in HPV-associated head and neck cancer" by NIH NIDCR. Her research interests are focused on the HPV-associated head and neck cancer.