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Recent Publications:

Tanoue Y, Toyoda T, Sun J, Mustofa MK, Tateishi C, Endo S, Motoyama N, Araki K, Wu D, Okuno Y, Tsukamoto T, Takeya M, Ihn H, Vaziri C, Tateishi S. Differential Roles of Rad18 and Chk2 in Genome Maintenance and Skin Carcinogenesis Following UV Exposure.聽 J Invest Dermatol. 2018 May 31. pii: S0022-202X(18)32036-0. doi: 10.1016/j.jid.2018.05.015. [Epub ahead of print]

Yang Y, Gao Y, Zlatanou A, Tateishi S, Yurchenko V, Rogozin IB, Vaziri C.聽 Diverse roles of RAD18 and Y-family DNA polymerases in tumorigenesis聽 Cell Cycle. 2018 May 8:1-11. doi: 10.1080/15384101.2018.1456296. [Epub ahead of print]

Diverse roles of RAD18 and Y family DNA polymerases in tumorigenesis

In this invited review we discuss the significance of our recent findings that TLS is aberrantly activated in cancer and confers tolerance of oncogenic stress

Yang Y, Gao Y, Mutter-Rottmayer L, Zlatanou A, Durando M, Ding W, Wyatt D, Ramsden D, Tanoue Y, Tateishi S, Vaziri C.聽 DNA repair factor RAD18 and DNA polymerase Pol魏 confer tolerance of oncogenic DNA replication stress.聽 J Cell Biol. 2017 Oct 2;216(10):3097-3115. doi: 10.1083/jcb.201702006. Epub 2017 Aug 23.

DNA repair factor RAD18 and DNA polymerase Pol魏 confer tolerance of oncogenic DNA replication stress

In this study we showed that RAD18-mediated TLS allows cells to tolerate oncogene-induced DNA damage.聽 In the absence of TLS, oncogene-induced DNA damage leads mitotic catastrophe.聽 These results explain our previous finding that many cancer cells pathologically activate TLS (Gao et al., Nature Communications 2016).

This article was selected by JCB for inclusion in a special collection of articles that advanced the fields of Nuclear organization and function (http://jcb.rupress.org/cc/nuclear-organization-and-function). From the journal web site: 鈥淚n this special collection, JCB Editorial Board Member Ana Pombo and Senior Scientific Editor Melina Casadio selected some of JCB’s most highly read recent content exploring chromatin structure and how it relates to gene expression and genome functions such as DNA replication and repair. This collection sheds light on genome organization and chromosome conformation, chromatin partners and dynamics during development and disease, and how emerging imaging technologies advance the field.鈥�

Li J, Liu J, Liang Z, He F, Yang L, Li P, Jiang Y, Wang B, Zhou C, Wang Y, Ren Y, Yang J, Zhang J, Luo Z, Vaziri C, Liu P. (2017) Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient tumors growth. Cell Death Dis. Mar 16;8(3):e2673. doi: 10.1038/cddis.2017.46.

Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient tumors growth

Gao Y, Mutter-Rottmayer E, Zlatanou A, Vaziri C, Yang Y. (2017) Mechanisms of Post-Replication DNA Repair. Genes (Basel) 8;8(2). pii: E64. doi: 10.3390/genes8020064.

Mechanism of Post Replication DNA Repair

Liang Z, Li W, Liu J, Li J, He F, Jiang Y, Yang L, Li P, Wang B, Wang Y, Ren Y, Yang J, Luo Z, Vaziri C, Liu P. (2017) Simvastatin suppresses the DNA replication licensing factor MCM7 and inhibits the growth of tamoxifen-resistant breast cancer cells. Sci Rep. 7:41776. doi: 10.1038/srep41776.

Simvastatin suppresses the DNA replication licensing factor MCM7 and inhibits the growth of tamoxifen-resistant breast cancer cells

Mutter-Rottmayer E, Gao Y, Vaziri C. (2016) Cancer cells activate damage-tolerant and error-prone DNA synthesis. Mol Cell Oncol. 3(6):e1225547. doi: 10.1080/23723556.2016.1225547.

Cancer cells activate damage tolerant and error prone DNA synthesis

Gao Y, Tateishi S., Vaziri C. (2016) Pathological Trans-Lesion Synthesis in Cancer.聽 Cell Cycle 2016 15(22):3005-3006.

Pathological trans lesion synthesis in cancer

Gao Y, Mutter-Rottmayer E, Greenwalt A M, Goldfarb D, Yan F, Yang Y, Martinez RC, Pearce KH, Tateishi S, Major MB, Vaziri C. (2016) A Neomorphic cancer cell-Specific Role of MAGE-A4 in Trans-Lesion Synthesis. Nature Commun. 2016 Jul 5;7:12105. doi: 10.1038/ncomms12105聽

A neomorphic cancer cell-specific role of MAGE-A4 in trans-lesion synthesis

This study identifies a novel mechanism by which cancer cells deploy a mis-expressed germ cell protein (MAGE-A4) to activate TLS and become DNA damage-tolerant.聽

Yang Y, Poe JC, Yang L, Fedoriw A, Desai S, Magnuson T, Li Z, Fedoriw Y, Araki K, Gao Y, Tateishi S, Sarantopoulos S, Vaziri C. (2015) Rad18 confers hematopoietic progenitor cell DNA damage tolerance independently of the Fanconi Anemia pathway in vivo. Nucleic Acids Res. 2016 44(9):4174-88

Rad18 confers hematopoietic progenitor cell DNA damage tolerance independently of the Fanconi Anemia pathway in vivo