Dawit Kidane, Ph.D.

Dawit Kidane Profile Pic

Assistant Professor of Pharmacology & Toxicology

The Kidane Lab

Kidane Lab Images

Research Interests

My laboratory is devoted to understand how basic mechanisms of DNA repair impact cancer etiology and response to chemotherapies. The major focus of the group is to uncover the biological role of DNA repair in cancer cells and provide potential new strategies to exploit genetic vulnerability for better chemotherapeutic response.

My laboratory research has two main interests:

1. Base excision repair and genomic instability

Reactive oxygen and nitrogen species (RONs) interact with DNA and induce various forms of DNA damage including single-and double-strand breaks, abasic sites, and nucleotide modification, all of which contribute to tumor initiation. RONs induced DNA damage is repaired by base excision repair (BER). The BER pathway deals with base damage, the most common insult to cellular DNA. BER is initiated by DNA glycosylases that recognize damaged bases, excise the lesions, and provide substrates for later enzymes in the pathway. When these pathways are compromised, there is an increase in genomic instability and cellular transformation, which can lead to cancer. Since the BER pathway has become a target for cancer therapies, it is vital to understand how germline (heritable variation in the lineage of population) and BER gene mutations in tumors variants induce genomic instability and alter cellular responses to DNA damaging agents. Using the Cancer Genome Atlas (TCGA) and the 1000 Genomes database, we have identified several cancer-associated and germline variants of BER genes (Single-nucleotide polymorphism) respectively. However, the biological functions of these mutations and the effect in response to chemotherapy are not known. Our study will determine i) how cancer-associated variants of BER genes (such as POLB, NEIL3) induce genomic instability; ii) cellular response to DNA damaging agents; iii) how to manipulate BER mutations in tumors to restore sensitivity of chemotherapy resistant cancer cells. Our work utilizes a combination of biochemistry, cell biology, and genetically engineered mice to study BER pathways involved in genomic instability and cancer. The long-term objective of my laboratory is to understand how aberrant BER is linked to carcinogenesis and to develop a novel approach for discovering specific genetic vulnerabilities in cancer cells that can be exploited for the development of therapeutics.

2. Interplay between infection, inflammation and DNA repair

A second area of interest in my laboratory is to uncover the complex relationship between infections induced inflammation, genomic instability, and cancer. Despite huge research efforts to understand the interaction between hosts and pathogens during an infection, it is very difficult to translate the generated fundamental knowledge into strategy to reduce infection-mediated cancer. Bacterial infection is one of the environmental factors that cause chronic inflammation, host DNA damage, and increase the risk of cancer. Helicobacter pylori is a gram-negative bacterial and colonizes the gastric mucosa of half of the world’s population and is a class I carcinogen. While eradication of H. pylori by antibiotic treatment can be relatively simple to accomplish, preventing the global burden of gastric cancer through H. pylori eradication can be a challenging task. Some of the challenges demonstrated that H. pylori mediated gastric cancer is a slow process and it can take decades. In addition a number of earlier human chemoprevention trials had addressed the effect of H. pylori eradication on precancerous lesions rather than using gastric cancer. Although it is well accepted that activation of host DNA damage response is a common theme of infections with H. pylori, more detailed study is still needed to better understand the “how” and “why” of long-term interaction between the host and pathogens. Our recent finding shows that upon H. pylori infection, base excision repair (BER) intermediate (AP sites) accumulate and lead to increased levels of double-strand breaks (DSBs) at different stages of cell cycles (Kidane D, et al 2014, Oncogenesis) suggest that BER is critical to repair oxidative DNA damage induced with H. pylori infection. We believe that more work is needed to elucidate mechanisms how H. pylori infection manipulate the host immune system and DNA repair to promote genomic instability and malignant transformation. Therefore, the goals of our study are i) to shade lights how DNA repair promote H. pylori- mediated gastric cancer using mouse model with reasonable short period of time; ii) to develop new therapeutic strategies using DNA repair inhibitor. Our study will lead to a better understanding of H. pylori infection mediated DNA damage response, improve our knowledge of infection induced cancer and refine our preclinical data to design therapeutic strategies for future.


Alex Klattenhoff, Msc. Lab Manger
Debolina Ray, Ph.D. Postdoctoral Associate
Elizabeth Alvarez, Pharma, D. student
Chad McCants, Undergraduate student
Oanh Tran, Undergraduate student


Stephan Clayton
Jenna Rozacky
Lidiya Lulseged

Selected Peer-Reviewed Publications

  1. Rozacky, J., Nemec, A.A., Sweasy J.B. and Kidane D. (2015). Gastric cancer associated variant of DNA polymerase beta (Leu22Pro) promotes replication associated double strand breaks. Oncotarget 2015.
  2. Kidane, D., Murphy DL and Sweasy JB. (2014) Accumulation of abasic sites induces genomic instability in normal human gastric epithelial cells during Helicobacter pylori infection.Oncogenesis;3:e128
  3. Kidane, D  Wook Jin Chae, Jennifer Czochor, Kristin A. Eckert, Peter Glazer, Alfred L.M. Bothwell, Joann B. Sweasy  (2014). Interplay Between DNA Repair and Inflammation, and the Link to Cancer  Crit Rev Biochem Mol Biol 49(2) 116-39. PMID 24410153.
  4. Senejani, A.G; Liu, Y; Kidane, D; Stephen E; Maher, S.E; Zeiss,C.J; Park,H.J; Kashgarian,M; Jennifer M. McNiff, J.M  Zelterman8,D;. Bothwell, A.LM, Sweasy J.B (2014). Mutation of POL B Causes Lupus in Mice. Cell Rep. 6(1):1-8.
  5. Tadesse, S. Kidane D., Guller, S., Luo,T.,  Arcuri,F.,  Toti, P., Norwitz, E.R (2014). In vivo and in vitro  evidence for DNA damage in preeclampsia. PLoS One. 9(1):e86791
  6. Galick, HA., Kathe,S.,  Minmin Liu Susan Robey-Bond, Kidane, D; Susan S. Wallace,SS; Joann B. Sweasy . (2013) A Germline Variant of Human NTH1 DNA Glycosylase Induces Genomic Instability and Cellular Transformation. Proc Natl Acad Sci 27;110(35):14314-9.
  7. Kidane. D, Sakkas, D, Nottoli, T, McGrath, J, and Sweasy J. B. Sweasy. Kinesin 5B (KIF5B) Is Required for Progression through Female Meiosis and Proper Chromosomal Segregation in Mitotic Cells. PLoS One. 2013;8(4):e58585.
  8. Kidane. D, Sweasy, J.B. Graumann, PL. and Alonso, JC. (2012). Cell pole: The site of  cross talk between DNA repair and DNA uptake machinery. Crit Rev Biochem Mol Biol 47(6): 531-55
  9. Kidane, D and Sweasy J.B. (2012). Tipping the Balance the Powerhouse of Cells to Protect Colorectal Cancer. Perspective. PLoS Genet. 2012 Jun;8(6):e1002758.
  10. Kidane, D, Keh A, Liu Y, Sweasy J.B. (2011). DNA polymerase Beta is critical for genomic stability in sperm cell.  DNA repair (Amst) PMID: 21333614.
  11. Kidane D Jonason, A.S, Gorton T.S, Mihaylov I, Ashley T, Keh A, Liu Y, Banerjee U, Zelterman D and Sweasy J.B. (2010). DNA Polymerase Beta is Critical for Meiotic Synapsis. EMBO Journal. PMID: 20019666.
  12. Kidane .D, Carrasco B, Manfredi C, Tadesse S, Alonso JC, Graumann PL. (2009). Visual evidence for Horizontal gene transfer in competentBacillus subtilis cells. PLoS Genet. 2009 Sep
  13. Mascarenhas J, Sanchez H, Tadesse S, Kidane D, Krishnamurthy M, Alonso JC, Graumann PL. (2006) Bacillus subtilis SbcC protein plays an important role in DNA inter-strand cross-link repair BMC Mol Biol. 7 (1): 20 PMCID: PMC1533848
  14. Genetu A, Gadisa E, Aseffa A, Barr S, Lakew M, Jirata D, Kuru T,Kidane D, Hunegnaw M Gedamu L. (2006) Leishmania aethiopica: Strain identification and characterization of superoxide dismutase-B genes. Exp Parasitol. 113(4): 221-226. PMID: 16516199.
  15. Sanchez H, Kidane D, Castillo Cozar M, Graumann PL, Alonso JC. (2006). Recruitment of Bacillus subtilis RecN to DNA double-strand breaks in the absence of DNA end processing. J Bacteriol. 188(2): 353-360.PMCID: PMC1347269
  16. Kidane D, Graumann PL. (2005) Dynamic formation of RecA filaments at DNA double strand break repair centers in live cells. J Cell Biol. 170(3): 357-366. PMCID:   PMC2171471
  17. Sanchez H, Kidane D, Reed P, Curtis FA, Cozar MC, Graumann PL, Sharples GJ, Alonso JC. (2005) The RuvAB branch migration translocase and RecU Holliday junction resolvase are required for double stranded DNA break repair in Bacillus  subtilis. Genetics. 171(3): 873-883. PMCID: PMC1456856
  18. Kidane D, Graumann PL. (2005) Intracellular protein and DNA dynamics in competent Bacillus subtilis cells. Cell. 122(1): 73-84.PMID: 16009134
  19. Kidane D, Sanchez H, Alonso JC, Graumann PL. (2004) Visualization of DNA double-strand break repair in live bacteria reveals dynamic recruitment of Bacillus subtilis RecF, RecO and RecN proteins to distinct sites on the nucleoids. Mol Microbiol. 52(6): 1627-1639. PMID: 15186413

Complete List of Published Work in MyBibliography:  


Postdoctoral Position Availability and Details: Postdoctoral positions are available in the areas of molecular cancer biology and DNA repair. Please submit a CV.

Graduate student (Ph.D) position: Available in the area of molecular cancer and DNA repair. Please visit Pharmacology and Toxicology Handbook  for Specific requirements for admission to the Pharmacology & Toxicology Ph.D. Program. and send your CV to dawit.kidane@austin.utexas.edu

Contact Information
Campus location:
DPRI 2.220

The University of Texas at Austin
Division of Pharmacology and Toxicology
Dell Pediatric Research Institute
1400 Barbara Jordan Blvd.
Austin, TX 78723

US Mail Address:
The University of Texas at Austin
DPRI 2.220
1 University Station, C0850
Austin, TX 78712-0128

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DPRI 2.220
The University of Texas at Austin
Austin, TX 78712