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Joann Sweasy, PhD

Director, University of Arizona Cancer Center

Degrees and Appointments

  • B.A., Biology and Chemistry, Arcadia University, 1980
  • Ph.D., Microbiology, Rutgers University, 1989
  • Postdoctoral Fellow, University of Washington, 1993
  • Member NCI Subcommittee A, NCI Designated Cancer Centers 2017 - 2022

Awards and Honors

  • Arcadia University Women’s Board Scholarship, 1977-1980
  • American Institute of Chemists Medal, 1980
  • Phi Kappa Phi Honor Society, elected 1980
  • Merck Predoctoral Fellow, 1987-1989
  • Genetics Society of America Travel Award, 1989
  • National Research Service Award, National Cancer Institute, 1990-1993
  • Argall and Anna Hull Fellowship, 1994
  • American Cancer Society Junior Faculty Research Award, 1996
  • Donaghue Investigator Award, 2000-2005
  • Environmental Mutagenesis and Genomics Society Award, 2016
  • Yale University Postdoctoral Mentoring Award, 2017

Dr. Sweasy is an internationally recognized expert the genetics, cell biology, and biochemistry of DNA repair. For the past 25 years her laboratory has been consistently funded by the National Cancer Institute to study the molecular basis of mutagenesis and dysfunctional DNA repair as they relate to human diseases including cancer and autoimmunity. Dr. Sweasy’s research focuses on how aberrant DNA repair leads to mutations that result in human diseases, such as cancer. A major focus of her laboratory is to understand how genetic variants in DNA repairs genes, including genes that function in homology-directed repair, non-homologous end-joining and base-excision repair impact cancer risk and treatment.

The current focus of Dr. Sweasy's research is on cancer and autoimmunity.  A mutator phenotype and chromosomal instability lead to cancer.  Her research team probes the underlying molecular mechanisms of cancer as a result of aberrant DNA repair using biophysics, genetics, and cell biology.  Dr. Sweasy’s research team recently discovered that mutations in DNA repair genes lead to the development of the autoimmune disease of lupus and are employing novel mouse models based on human lupus to uncover the molecular basis of this disease. They also discovered that dynamic conformational changes are important for accurate DNA synthesis. The team has also shown that human germline and somatic genetic variants of base excision repair genes are linked to carcinogenesis because they are unable to properly remove damaged DNA bases, leading to genomic instability, mitotic catastrophe, and other cancer-associated phenotypes.

Personal Statement

I am the Director of the University of Arizona Cancer Center. I also serve as a Member of NCI-subcommittee A.  Previously, I served as Associate Director for Basic Sciences at the Yale Comprehensive Cancer Center.  In this capacity, I led strategic planning for basic sciences in the Cancer Center, directed the development of translational research infrastructure and directed the pilot and limited opportunity funding program.   As the principle investigator of the American Cancer Society Institutional Research Grant, I developed and led a mentoring program for early stage investigators. I have been continuously funded by the NCI since 1994 for my research on the genetics, cell biology, and biochemistry of DNA repair and the roles of aberrant DNA repair in cancer and autoimmunity.  For this work I was awarded the 2016 Environmental Mutagenesis and Genomics Society Award. I am an elected member of the Connecticut Academy of Sciences and Engineering and currently hold the Nancy C. and Craig L. Berge Endowed Chair for the Director of the Cancer Center. I have trained nine graduate students and 22 postdoctoral associates. I was awarded the 2017 Yale Postdoctoral Mentoring Award. Over 50% of my trainees are women and include persons from diverse backgrounds. I have also served as Director of Graduate Studies of the Microbiology Program, in which I oversaw the rigorous education of graduate students. Several of my projects are collaborative in nature and as the lead PI, I have successfully directed the studies, ensuring scientific rigor and the use of unbiased methodology, resulting in the publication of several high-quality papers in peer-reviewed journals

Complete List of Published Work in My Bibliography

Selected Publications

Sweasy JB, Lang T, Starcevic D, Sun KW, Lai CC, DiMaio D, Dalal S. (2005). Expression of DNA polymerase beta cancer-associated variants in mouse cells results in cellular transformation. Proc. Natl. Acad. Sci. U.S.A.102: 14350-14355. PMCID: PMC1242307
Marsden, C.G., Jensen, R., Morrical, S., Wallace, S.S., Sweasy, J.B. (2016). RAD51 G151D induces a hyper-recombination phenotype. PLoS Genet. 12: e1006208. PMCID: PMC4981402
Nemec, A.A., Abriola, L., Merkel, J.S., Glazer, P.M, Sweasy, J.B. (2017). DNA polymerase beta germline variant fidelity confers cellular response to cisplatin therapy Molecular Cancer Research 15:269-280. PMCID: PMC5334281
Galick HA, Marsden CG, Kathe S, Dragon JA, Volk L, Nemec AA, Wallace SS, Prakash A, Doublié S, Sweasy JB. (2017) The NEIL1 G83D germline DNA glycosylase variant induces genomic instability and cellular transformation. Oncotarget 8:85883-85895.
Kidane D, Jonason AS, Gorton TS, Mihaylov I, Pan J, Keeney S, de Rooij DG, Ashley T, Keh A, Liu Y, Banerjee U, Zelterman D, Sweasy JB. (2010). DNA polymerase beta is critical for mouse meiotic synapsis. EMBO J. 29: 410-23 PMCID: PMC2824467
Lokanga, R.A., Senejani, A.G., Sweasy, J.B., Usdin, K. (2015). Heterozygosity for a hypomorphic Polβ mutation reduces the expansion frequency in a mouse model of the Fragile X-related disorders. PLoS Genet. 11:e1005181. PMCID: PMC4981402
Senejani AG, Dalal S, Liu Y, Nottoli TP, McGrath JM, Clairmont CS, Sweasy JB. (2012). Y265C DNA Polymerase beta knockin mice survive past birth and accumulate base excision repair intermediate substrates Proc. Natl. Acad. Sci. U.S.A.109: 6632-7 PMCID: PMC3310078
Senejani AG, Liu Y, Kidane D, Maher SE, Zeiss CJ, Park HJ, Kashgarian M, McNiff JM, Zelterman D, Bothwell AL, Sweasy JB. (2014). Mutation of POLB Causes Lupus in Mice. Cell Rep. 16: 1-8 PMCID: PMC3916967