Member Biography

David A. Boothman, Ph.D.
David Boothman

David Boothman, Ph.D.

980 W. Walnut Street
Walther Hall R3 C519
Indianapolis, IN 46202
Phone: (317) 278-7777

Research Program Membership

Full member:

Sidney and Lois Eskenazi Professor of Hematology-Oncology
IU School of Medicine

Department of Biochemistry and Molecular Biology
IU School of Medicine

Associate Director of Translational Research
IU Simon Cancer Center

Dr. Boothman's research interests include:

The overall mission of my laboratory is to understand and exploit cell stress responses in cancer versus normal cells. There are three ongoing projects in the laboratory focused on: i) DNA double strand break (DSB) repair and the specific roles of RNA transcription termination factors in the regulation and control of RNA Pol II-mediated R-loop formation, and the impact of loss of RNA termination factors (e.g., RPRD1B, RPRD1A and XRN2) on DSB repair and sensitivities of cancers to DNA damaging agents and DNA repair inhibitors; ii) EMT, migration and metastasis and the influences of, or changes in, metabolism during TGFß1-driven EMT; and iii) exploiting NQO1 bioactivatable drugs for improved therapy of cancers that have elevated levels of NAD(P)H:quinone oxidoreductase 1 (NQO1), including cancers of the lung (NSCLC), pancreas (PDA), breast (including TNBC), and prostate. Dr. Boothman has identified several cell stress response pathways, such as Ku70 binding protein #5 (kub5/hera, K-H/RPRD1B) XRN2 or RPRD1A loss, the ATM-IGF-1-sCLU pathway, and the NQO1 bioreduction pathway, with which to exploit using unique and novel strategies. His lab has developed mechanisms and/or drugs to exploit these for improved therapy of NSCLC, pancreatic, prostate, breast, and colon cancers. Recent systems have been derived for the RPRD1B/Kub5/Hera (K/H) gene in cancer cell lines, but where CDK1, BRCA1/2, PARP1 or Artemis have been modified for metastatic studies.

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More Publications »

Ph.D. - University of Miami, Coral Gables, FL 1986