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Samuel W. Brady, PhD
Samuel W. Brady, PhD


  • BS (Molecular Biology) - Brigham Young University, Provo, UT
  • PhD (Cancer Biology) - University of Texas MD Anderson Cancer Center, Houston, TX
  • Postdoctoral Fellow - University of Utah, Salt Lake City, UT

Research Interests

My lab brings together cancer genomics and pharmacology to identify new approaches to treat pediatric cancer. Particular areas of interest include:

  • Using cancer mutational signatures to identify new treatment and preventative approaches.
  • Identifying therapeutic vulnerabilities associated with driver rearrangements and other mutations in cancer.

All research in the lab begins with the identification of striking findings from patient genomic data, which fuels hypotheses for improved cancer treatment approaches. These hypotheses are then tested using experimental approaches.

Selected Publications

Brady SW*, Roberts KG*, Gu Z, Shi L, Pounds S, Pei D, Cheng C, Dai Y, Devidas M, Qu C, Hill AN, Payne-Turner D, Ma X, Iacobucci I, Baviskar P, Wei L, Arunachalam S, ... Loh ML, Hunger SP, Zhang J, Mullighan C. The genomic landscape of pediatric acute lymphoblastic leukemia. Nature Genetics 54:1376-1389, 2022.

Brady SW, Gout AM, Zhang J. Therapeutic and prognostic insights from the analysis of cancer mutational signatures. Trends in Genetics 38:194-208, 2022. 

Yang F*, Brady SW*, Tang C*, Sun H*, Du L*, Barz MJ, Ma X, Chen Y, Fang H, Li X, Kolekar P, Pathak O, Cai J, Ding L, Wang T, von Stackelberg A, Shen S, Eckert C, Klco JM, Chen H, Duan C, Liu Y, Li H, Li B, Kirschner-Schwabe R, Zhang J, Zhou BS. Chemotherapy and mismatch repair deficiency cooperate to fuel TP53 mutagenesis and ALL relapse. Nature Cancer 2:819-834, 2021.

Brady SW*, Lu Y*, Ma X, Gout AM, Hagiwara K, Zhou X, Wang J, Macias M, Chen X, Easton J, Mulder HL, Rusch M, Wang L, Nakitandwe J, Lei S, Davis EM, Naranjo A, Cheng C, Maris JM, Downing JR, Cheung NV, Hogarty MD, Dyer MA, Zhang J. Pan-neuroblastoma analysis reveals age- and signature-associated driver alterations. Nature Communications 11:5183, 2020.

Li B*, Brady SW*, Ma X*, Shen S*, Zhang Y*, Li Y*, Szlachta K, Dong L, Liu Y, Yang F, Wang N, Flasch DA, Myers MA, Mulder HL, Ding L, Liu Y, Tian L, Hagiwara K, Xu K, Zhou X, Sioson E … Easton J, Zhu X, Zhang J, Cheng C, Raphael BR, Tang J, Downing JR, Alexandrov LB, Zhou BS, Pui C, Yang JJ, Zhang J. Therapy-induced mutations drive the genomic landscape of relapsed acute lymphoblastic leukemia. Blood 135:41-55, 2020.

Brady SW, Ma X, Zhou BS, Pui C, Yang JJ, Zhang J. Therapy-induced mutagenesis in relapsed ALL is supported by mutational signature analysis. Blood 136:2235-2237, 2020.

Brady SW*, Ma X*, Bahrami A, Satas G, Wu G, Newman S, Rusch M, Putnam DK, Mulder HL, Yergeau D, Edmonson MN, Easton J, Alexandrov LB, Chen X, Mardis ER, Wilson RK, Downing JR, Pappo AS, Raphael BJ, Dyer MA, Zhang J. The Clonal Evolution of Metastatic Osteosarcoma as Shaped by Cisplatin Treatment. Molecular Cancer Res 17:895-906, 2019.

Brady SW, McQuerry J, Qiao Y, Piccolo S, Shrestha G, Layer R, Pedersen B, Jenkins D, Esch A, Selitsky S, Parker J, Anderson L, Dalley B, Factor R, Reddy C, Boltax J, Li D, Moos P, Gray J, Heiser L, Johnson E, Buys S, Cohen A, Quinlan A, Marth G, Werner T, Bild A. Combating subclonal evolution of resistant cancer phenotypes. Nature Communications 8:1231, 2017.

Brady SW, Zhang J, Tsai M-H, Yu D. PI3K-independent mTOR activation promotes lapatinib resistance and IAP expression that can be effectively reversed by mTOR and Hsp90 inhibition. Cancer Biology & Therapy 16:402-411, 2015.

Brady SW, Zhang J, Seok D, Wang H, and Yu D. Enhanced PI3K p110α Signaling Confers Acquired Lapatinib Resistance That Can Be Effectively Reversed by a p110α-Selective PI3K Inhibitor. Molecular Cancer Therapeutics 13:60-70, 2014.

*Equal contribution

Last update: August 2023