David Goodrich


Special Interests:

Understanding molecular mechanisms underlying tumor suppression mediated by the RB1 and TP53 genes Identifying genes involved in prostate cancer metastasis Discerning how transcriptionally formed R-loops contribute to cancer initiation and progression Understanding molecular mechanisms underlying the non-genetic adaptations of cancer cells to selective pressures like metastasis and therapy Elucidating how tumor suppression genes control cancer lineage plasticity and acquired therapeutic resistance

About David Goodrich


View the Goodrich Lab


Roswell Park Comprehensive Cancer Center

  • Distinguished Professor of Oncology
  • Member, Molecular Pharmacology and Cancer Therapeutics Graduate Program
  • Associate Dean for Postdoctoral Education
  • Department of Pharmacology & Therapeutics


Education and Training:

  • 1989 - PhD - Molecular Biology, University of California, Berkeley, CA
  • BS, Molecular Biology, University of Wisconsin, Madison, WI

Honors & Awards:

  • RPMI Award
  • Dean’s Award for Excellence in Graduate Education
  • Wilson Scholar
  • Leukemia Society Fellow
  • Giannini Medical Research Fellow
  • NRSA Predoctoral Fellow
  • Phi Beta Kappa
  • Knapp Research Fellow
  • Ingersol Prize in Physics


Research Overview:

The long-term goals of my laboratory are to understand how genetic alterations in tumor suppressor genes drive cancer initiation, progression, and therapeutic resistance. The tumor suppressor genes we study are some of the most frequently altered genes in human cancer. Understanding how these genes function will refine our fundamental understanding of cancer and suggest novel therapeutic approaches to treat it. Our primary experimental approaches involve creation of genetically engineered mouse strains and patient derived organoids. Characterizing the effects of engineered genetic alterations helps us elucidate molecular mechanisms underlying cancer phenotypes of interest.

Our current primary focus is on cancer lineage plasticity, a phenomenon whereby cancer cells reprogram themselves to an alternative lineage or phenotypic state in order to adapt to selective pressures. We are finding that mutations in key tumor suppressor genes can increase cancer lineage plasticity, endowing these cancers with increased ability to metastasize and evade therapy.

We study prostate and lung cancer primarily, two important cancers where lineage plasticity has been documented to promote resistance to molecularly targeted therapies. Our goal is to discover underlying molecular mechanisms and leverage these mechanisms to devise novel therapeutic approaches. For example, we are testing whether targeting epigenetic regulatory factors or lineage specifying transcription factors can suppress cancer lineage plasticity and improve therapeutic outcomes using both mouse models and human clinical trials.

Meenalakshmi Chinnam
Mauricio Flores
Jena Hazen
Neha Jaiswal
Yanqing Wang
Xiaojing Zhang

Goodrich Lab


Full Publications list on PubMed

Pearson, J.D., Huang, K., Pacal, M., McCurdy, S.R., Lu, S., Aubry, A., Yu, T., Wadosky, K.M., Zhang, L., Wang, T., Gregorieff, A., Ahmad, M., Dimaras, H., Langille, E., Cole, S.P.C., Monnier, P.P., Lok, B.H., Tsao, M., Akeno, N., Schramek, D., Wikenheiser-Brokamp, K.A., Knudsen, E.S., Witkiewicz, A.K., Wrana, J.L., Goodrich, D.W., Bremner, R. Binary pan-cancer classes with distinct vulnerabilities defined by pro- or anti-cancer YAP/TEAD acticity. Cancer Cell 39: 1115-1134, 2021.

Park, S.H., Fong, K.-W., Kim, J., Wang, F., Lu, X., Lee, Y., Brea, L.T., Wadosky, K., Guo, C., Abdulkadir, S.A., Crispino, J.D., Fang, D., Ntziachristos, P., Liu, X., Li, X., Wan, Y., Goodrich, D.W., Zhao, J.C., Yu, J. Posttranslational regulation of FOXA1 by Polycomb and BUB3/USP7 deubiquitin complex in prostate cancer. Sci. Adv. 7: eabe2261, 2021.

Davies, A., Nouruzi, S., Ganguli, D., Namekawa, T., Thaper, D., Linder, S., Karaoglanoglu, F., Omur, M., Kim, S., Kobelev, M., Kumar, S., Sivak, O., Bostock, C., Bishop, J., Hoogstraat, M., Talal, A., Stelloo, S., van der Poel, H., Bergman, A.M., Ahmed, M., Fazli, L, Huang, H. Tilley, W.D., Goodrich, D.W., Feng, F.Y., Gleave, M., He, H.H., Hach, F., Zwart, W., Beltran, H., Seith, L., Zoubeidi, A. An androgen receptor switch underlies lineage infidelity in treatment-resistant prostate cancer. Nat. Cell. Biol. 23: 1023-1034, 2021.

Ku S.-Y., Rosario, S., Wang, Y., Mu, P., Seshardri, M., Goodrich, Z.W., Goodrich, M.M., Labbe, D.P., Gomez, E.C., Wang, J., Long, H.W., Xu, B., Brown, M., Loda, M., Sawyers, C.L., Ellis, L., Goodrich, D.W. Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance. Science. 355: 78-83, 2017.

Mu, P., Zhang, Z., Benelli, M., Karthaus, W.R., Hoover, E., Chen, C.-C., Wongvipat, J., Ku, S.-Y., Gao, D., Cao, Z., Shah, N., Adams, E.J., Abida, W., Watson, P.A., Prandi, D., Huang, C.-H., Stanchina, E., Lowe, S.W., Ellis, L., Beltran, H., Rubin, M.A., Goodrich, D.W., Demichelis, F., Sawyers, C.L. SOX2 promotes lineage plasticity and antiandrogen resistance in TP53 and RB1 deficient prostate cancer. Science. 355: 84-88, 2017.