David Goodrich


Research 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


I trained as a molecular biologist and currently serve as Distinguished Professor of Oncology in the Department of Pharmacology & Therapeutics at Roswell Park Comprehensive Cancer Center. I also serve as Associate Dean for Postdoctoral Education.

I earned my Bachelor’s degree in 1984 from the University of Wisconsin at Madison. There as a Knapp Research Fellow, I studied molecular mechanisms regulating the immune system in the laboratory of Dr. Colleen Hayes. I matriculated at the University of California at Berkeley to pursue my doctoral degree with support from a National Research Service Award predoctoral fellowship. There I studied retroviral oncogenes in the laboratory of Dr. Peter Duesberg, earning a PhD in 1989. This research sparked my interest in cancer biology, so I traveled to the University of California at San Diego to initiate research in the then emerging field of tumor suppressor genes. As a Giannini and Leukemia Society Fellow, I discovered that the recently identified retinoblastoma tumor suppressor gene encoded a protein that regulates the cell division cycle.

In 1994 I moved to the University of Texas MD Anderson Cancer Center to join the faculty in the Department of Tumor Biology and continue my research on the retinoblastoma tumor suppressor gene. There I discovered that cyclin dependent kinases regulate the retinoblastoma tumor suppressor protein by site specific phosphorylation, providing scientific rationale for currently FDA approved therapies targeting cyclin dependent kinases. In 2001 I moved my laboratory to the Department of Pharmacology & Therapeutics at Roswell Park Comprehensive Cancer Center. In recent years my lab has focused its attention on non-canonical functions of tumor suppressor genes, including how genetic alterations in these genes drive cancer lineage plasticity, metastasis, and therapeutic resistance. We are using this information to identify new ways to improve therapeutic outcomes by suppressing cancer lineage plasticity.

View the Goodrich Lab


Roswell Park Comprehensive Cancer Center
  • Distinguished Professor of Oncology
  • Associate Dean for Postdoctoral Education
  • Department of Pharmacology & Therapeutics
  • Director, Genitourinary Research
  • Department of Urology


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

Zhang, L., Liu, C., Zhang, B., Zheng, J., Singh, P., Bshara, W., Wang, J., Gomez, E.C., Zhang, X., Wang, Y., Zhu, X., Goodrich, D.W. Pten loss expands the histopathological diversity and lineage plasticity of lung cancers initiated by Rb1/Trp53 deletion. J. Thorac. Oncol. In Press, 2022. https://doi.org/10.1016/j.jtho.2022.11.019.

Chan, J.M., Zaidi, S., Love, J.R., Zhao, J.L., Setty, M., Wadosky, K.M., Gopalan, A., Choo, Z.-N., Persad, S., Choi, J., Laclair, J., Lawrence, K.E., Chaudhary, O., Xu, T., Masilionis, I., Linkov, I., Wang, S., Lee, C., Barlas, A., Morris, M.J., Mazutis, L., Chaligne, R., Chen, Y., Goodrich, D.W., Karthaus, W.R., Pe’er, D., Sawyers, C.L. Lineage plasticity in prostate cancer depends on JAK/STAT inflammatory signaling. Science 377:1180-1191, 2022.

Kumar, R., Chaudhary, A.K., Woytash, J., Inigo, J.R., Gokhale, A.A., Bshara, W., Attwood, K., Wang, J., Spernyak, J., Rath, E., Yadav, N., Haller, D., Goodrich, D.W., Tang, D.G., Chandra, D. A mitochondrial unfolded protein response inhibitor suppresses prostate cancer growth in mice via HSP60. J. Clin. Invest. 132(13):e149906.doi: 10.1172/JCI149906, 2022

Chinnam, M., Xu, C., Lama, R., Zhang, X., Cedeno, C.D, Wang, Y., Stablewski, A.B., Goodrich, D.W., Wang, X. MDM2 E3 ligase activity is essential for p53 regulation and cell cycle integrity. PLOS Genet. 18(6): e1010293. doi.org/10.1371/journal.pgen.1010293, 2022 (corresponding authors).

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.

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.