Area of research
Oncology · Cancer Research
Research interest
My research is focused on mechanisms of therapy resistance with major efforts in drug discovery and development. I have practiced medicine (medical oncology/colorectal cancer) since completing internal medicine residency and medical oncology fellowship training at Johns Hopkins by 1994. I direct a basic science lab focused on the p53 pathway, cell death, drug resistance, and novel therapeutics. I discovered the p21 (WAF1) cell cycle inhibitor as a p53 target gene and mediator of p53-dependent tumor suppression, the most highly-cited original paper published in Cell . Since the early-1990’s I have been unraveling signaling in the p53 pathway involved in tumor suppression and cancer therapeutic response/resistance.
The evolving landscape of antibody-drug conjugates (ADCs) for treatment of prostate cancer
TRAIL agonists rescue mice from radiation-induced lung, skin, or esophageal injury
Corrigendum to Targeting apoptotic pathways for cancer therapy
Correction: Potential role for Cathepsin D in p53-dependent tumor suppression and chemosensitivity
BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC).
XPO1 R749Q Mutations Co-occur with POLE Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance.
Supplementary Figure S1 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Supplementary Figure S3 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Supplementary Table S1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Supplementary Table S2 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Data from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Supplementary Table S2 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Supplementary Table S3 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Table 1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Author response: The context-dependent epigenetic and organogenesis programs determine 3D vs. 2D cellular fitness of MYC-driven murine liver cancer cells
Author response: Pharmacologic inhibition of BAF chromatin remodeling complexes as a therapeutic approach to transcription factor-dependent cancers
Figure 2 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Supplementary Figure S6 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Data from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Table 3 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Figure 1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Supplementary Figure S4 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Supplementary Figure S5 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Supplementary Figure S2 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Author response: Pharmacologic inhibition of BAF chromatin remodeling complexes as a therapeutic approach to transcription factor-dependent cancers
Supplementary Table S1 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
Supplementary Figure S7 from <i>XPO1</i><sup><i>R749Q</i></sup> Mutations Co-occur with <i>POLE</i> Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance
AI enabled exome and transcriptome liquid biopsy platform spanning the continuum of care in oncology
Table 2 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)