Tanya Dorff, MD, discusses the main findings from a phase 1 study of patients with metastatic castration-resistant prostate cancer.
Tanya Dorff, MD, a medical oncologist, section chief of Genitourinary Disease Program, and associate professor in the Department of Medical Oncology & Therapeutics Research at City of Hope, discusses the main findings from a phase 1 study (NCT03873805) of patients with metastatic castration-resistant prostate cancer (mCRPC).
In the study, investigators are looking to determine the toxicity profile of prostate stem cell antigen (PSCA)-chimeric antigen receptor (CAR) T cells, as well as the dose-limiting toxicities. Secondary end points of the trial are CAR T cells persistence, expansion of CAR T cells, disease response, overall survival, progression-free survival, PSCA expression, and serum cytokine profile.
Patients included in the study must be aged 18 years and older with an ECOG performance status 0-2, have documented mCRPC with PSCA-positive tumor expression as evaluated by City of Hope Pathology Care, and no known contraindications to leukapheresis, steroids, or tocilizumab (Actemra).
According to preliminary findings from the study, PSCA CAR T cells induced an antitumor effect when dosed at 100 million CAR T cells or higher and given with lymphodepleting chemotherapy in this patient population.
Transcription:
0:08 | The most important conclusion that can be drawn from our study is that there is the ability of CAR T-cell therapy to have an impact in prostate cancer. We wouldn't expect to solve this with just 12 patients. So, we know there's more work to be done. But there's a clear signal that this is a promising therapeutic modality. Also, that prostate stem cell antigen, which is a new target in prostate cancer, can induce anti-prostate cancer responses.
0:40 | Finally, I think it's important that we've validated what was learned preclinically, that CAR T cells, when we're using them in solid tumors, we still do need to add in that lymphodepleting chemotherapy that impacts the tumor microenvironment in a very significant way and leads to some of these responses that we've seen.
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