Howard Scher

About Howard Scher

Cell signaling in cancer causes uncontrolled cell growth and many clinical properties of cancer, such as metastases. Two major pathways of cell signaling in prostate cancer are initiated through a cascade of biochemical pathways. One is regulated through the androgen receptor (AR), the engine of prostate cancer, another is called PI3 Kinase (PI3K) which responds to growth factors on the outside of the cell that send signals for inappropriate cell growth. This team recently showed that targeting just one of these pathways in anticancer therapy has limited benefit because cancer cells adapt to the medication by turning on the other pathway. Therefore, it is crucial to target both the PI3K and AR pathways through combination therapy for effective and durable treatment. Dr. Scher and his team plan to inhibit individual steps in the PI3K pathway and investigate the cancer cell adaptation and survival response in detail. The technical plan will involve investigations of the results of inhibiting either of these pathways and the benefit of combined therapy. This information will then be used to design clinical trials that co-target these two dominant signaling pathways in prostate cancer patients.
Potential patient benefit: Successful clinical trials with combined signaling inhibition with medications against PI3K and AR will provide patients with improved therapy for advanced prostate cancer and better outcomes.

Howard Scher, MD –

Memorial Sloan-Kettering Cancer Center
Development of Combined Inhibition of AR and PI3K Signaling as a Therapeutic Strategy for Advanced Prostate Cancer

Co-Investigators:

Charles Sawyers, MD; Brett Carver, MD; Neal Rosen, MD, PhD