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Marcelo Ehrlich, PhD

Marcelo Ehrlich, PhD

Grant Status
Active

Institution
Tel Aviv University

Grant Type
Project Grant

Project Title
Improved Bladder Cancer Immunotherapy: Adenovirus IRF1 Delivery and Histone Deacetylase Inhibition

Tumor Types

Research Topics
Bladder Cancer


About the Investigator:

Dr. Marcelo Ehrlich’s research focuses on understanding cell signaling and virus-cell interactions and how they can be harnessed for virus-based immunotherapy.  He received his BSc, MSc in Cell Biology and PhD in Neurobiochemistry degrees from Tel Aviv University. After postdoctoral training at the Harvard Medical School in Massachusetts, he returned to Tel Aviv University, where he is now a Professor of Cell Biology at the Shmunis School of Biomedicine and Cancer Research in the Faculty of Life Sciences.

About the Research:

This research, which involves cancer cell biology and molecular virology, is a collaboration between the Ehrlich and Bacharach laboratories, which specialize in these areas, respectively. This project aims to improve immunotherapy for advanced bladder cancer by combining an adenovirus that delivers the transcription factor Interferon Regulatory Factor 1 (IRF1) with Histone Deacetylase Inhibitors (HDACis). The former is endowed with the abilities to induce cancer-cell death and stimulate anti-tumor immunity, while the latter may enhance gene-inducing abilities of IRF1 via chromatin modifications. However, preliminary studies showed that HDACis hinder expression of endogenous IRF1. To circumvent this limitation, a modified adenoviral vector, AdV-IRF1ΔUTRs, was created to enhance delivery and expression of IRF1. Combining this vector with SAHA, an FDA-approved HDACi, boosts the effectiveness of treatment by increasing the number of infected cancer cells, enhancing immune responses, and inducing cancer cell death. The next steps include testing this combination in both human and mouse bladder cancer cells and evaluating its effectiveness in animal models. This approach leverages the unique capabilities of HDACis to maximize the anti-tumor effects of IRF1.

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