UCLA Oncologist Pursues Promise of CSF1R Inhibitor Combos

Published: Monday, Apr 09, 2018
Zev Wainberg, MD

Zev Wainberg, MD
The future of anticancer strategies aimed at colony stimulating factor 1 receptor (CSF1R) most likely lies in combinations that include immune checkpoint therapies and chemotherapy, according to Zev A. Wainberg, MD.


Wainberg, an associate professor of medicine and co-director of the gastrointestinal (GI) oncology program at UCLA Medical Center in Santa Monica, California, focuses on the molecular classification of GI malignancies and the development of novel therapeutics.

He has been involved in the development of CSF1R inhibitors pexidartinib and cabiralizumab and is serving as the lead investigator for a clinical trial evaluating cabiralizumab in combination with nivolumab (Opdivo) in patients with pancreatic cancer. Wainberg presented data from the pancreatic cancer cohort of this trial at the 2017 Annual Meeting of the Society for Immunotherapy of Cancer (NCT02526017).

What is the function of CSF1R in normal cells, and how is it involved in promoting cancer?

In a normal cell, it’s not entirely clear what the role is of CSF1R. It does help to stimulate macrophage growth, and it does help on some level to ensure that certain macrophages continue to grow and function. In cancer cells, it serves the same purpose. The problem is that in this setting it’s generally a driver for tumor-associated macrophages [TAMs]—those that are more inclined to be critical for tumor development.

How is CSF1R being targeted for anticancer therapy, and what is your interest in that?

The concept of targeting CSF1R stems from the notion, made clear in several scientific publications, that blockage of CSF1R will destabilize TAMs and perhaps even convert them to more functional macrophages—those that really serve a useful purpose. By blocking the primary growth stimulator of those macrophages, which is the CSF1R, the concept has been put forward that it will deplete those TAMs and lead to less growth potential of the tumors themselves.

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