Abstract

Mel Greaves: Cancer through the Lens of Evolution

Highlights

  • The recent FDA approval of a BH3 mimetic, venetoclax, for CLL, was a cancer breakthrough

  • What do you see as the main opportunities and challenges for effective translation of these therapies? The life-death switch controlled by the BCL-2 family operates downstream from oncogenic mutations affecting numerous signaling pathways

  • As with traditional cancer therapeutics, the challenge is how to use BH3 mimetics without causing unacceptable collateral damage. This requires deepening our understanding of the balance of pro- and antiapoptotic proteins within all normal cell types and tumors, so that we can better predict which BH3 mimetic will be the most effective in a particular tumor type, and which normal cell types would be most at risk with the regimen that is most effective for the tumor

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Summary

Introduction

The recent FDA approval of a BH3 mimetic, venetoclax, for CLL, was a cancer breakthrough. BH3 mimetics should be effective for many cancer cell types. As with traditional cancer therapeutics, the challenge is how to use BH3 mimetics without causing unacceptable collateral damage. The prospects for BH3 mimetic cancer therapy are enormously exciting.

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