Systematic Mapping Of Bcl-2 Gene Dependencies In Cancer Reveals Molecular Determinants Of Bh3 Mimetic Sensitivity

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Systematic Mapping Of Bcl-2 Gene Dependencies In Cancer Reveals Molecular Determinants Of Bh3 Mimetic Sensitivity

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PROJECT TOPIC AND MATERIAL ON SYSTEMATIC MAPPING OF BCL-2 GENE DEPENDENCIES IN CANCER REVEALS MOLECULAR DETERMINANTS OF BH3 MIMETIC SENSITIVITY

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  • Name: Systematic Mapping Of Bcl-2 Gene Dependencies In Cancer Reveals Molecular Determinants Of Bh3 Mimetic Sensitivity
  • Type: PDF and MS Word (DOC)
  • Size: [70 KB]
  • Length: [56] Pages

 

 

 

Introduction

The process of intrinsic apoptosis is tightly regulated by the BCL-2 family of proteins. In human cancers, the anti-apoptotic BCL-2 proteins play a critical role in protecting cells, which are often “primed” for apoptosis, from committing to irreversible cell death1. To date, the most well described of the anti-apoptotic BCL-2 genes are BCL-2, BCL-XL, and MCL-1, and recently, following over a decade of extensive research effort, potent and selective inhibitors of each of these proteins were developed. Much is known about the cancer types that respond well to selective BCL-2 inhibitors, and indeed the BCL-2 inhibitor venetoclax (ABT-199) is now FDA approved to treat certain leukemias such as chronic lymphocytic leukemia (CLL)2,3. In contrast, outside of a small number of studies in select cancer types, little is known regarding which cancers might respond well to single agent BCL-XL or MCL-1 inhibition4,5,6,7. Finally, to the best of our knowledge, no studies have systematically examined the dependencies of cancers on combinations of BCL-2 family proteins.

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