Related Experiment Video
Updated: Jun 3, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
Published on: January 31, 2018
MYC, PARP1, and chemoresistance: BIN there, done that?
1Cancer Institute of New Jersey, Robert Wood Johnson Medical School-University of Medicine and Dentistry of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08901, USA. ganesash@umdnj.edu
Abstract:
Dysregulation of c-MYC plays a critical role in the development of many human cancers. New evidence has uncovered a previously unknown mechanism whereby increased abundance of c-MYC can promote poly(ADP-ribose) polymerase (PARP)-dependent DNA repair pathways and induce relative chemoresistance. The adaptor protein BIN1, whose expression is regulated by c-MYC, interacts with PARP1 and inhibits its enzymatic activity. A model has been proposed in which increased abundance of c-MYC indirectly leads to decreased BIN1 expression, in turn leading to increased PARP activity and resistance to DNA-damaging agents. The clinical implications of these findings are discussed.
More Related Videos
08:46Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
Published on: December 9, 2015
07:53Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter
Published on: April 17, 2026
Related Concept Videos
Treatment Resistant Cancers
Abnormal Proliferation
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Restarting Stalled Replication Forks
Conservative Site-specific Recombination and Phase Variation
The recognition sites for Cre recombinase called LoxP...
Combination Therapies and Personalized Medicine
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...