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Research yields new agent for some drug-resistant non-small cell lung cancers
Date:12/23/2009

ts have severe side effects such as skin rashes and diarrhea.

All current EGFR inhibitors have a structural "backbone" known as a quinazoline core. They lodge in a notch on EGFR normally reserved for a molecule known as ATP, which delivers chemical energy to the cell. By blocking ATP from binding to EGFR, the inhibitors prevent EGFR from sending signals that are essential to keep the tumor cells growing.

Over time, however, the tumor cells develop additional abnormalities in EGFR, enabling them to recommence their growth, even in the presence of Iressa or Tarceva. The most common of these abnormalities present in about 50 percent of patients with drug-resistant tumors is known as EGFR T790M.

Dana-Farber investigators hypothesized that current agents lose their potency because they don't bind as tightly or fully to the EGFR T790M protein as they ideally should. To improve the fit, researchers led by chemical biologist Nathanael Gray, PhD, prepared a group of inhibitors with a different structural scaffold, known as a pyrimidine core, which, it was thought, would mesh more thoroughly. They lab-tested the agents in NSCLC cells with EGFR T90M and found several that were up to 100 times more potent than quinazolines in restricting cell growth. As an unexpected bonus, these compounds were nearly 100 times less powerful at slowing the growth of cells with normal EGFR, suggesting they would be less likely to produce side effects than current drugs. The agent which performed the best is the pyrimidine WZ4002.

"This work provides a possible therapeutic chapter to a longstanding record of validating EGFR as a drug target," says Gray. "This has involved the identification of activating mutations in EGFR as a predictor of drug response, the discovery of multiple drug resistance mechanisms, and the elucidation of how these mutations work at an atomic level."

In follow-up experiments, Dana-Farber and BWH's Kwok-Kin Wong, MD, Ph
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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
Source:Eurekalert  

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