Particularly in non-small cell lung cancer, there's a population of patients who carry mutations in the epidermal growth factor receptor gene. These patients are much more likely to respond positively to small molecular tyrosine kinase inhibitors than those with wild-type EGFR. What is the mechanism that underlies this differential response to anti-EGFR therapy?
It seems this study by Cai-Hong Yun et al. is related to the phenomenon.
Something with the 3D structure.
http://www.eurekalert.org/pub_releases/2007-03/dci-srh031207.php
Other:
http://mct.aacrjournals.org/content/7/4/874.full
http://www.eurekalert.org/pub_releases/2011-02/esfm-oas022411.php
http://www.eurekalert.org/pub_releases/2010-04/esfm-btm042910.php
http://www.eurekalert.org/pub_releases/2009-12/tcob-anm120209.php
Regards,
Joachim (not a medic)
Mutations such as L858R and in-frame deletions in exon 19 of EGFR (all in the kinase domain of EGFR) confer over activation of kinase activity mainly by disrupting autoinhibitory interactions. This conformational change results in the the preferential binding of these small molecule inhibitors over the natural partner, ATP. Wild-type EGFR is not affected so. The result is a dampening of EGFR signaling. Tumours such NSCLC with these activating mutations in EGFR become "addicted" to this signaling pathway and thus these EGFR mutant patients respond best to these small molecule inhibitor therapies.
Very interesting. During years we found different results of chemotheraphy in different gallbladder cancers and we did not understand why. Your findings could explain these differences.
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