Abstract
Clinical implications of epidermal growth factor receptor (EGFR) epigenetic modification in lung cancer, proof of concept for dual multitargeted epigenetic therapy (MTET) in combination with egfr inhibitors
Highlights
Several categories of resistance have been speculated to be responsible for molecular resistance in epidermal growth factor receptor (EGFR) mutated and treated cases with EGFR inhibitors
50% of the acquired resistance developed to erlotinib or gefitinib is linked to T790M mutation and the proportion could be underestimated as more accurate prevalence of 68% was achieved using LNA-PCR/sequencing assay
We study a case series of 2 patients with such phenomenon and report a significant effect size in their response when epigenetic therapies are implemented under the multitargeted Epigenetic Therapy protocol (MTET)
Summary
Several categories of resistance have been speculated to be responsible for molecular resistance in EGFR mutated and treated cases with EGFR inhibitors. Due to connection of Hepatocyte growth factors to Met pathway, it is speculated that in about 61 percent of cases, studies in Japan, HGF overexpression was responsible in promoting drug resistance. This mechanism is INDEPENDENT of TKI pathways [6]. That said application of several dual targeted therapies to target Pi3k/Akt, has not resulted in improved survival in these patients. Her 2 alteration is seen in about 2 percent of cases [7]. Epidermo mesenchymal Transition (EMT) phenotypic transformation has been proven in at least 5 percent of cases with EGFR resistance as main mechanism [810]
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