Egfr T790m, Frontiers An Observational Study Of Acquired Egfr T790m Dependent Resistance To Egfr Tki Treatment In Lung Adenocarcinoma Patients In Taiwan Oncology

Egfr t790m is present in 042 of aacr genie cases with lung adenocarcinoma and non small cell lung carcinoma having the greatest prevalence.

Can you survive stage 4 mesothelioma with no treatment. Egfr egfr t790m. . Patients with this mutation respond well to third generation tyrosine kinase inhibitors but obtaining a tissue biopsy to confirm the mutation poses risks and is often not feasible.

T790m is a point mutation in the egfr gene that is most frequently reported to associate with the resistance to first line egfr tki treatment. Top disease cases with egfr t790m. Patients carrying egfr mutations known as activating mutations may benefit from first or second or third generation tkis.

Even though lung cancer patients harboring a mutation in the epidermal growth factor receptor egfr gene exhibit an initial dramatic response to egfr tyrosine kinase inhibitors egfr tkis acquired resistance is almost inevitable after a progression free period of approximately 10 monthsa secondary point mutation that substitutes methionine for threonine at amino acid position 790 t790m. Despite remarkable initial responses patients eventually develop progressive disease with the most common cause of resistance to first line egfr tkis being the acquired t790m mutation. Threonine is a small polar amino acid.

Targeted therapies often work well for a period of time but then stop working. T790m also known as thr790met is a gatekeeper mutation of the epidermal growth factor receptor egfr. The thirdgeneration epidermal growth factor receptor egfr tyrosine kinase inhibitors tki osimertinib is the current standard of care for patients with advanced egfrpositive nonsmall cell lung cancer nsclc who acquired t790m mutation after receiving earliergeneration tkis therapy osimertinib significantly improves objective response rate orr and progression.

This means the cancer develops resistance to the treatment. Biomarker directed therapies view therapies for egfr t790m. Tumor specimens from patients should be tested for the presence of egfr mutations prior to tki treatment.

About 60 of non small cell lung cancer nsclc patients develop resistance to targeted epidermal growth factor receptor egfr inhibitor therapy through the egfr t790m mutation. Nsclc comprises approximately 85 of all lung cancers. Current data suggests that patients with metastatic nsclc and the t790m mutation may benefit from t790m targeted therapy eg osimertinib.

Therefore testing using plasma specimens is most appropriate for consideration in patients from whom a tumor biopsy cannot be obtained. The efficacy of tagrisso osimertinib has not been established in the egfr t790m plasma positive tissue negative or unknown population and clinical data for t790m plasma positive patients are limited. The mutation substitutes a threonine t with a methionine m at position 790 of exon 20 affecting the atp binding pocket of the egfr kinase domain.

Various third generation egfr tkis have been developed to specifically target this acquired mutation of which osimertinib is currently the only approved agent. Rapid detection of the egfr t790m mutation in non small cell lung cancer patients as an alternative for egfr analysis of tissue.