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  • 09월 20일 16시 이후 : 초록수정 불가능, 일정확인 및 검색만 가능

제126회 대한화학회 학술발표회 및 총회 Resistance to tyrosine kinase inhibitors originated from the altered EGFR mutant-specific interactome

2020년 9월 18일 17시 49분 40초
MEDI.P-437 이곳을 클릭하시면 발표코드에 대한 설명을 보실 수 있습니다.
10월 21일(수) 17:30~18:00
Medicinal Chemistry
저자 및
Minh Hung Vu, Min-Sik Kim1,*
New Biology, Daegu Gyeongbuk Institute of Science & Technology, Korea
1Department of New Biology, DGIST, Korea
Non-small cell lung cancer (NSCLC) is the major class of lung cancers and constitutes for more than 80% of patients diagnosed in the metastatic stage. NSCLC is believed to be progressed with genomic alterations such as mutations on EGFR or KRAS and amplifications of HER2 or MET. Thus, targeting of activating mutations within epidermal growth factor receptor (EGFR) using tyrosine kinase inhibitors (TKIs) has been the standard of care for patients with NSCLC. Although progression-free survival was initially appeared to be improved, overall mortality at the end remains dismal mainly due to the resistance to TKIs. Studies have been carried out to understand causes of acquired EGFR-TKIs resistance. Nevertheless, how the resistance is acquired during the course of TKI treatment remains to be understood. To resolve this challenging question on the origin of the TKI resistance, we hypothesize that TKI may alter EGFR interactome which leads to acquired resistance through de novo mutation of EGFR. To test our hypothesis, we will characterize mass spectrometry-based EGFR interactomes upon TKI treatment on lung cancer cell lines harboring acquired TKI resistance mutations such as EGFR T790M mutation, c-MET amplification and HER2 amplification. This result would deepen our understanding about acquired EGFR-TKIs resistance mechanisms and may reveal targets for preventing TKIs resistance development. *Keywords: NSCLC, EGFR mutations, TKI resistance, EGFR interactomes.