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Ref Type Journal Article
PMID (31045832)
Authors Wu K, Guo C, Li R
Title Clinical characterization of icotinib-induced chemoresistance in erlotinib-treated lung adenocarcinoma patient with EGFR mutations: A case report.
URL
Abstract Text Mounting evidences reveal that mutation of epidermal growth factor receptor (EGFR) may induce the resistance of tyrosine kinase inhibitors (TKIs). TKI-resistant lung cancer cells are sensitive to inhibition of the EGFR pathway. This case report aimed to characterize the therapeutic benefits of erlotinib, a targeted drug, on an advanced lung cancer patient with somatic EGFR mutation.A 52-year-old non-smoking Chinese woman was suffered from pneumonia-based chest pains, and the patient was diagnosed as advanced lung cancer through medical imaging, thoracoscopy, and pathological examination.Blood tests, pathological examination, thoracoscopy, computed tomography (CT)/positron emission computed tomography (PET) scans, next-generation sequencing (NGS) testing were subjected to the patient's samples before and after targeted drug treatments.After icotinib-induced resistance, the chemoresistance mechanism was involved in EGFR mutations before being prescribed with erlotinib.The therapeutic effectiveness of icotinib for 4-month showed undetected carcinomatous metastasis. The lung tumor sizes were reduced, and improved quality of life (QOL) was described by the patient. Followed by monotherapy with erlotinib for 1.5-year, the icotinib-resistant patient benefited from longer survival rate without tumor enlargement and neoplastic metastasis. In therapeutic duration of erlotinib, T790M mutation of EGFR, R248W mutation of tumor protein p53 (TP53), K844S mutation of retinoblastoma protein 1 (RB1) were identified through NGS test.In conclusion, the anti-cancer benefits of icotinib and erlotinib against advanced lung cancer may contribute to suppress neoplastic growth and metastasis. Further, erlotinib exerts potent efficacy for extended survival rate of patient because detectable mutations may not or limitedly induce erlotinib-resistance. In addition, reduced circulating hormones by menopause may enhance the therapeutic effectiveness of erlotinib.

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Molecular Profile Treatment Approach
Gene Name Source Synonyms Protein Domains Gene Description Gene Role
Therapy Name Drugs Efficacy Evidence Clinical Trials
Drug Name Trade Name Synonyms Drug Classes Drug Description
Gene Variant Impact Protein Effect Variant Description Associated with drug Resistance
RB1 K844S missense unknown RB1 K844S lies within domain C of the Rb1 protein (UniProt.org). K844S has been identified in the scientific literature (PMID: 31045832), but has not been biochemically characterized and therefore, its effect on Rb1 protein function is unknown (PubMed, Oct 2023).
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References