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The Analysis Of Treatment Effect By Different Strategies For Advanced Lung Adenocarcinoma Patients With EGFR Sensitive Mutation Positive

Posted on:2020-01-14Degree:MasterType:Thesis
Country:ChinaCandidate:X MiaoFull Text:PDF
GTID:2404330575989678Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
OBJECTIVE: Epidermal growth factor receptor(EGFR)is the most common and widely used target for non-small-cell lung cancer(NSCLC).EGFR tyrosine kinase inhibitors(TKI)competitively bind to the EGFR tyrosine kinase domain,affecting downstream pathways,leading to tumor apoptosis.Numerous studies have confirmed that EGFR-sensitive mutations are associated with the efficacy and survival benefit of a generation of EGFR-TKI.However,in clinical work,it was found that the efficacy of EGFR-TKI was maintained only for 10 months,which was prone to drug resistance.Studies have attempted to treat EGFR-sensitive mutations in combination with EGFR-TKI in combination with standard chemotherapy.The survival status of patients with different treatment strategies at home and abroad needs further observation.This retrospective study looked at the differences in the efficacy and adverse effects of different treatment strategies in patients with advanced lung adenocarcinoma with EGFR-sensitive mutations.Methods: The clinical data of patients with stage IIIB to stage IV EGFR-sensitive mutations in lung adenocarcinoma were collected.According to the first-line treatment strategy,they were divided into chemotherapy group(group A),targeted treatment group(group B),and targeted maintenance treatment group after chemotherapy(group C).The patient's progression-free survival(PFS),overall response rate(ORR),and disease control rate(DCR)were observed.The survival of patients with malignant pleural effusion(MPE)and brain metastases was analyzed.Results: A total of 208 patients were enrolled,52 in group A,92 in group B,and 64 in group C.The median PFS of the three groups A,B,and C were 6.61 months,10.56 months,and 14.30 months,respectively,and the difference was statistically significant(P<0.001).The 1-year survival rate were 34.6%,56.5%,and 62.5%,respectively,and the difference was statistically significant(P=0.007).The2-year survival rate was 7.7%,17.4%,and 26.6%,respectively,and the difference was statistically significant(P=0.030).The three groups of ORR were 21%,67%,and 75%,respectively,and the difference was statistically significant(P < 0.001).The three groups of DCR were 83%,90%,and 95%,respectively,and the difference was not statistically significant(P=0.080).PFS in patients with pleural effusion was significantly different between the three groups(P < 0.001),PFS was also significantly different in patients with brain metastases(P = 0.001),and group B and C were significantly better than group A.There was no significant difference in the survival of patients with pleural effusion and those without pleural effusion in group B,and those with brain metastasis and those without brain metastasis.There were differences in adverse reactions between the three groups.The common adverse reactions in group A were hematological toxicity(including anemia,leukopenia,neutropenia,and thrombocytopenia),liver function damage,and nausea and vomiting.Common adverse reactions in group B are diarrhea,rash or hemorrhoids.Adverse reactions above group C were visible.All three groups of adverse reactions were within acceptable limits.Conclusion: First-line targeted therapy for patients with advanced lung adenocarcinoma with sensitive mutations significantly improved PFS,ORR,and DCR in patients compared with chemotherapy.PFS targeted for maintenance therapy after chemotherapy was significantly improved compared with targeted therapy.In patients with brain metastases or pleural effusions,first-line targeted therapy and targeted maintenance therapy after chemotherapy still have good efficacy.Although the above adverse events are different,they are all within an acceptable range.
Keywords/Search Tags:Lung adenocarcinoma, Epidermal growth factor receptor-tyrosine, kinase inhibitor, Malignant pleural effusion, Brain metastasis
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