R. Rao, Z. Otaibi, Matthew Bartock, Mamatha Gaddam, A. Zaidi, B. Jobe, G. Finley
{"title":"肺癌分子检测的医师态度和流行程度","authors":"R. Rao, Z. Otaibi, Matthew Bartock, Mamatha Gaddam, A. Zaidi, B. Jobe, G. Finley","doi":"10.12788/JCSO.0326","DOIUrl":null,"url":null,"abstract":"Lung cancer is the leading cause of cancer death in the United States. It is estimated that there will be 222,500 new cases of lung cancer and 155,870 deaths from lung cancer in 2017. Non–small-cell lung carcinoma (NSCLC) accounts for 80%-85% of lung cancers, with adenocarcinoma being the most common histologic subtype. Other less common subtypes include squamous-cell carcinoma, large-cell carcinoma, and NSCLC that cannot be further classified.1 Nearly 70% of patients present with locally advanced or metastatic disease at the time of diagnosis and are not candidates for surgical resection.2 For that group of patients, the mainstay of treatment is platinumbased chemotherapy with or without radiation therapy. Patients who are chemotherapy naive often experience a modest response, however; durable remission is short lived, and the 5-year survival rate remains staggeringly low.3 Improved understanding of the molecular pathways that drive malignancy in NSCLC has led to the development of drugs that target specific molecular pathways.4 By definition, these driver mutations facilitate oncogenesis by conferring a selective advantage during clonal evolution.5 Moreover, agents targeting these pathways are extremely active and induce durable responses in many patients.6,7,8 Predictive biomarkers in NSCLC include anaplastic lymphoma kinase (ALK) fusion oncogene and sensitizing epidermal growth factor receptor (EGFR) mutations. Mutations in the EGFR tyrosine kinase are observed in about 15%-20% of NSCLC adenocarcinomas in the United States and upward of 60% in Asian populations. They are also found more frequently in nonsmokers and women.6 The two most prevalent mutations in the EGFR tyrosine kinase domain are in-frame deletions of exon 19 and L858R substitution in exon 21, representing about 45% and 40% of mutations, respectively.9 Both mutations result in activation of the tyrosine kinase domain, and both are associated with sensitivity to the small-molecule tyrosine","PeriodicalId":75058,"journal":{"name":"The Journal of community and supportive oncology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Physician attitudes and prevalence of molecular testing in lung cancer\",\"authors\":\"R. Rao, Z. Otaibi, Matthew Bartock, Mamatha Gaddam, A. Zaidi, B. Jobe, G. Finley\",\"doi\":\"10.12788/JCSO.0326\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Lung cancer is the leading cause of cancer death in the United States. It is estimated that there will be 222,500 new cases of lung cancer and 155,870 deaths from lung cancer in 2017. Non–small-cell lung carcinoma (NSCLC) accounts for 80%-85% of lung cancers, with adenocarcinoma being the most common histologic subtype. Other less common subtypes include squamous-cell carcinoma, large-cell carcinoma, and NSCLC that cannot be further classified.1 Nearly 70% of patients present with locally advanced or metastatic disease at the time of diagnosis and are not candidates for surgical resection.2 For that group of patients, the mainstay of treatment is platinumbased chemotherapy with or without radiation therapy. Patients who are chemotherapy naive often experience a modest response, however; durable remission is short lived, and the 5-year survival rate remains staggeringly low.3 Improved understanding of the molecular pathways that drive malignancy in NSCLC has led to the development of drugs that target specific molecular pathways.4 By definition, these driver mutations facilitate oncogenesis by conferring a selective advantage during clonal evolution.5 Moreover, agents targeting these pathways are extremely active and induce durable responses in many patients.6,7,8 Predictive biomarkers in NSCLC include anaplastic lymphoma kinase (ALK) fusion oncogene and sensitizing epidermal growth factor receptor (EGFR) mutations. Mutations in the EGFR tyrosine kinase are observed in about 15%-20% of NSCLC adenocarcinomas in the United States and upward of 60% in Asian populations. They are also found more frequently in nonsmokers and women.6 The two most prevalent mutations in the EGFR tyrosine kinase domain are in-frame deletions of exon 19 and L858R substitution in exon 21, representing about 45% and 40% of mutations, respectively.9 Both mutations result in activation of the tyrosine kinase domain, and both are associated with sensitivity to the small-molecule tyrosine\",\"PeriodicalId\":75058,\"journal\":{\"name\":\"The Journal of community and supportive oncology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Journal of community and supportive oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.12788/JCSO.0326\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of community and supportive oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12788/JCSO.0326","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Physician attitudes and prevalence of molecular testing in lung cancer
Lung cancer is the leading cause of cancer death in the United States. It is estimated that there will be 222,500 new cases of lung cancer and 155,870 deaths from lung cancer in 2017. Non–small-cell lung carcinoma (NSCLC) accounts for 80%-85% of lung cancers, with adenocarcinoma being the most common histologic subtype. Other less common subtypes include squamous-cell carcinoma, large-cell carcinoma, and NSCLC that cannot be further classified.1 Nearly 70% of patients present with locally advanced or metastatic disease at the time of diagnosis and are not candidates for surgical resection.2 For that group of patients, the mainstay of treatment is platinumbased chemotherapy with or without radiation therapy. Patients who are chemotherapy naive often experience a modest response, however; durable remission is short lived, and the 5-year survival rate remains staggeringly low.3 Improved understanding of the molecular pathways that drive malignancy in NSCLC has led to the development of drugs that target specific molecular pathways.4 By definition, these driver mutations facilitate oncogenesis by conferring a selective advantage during clonal evolution.5 Moreover, agents targeting these pathways are extremely active and induce durable responses in many patients.6,7,8 Predictive biomarkers in NSCLC include anaplastic lymphoma kinase (ALK) fusion oncogene and sensitizing epidermal growth factor receptor (EGFR) mutations. Mutations in the EGFR tyrosine kinase are observed in about 15%-20% of NSCLC adenocarcinomas in the United States and upward of 60% in Asian populations. They are also found more frequently in nonsmokers and women.6 The two most prevalent mutations in the EGFR tyrosine kinase domain are in-frame deletions of exon 19 and L858R substitution in exon 21, representing about 45% and 40% of mutations, respectively.9 Both mutations result in activation of the tyrosine kinase domain, and both are associated with sensitivity to the small-molecule tyrosine