Elizabeth McQuitty, Wei Zhang, Heather Hendrickson, Fermin O. Tio, Jaishree Jagirdar, Randall Olsen, and Philip T. Cagle (2014) Lung Adenocarcinoma Biomarker Incidence in Hispanic Versus Non-Hispanic White Patients. Archives of Pathology & Laboratory Medicine: March 2014, Vol. 138, No. 3, pp. 390-394.
ORIGINAL ARTICLES
Elizabeth McQuitty , MD; Wei Zhang , MD; Heather Hendrickson , MB, MBA; Fermin O. Tio , MD; Jaishree Jagirdar , MD; RandallOlsen , MD, PhD; Philip T. Cagle , MD
From the Department of Pathology, University of Texas Health Sciences Center, San Antonio (Drs Zhang and Jagirdar); the Department of Anatomic and Clinical Pathology, South Texas Veterans Health Care System, San Antonio (Dr Tio); and the Department of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas (Drs McQuitty, Olsen, and Cagle and Ms Hendrickson). Dr McQuitty is now with the Department of Pathology and Immunology, Baylor College of Medicine, Houston.
Context.—Lung cancer is the leading cause of cancer deaths in the United States and worldwide. Biomarker testing is critical to personalized therapy in lung adenocarcinoma and has been extensively investigated in non-Hispanic whites, Asians, and African Americans. However, little information addresses the underlying genetic changes in lung adenocarcinoma among Hispanic patients in the United States.
Objective.—To identify targetable biomarkers other than EGFR and EML4-ALK in Hispanic patients with lung adenocarcinoma.
Design.—We tested DNA extracted from 85 lung adenocarcinoma specimens collected from 40 Hispanic and 43 non-Hispanic white patients for previously reported mutations in KRAS, MET, BRAF, mTOR, STAT3, JAK2, PIK3CA, AKT1 through AKT3, and PTEN with a custom Sequenom massARRAY assay (Sequenom, San Diego, California).
Results.—Mutations in KRAS were identified in 11 cases (13%; 6 Hispanic [7%], 5 non-Hispanic white [6%]) and had no correlation with sex, age, or smoking history. Mutations in PIK3CA were identified in 2 of the 40 Hispanic patients (5%), including one patient (2.5%) with a concurrent KRAS mutation. The tumors were wild type for all other genes tested.
Conclusions.—Targetable biomarkers other than EGFR and EML4-ALK were identified in 7 of the 40 Hispanic patients (18%) and 5 of the 43 non-Hispanic white patients (12%), suggesting a similar mutational frequency. Our highly multiplexed genotyping assay detected actionable mutations in 14% (12 of 83) more patients than would have been identified by EGFRand EML4-ALK testing alone.
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