Saturday, March 29, 2014

From Elizabeth McQuitty and colleagues: EGFR Mutations in US Hispanic Versus Non-Hispanic White Patients With Lung Adenocarcinoma

Wei Zhang MDElizabeth B. McQuitty MDRandall Olsen MD, PhDHongxin Fan MDHeather Hendrickson MB(ASCP)CM, MBAFermin O. Tio MDKeith Newton MB(ASCP)CMPhilip T. Cagle MDJaishree Jagirdar MD
From the Department of Pathology (Dr Zhang), Molecular Diagnostics Laboratory (Dr Fan), and Department of Pathology (Dr Jagirdar), The University of Texas Health Science Center at San Antonio, and Laboratory Service, Audie L. Murphy Memorial Veterans Affairs Medical Center (Dr Tio), San Antonio; and Department of Pathology and Immunology, Baylor College of Medicine (Dr McQuitty), and Department of Pathology and Genomic Medicine, The Methodist Hospital (Drs Olsen and Cagle, Ms Hendrickson, and Mr Newton), Houston, Texas.
Context.—Lung cancer is the leading cause of cancer deaths worldwide. First-generation tyrosine kinase inhibitors improve progression-free survival in lung cancers with epidermal growth factor receptor (EGFR) mutations. EGFR mutations occur predominantly in exons 19 and 21 in lung adenocarcinomas of Asians (30%), whites (15%), and African Americans (19%). However, minimal information exists on the prevalence or type of genetic changes that occur in lung cancers in US Hispanic patients. We investigated the EGFR mutation frequency in primary lung adenocarcinomas in US Hispanics compared with non-Hispanic whites.
Objective.—To evaluate EGFR mutations in lung adenocarcinomas from US Hispanic patients compared with those from non-Hispanic white patients.
Design.—DNA samples were extracted from paraffin-embedded tissue of consecutive lung adenocarcinomas from 83 patients. Samples were collected from 40 Hispanics and 43 non-Hispanic whites. Mutations in EGFR were analyzed using a custom assay.
Results.—Fourteen of 83 patients (16.9%) had EGFR mutations in their tumor DNA, including 6 of 40 Hispanics (15.0%) and 8 of 43 non-Hispanic whites (18.6%). No association with age, sex, or tumor stage was identified. Smoking history could not be obtained for most of the 83 patients, although 8 of the 11 patients with EGFR mutations for whom smoking history was obtained were nonsmokers. Most of the tumors with EGFR mutations (12 of 14; 85.7%) were acinar with lepidic or papillary subtypes. EGFR mutations occurred in exon 19 (42.8%), exon 18 (28.6%), exon 20 (28.6%), and exon 21 (14.3%). Two cases had 2 mutations identified in different exons.
Conclusion.—The frequency of EGFR mutations is similar in US Hispanics compared with non-Hispanic whites.

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