title: Comparison of EGFR and KRAS mutations in primary and unpaired metastatic lung adenocarcinoma with potential chemotherapy effect.
abstract: Several recent studies have suggested that EGFR and KRAS mutations may be different in primary and metastatic tumors. It is also not well studied whether or not conventional chemotherapy has any effect on EGFR or KRAS mutations. In this study, we compared EGFR and KRAS mutations in primary and unrelated metastatic lung adenocarcinomas from retrospectively collected clinical cases. We also examined the potential effect of chemotherapy on EGFR and KRAS mutations in these 2 groups based on available clinical information. Using Johns Hopkins Hospital archives, 379 lung adenocarcinomas with EGFR and KRAS mutational analyses were included. Mutational status was determined by sequencing exons 18 to 21 of EGFR and codons 12 and 13 of KRAS. Clinical information was correlated. The overall mutational rates in primary and metastatic tumors were comparable. In 213 primary tumors, there was no significant difference of EGFR and KRAS mutational rates in the prechemotherapy and postchemotherapy groups (P > .05), whereas in 166 metastatic tumors, EGFR and KRAS mutations were 12.8% and 36.1% in the prechemotherapy group and 27.3% and 18.2% in the postchemotherapy group (P < .05). Although our study is an unpaired study, it suggests that mutational status in metastatic tumors may need to be tested, especially if the patient had chemotherapy before the test. Additional studies are needed to further investigate the mechanism and clinical significance of the findings.
authors: Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
authors: Delicia
authors: D
authors: Munfus-McCray
authors: Min
authors: M
authors: Cui
authors: Zhen
authors: Z
authors: Zhang
authors: Edward
authors: E
authors: Gabrielson
authors: Frederic
authors: F
authors: Askin
authors: Qing Kay
authors: QK
authors: Li
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000235:genetics* / Q000556:secondary; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D004252:DNA Mutational Analysis; D004273:DNA, Neoplasm / Q000235:genetics; D066246:ErbB Receptors / Q000235:genetics*; D005260:Female; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009154:Mutation; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D012189:Retrospective Studies; D013997:Time Factors; D055815:Young Adult; D018631:ras Proteins / Q000235:genetics*
chemical_list: D000970:Antineoplastic Agents; D004273:DNA, Neoplasm; C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; C512478:EGFR protein, human; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins