title: Pulmonary adenocarcinomas with micropapillary component significantly correlate with recurrence, but can be well controlled with EGFR tyrosine kinase inhibitors in the early stages.
abstract: Pulmonary adenocarcinoma with a micropapillary component (PA-MPC) is known to exhibit biologically aggressive behavior. The aim of this study was to evaluate the clinicopathological characteristics of early-stage PA-MPC and to investigate the correlation between PA-MPC and epidermal growth factor receptor (EGFR) or KRAS mutation status. We reviewed 440 PA patients who underwent resection. We defined PA-MPC as adenocarcinoma with MPC occupying at least 5% of the entire tumor. EGFR and KRAS mutations were detected using established methods. Of the 440 cases, 256 cases were classified as stage IA, of which 53 cases (20.7%) had MPC. The 5-year disease-free survival rates in the MPC-negative and MPC-positive groups of patients with stage IA tumors were 92.1% and 77.6%, respectively. The difference in these rates was statistically significant (p = 0.003), whereas the difference in overall survival between the groups was not statistically significant (p = 0.973). The mean percentage of MPC was 20.4% in the recurrent group and 18.3% in the non-recurrent group, with no significant correlation (p = 0.996). Of the 10 recurrent cases, 6 cases exhibited EGFR mutations; the 5 cases treated with a tyrosine kinase inhibitor (TKI) achieved long survival (median, 64.6 months). No KRAS mutations were detected in any of the 10 cases. PA-MPCs were strongly associated with recurrence, but were not influenced by the MPC percentage even in early-stage lesions. Moreover, PA-MPCs with recurrence were associated with relatively better survival. These findings indicate that PA-MPCs were biologically aggressive but could be controlled with EGFR-TKIs.
authors: Department of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
authors: Shinji
authors: S
authors: Sumiyoshi
authors: Akihiko
authors: A
authors: Yoshizawa
authors: Makoto
authors: M
authors: Sonobe
authors: Masashi
authors: M
authors: Kobayashi
authors: Masakazu
authors: M
authors: Fujimoto
authors: Tatsuaki
authors: T
authors: Tsuruyama
authors: Hiroshi
authors: H
authors: Date
authors: Hironori
authors: H
authors: Haga
mesh_terms: D000231:Adenocarcinoma, Papillary / Q000188:drug therapy* / Q000235:genetics / Q000401:mortality / Q000473:pathology / Q000601:surgery; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000627:therapeutic use; D018572:Disease-Free Survival; D066246:ErbB Receptors / Q000037:antagonists & inhibitors* / Q000235:genetics; D005260:Female; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000401:mortality / Q000473:pathology / Q000601:surgery; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009364:Neoplasm Recurrence, Local / Q000517:prevention & control*; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D011518:Proto-Oncogene Proteins / Q000235:genetics; D016283:Proto-Oncogene Proteins p21(ras); D016019:Survival Analysis; D055815:Young Adult; D018631:ras Proteins / Q000235:genetics
chemical_list: D000970:Antineoplastic Agents; C117307:KRAS protein, human; D047428:Protein Kinase Inhibitors; D011518:Proto-Oncogene Proteins; C512478:EGFR protein, human; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins