論文

査読有り 国際誌
2016年2月

Genetic alterations in lung adenocarcinoma with a micropapillary component.

Molecular and clinical oncology
  • Masashi Furukawa
  • ,
  • Shinichi Toyooka
  • ,
  • Kouichi Ichimura
  • ,
  • Hiromasa Yamamoto
  • ,
  • Junichi Soh
  • ,
  • Shinsuke Hashida
  • ,
  • Mamoru Ouchida
  • ,
  • Kazuhiko Shien
  • ,
  • Hiroaki Asano
  • ,
  • Kazunori Tsukuda
  • ,
  • Shinichiro Miyoshi

4
2
開始ページ
195
終了ページ
200
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3892/mco.2015.690

Pulmonary adenocarcinoma (PA) with a micropapillary component (PA-MPC) is known as an aggressive subtype of PA. The molecular profiles of PA-MPC have not been well characterized. the pathological reports of patients who underwent surgical resection for lung cancer between April, 2004 and May, 2012 were reviewed. Of the 674 patients diagnosed with PA, 28 were found to have MPC. A total of 138 resected PAs without MPC were selected in the same period to serve as age-, gender- and smoking status-matched controls to the PA-MPC group. Mutational status was determined by the following two methods: SNaPshot assay based on multiplex polymerase chain reaction (PCR), primer extension and capillary electrophoresis that was designed to assess 38 somatic mutations in 8 genes [AKT1, BRAF, endothelial growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), mitogen-activated protein kinase kinase 1, neuroblastoma RAS viral oncogene homolog, phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA) and phosphatase and tensin homolog]; and a PCR-based sizing assay that assesses EGFR exon 19 (deletions), EGFR exon 20 (insertions) and human epidermal growth factor receptor 2 exon 20 (insertions). echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase fusion gene (EML4-ALK) was screened by ALK immunohistochemistry and confirmed using the reverse transcription PCR assay and the break-apart fluorescence in situ hybridization assay. Regarding genetic alterations, 13 (46.4%) of the 28 PA-MPCs harbored mutually exclusive mutations: 9 (32.1%) EGFR mutations, 1 (3.6%) KRAS mutation and 3 (10.7%) EML4-ALK fusion genes. PAs without MPC harbored 42 (30.4%) EGFR mutations, 17 (12.3%) KRAS mutations, 3 (2.2%) EML4-ALK fusion genes and 1 (0.7%) PIK3CA mutation. EML4-ALK fusion genes appeared to occur significantly more frequently in PA-MPCs compared with PAs without MPC (P=0.027). Although the sample size was small, our study suggests that the molecular pathogenesis of PA-MPC may be different from that of other adenocarcinomas.

リンク情報
DOI
https://doi.org/10.3892/mco.2015.690
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26893860
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4734214
ID情報
  • DOI : 10.3892/mco.2015.690
  • ISSN : 2049-9450
  • PubMed ID : 26893860
  • PubMed Central 記事ID : PMC4734214

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