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Clinicopathological and genetic analyses of pulmonary enteric adenocarcinoma
  1. Fumi Okada1,
  2. Maiko Takeda1,
  3. Tomomi Fujii1,
  4. Tomoko Uchiyama1,
  5. Shoh Sasaki1,
  6. Minami Matsuoka1,
  7. Yuji Nitta1,
  8. Chiyoko Terada1,
  9. Katsuya Maebo1,
  10. Kohei Morita1,2,
  11. Eiwa Ishida2,
  12. Noriyoshi Sawabata3,
  13. Chiho Ohbayashi1
  1. 1Department of Diagnostic Pathology, Nara Medical University, Kashihara, Japan
  2. 2Department of Diagnostic Pathology, Nara Prefecture General Medical Center, Nara, Japan
  3. 3Department of Thoracic and Cardio-Vascular Surgery, Nara Medical University, Kashihara, Japan
  1. Correspondence to Dr Maiko Takeda, Nara Medical University School of Medicine, Department of Diagnostic Pathology, Kashihara, 634-8521, Japan; maikot{at}naramed-u.ac.jp

Abstract

Aims Pulmonary enteric adenocarcinoma (PEAC) is a rare variant of pulmonary adenocarcinoma. Due to its rarity, few pathological and molecular studies have been performed on PEAC. We herein conducted clinicopathological, immunohistochemical and molecular analyses of PEAC with a focus on its differentiation from invasive mucinous adenocarcinoma (IMA).

Methods We examined the clinicopathological features of 16 cases of PEAC and performed a genetic analysis using next-generation sequencing (NGS). The results obtained were compared with those for IMA.

Results The average age of patients with PEAC (seven men and nine women) was 72.9 years. A comparison of clinical data on PEAC and IMA revealed no significant differences in age, sex or smoking history. Fifteen PEAC cases had dirty necrosis. Immunohistochemically, the positive rates for each antibody in PEAC were as follows: CK7, 88% (14/16); CK20, 81% (13/16); CDX2, 88% (14/16); p53, 69% (11/16); MUC1, 100% (16/16); MUC2, 19% (3/16); MUC5AC, 69% (11/16); MUC6, 19% (3/16). The positive rates for these antibodies in IMA were 100%, 87%, 0%, 7%, 93%, 0%, 100% and 80%, respectively. EGFR mutations, the MET exon 14 skipping mutation, BRAF mutations, the ALK fusion gene and ROS-1 fusion gene were not detected in any cases of PEAC or IMA. Among PEAC cases, NGS identified KRAS mutations in seven (44%, 7/16) and TP53 mutations in nine (56%, 9/16). Among IMA cases, the most commonly mutated gene was KRAS (90%).

Conclusions The rates of dirty necrosis, immunopositivity for CDX2 and TP53 mutations were significantly higher, while that of KRAS mutations was significantly lower in PEAC cases than in IMA cases.

  • Pathology, Molecular
  • Lung Neoplasms
  • IMMUNOHISTOCHEMISTRY
  • Genes, Neoplasm

Data availability statement

Data are available upon reasonable request. Data are available on reasonable request. All data relevant to the study are included in the article or uploaded as online supplemental information. The individual datasets generated during and/or analysed during the current study are not publicly available due to privacy of research participants but are available from the corresponding author on reasonable request.

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Data availability statement

Data are available upon reasonable request. Data are available on reasonable request. All data relevant to the study are included in the article or uploaded as online supplemental information. The individual datasets generated during and/or analysed during the current study are not publicly available due to privacy of research participants but are available from the corresponding author on reasonable request.

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Footnotes

  • Handling editor Runjan Chetty.

  • Contributors FO contributed to the study design, data collection, a review of pathology samples, data analyses and the manuscript write-up. MT contributed as the corresponding author, a review of pathology samples, and manuscript editing. TF contributed to genetic analyses. TU, SS, MM, YN, CT, KM, KM and EI contributed to data collection and a review of pathology samples. NS contributed to data collection. CO contributed to the study design, a review of pathology samples, data analyses and manuscript editing. MT is responsible for the overall content as guarantor.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.