A subset of diffuse-type gastric cancer is susceptible to mTOR inhibitors and checkpoint inhibitors View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-03-12

AUTHORS

Hiroshi Fukamachi, Seon-Kyu Kim, Jiwon Koh, Hye Seung Lee, Yasushi Sasaki, Kentaro Yamashita, Taketo Nishikawaji, Shu Shimada, Yoshimitsu Akiyama, Sun-ju Byeon, Dong-Hyuck Bae, Keisuke Okuno, Masatoshi Nakagawa, Toshiro Tanioka, Mikito Inokuchi, Hiroshi Kawachi, Kiichiro Tsuchiya, Kazuyuki Kojima, Takashi Tokino, Yoshinobu Eishi, Yong Sung Kim, Woo Ho Kim, Yasuhito Yuasa, Shinji Tanaka

ABSTRACT

BackgroundMechanistic target of rapamycin (mTOR) pathway is essential for the growth of gastric cancer (GC), but mTOR inhibitor everolimus was not effective for the treatment of GCs. The Cancer Genome Atlas (TCGA) researchers reported that most diffuse-type GCs were genomically stable (GS). Pathological analysis suggested that some diffuse-type GCs developed from intestinal-type GCs.MethodsWe established patient-derived xenograft (PDX) lines from diffuse-type GCs, and searched for drugs that suppressed their growth. Diffuse-type GCs were classified into subtypes by their gene expression profiles.ResultsmTOR inhibitor temsirolimus strongly suppressed the growth of PDX-derived diffuse-type GC-initiating cells, which was regulated via Wnt-mTOR axis. These cells were microsatellite unstable (MSI) or chromosomally unstable (CIN), inconsistent with TCGA report. Diffuse-type GCs in TCGA cohort could be classified into two clusters, and GS subtype was major in cluster I while CIN and MSI subtypes were predominant in cluster II where PDX-derived diffuse-type GC cells were included. We estimated that about 9 and 55% of the diffuse-type GCs in cluster II were responders to mTOR inhibitors and checkpoint inhibitors, respectively, by identifying PIK3CA mutations and MSI condition in TCGA cohort. These ratios were far greater than those of diffuse-type GCs in cluster I or intestinal-type GCs. Further analysis suggested that diffuse-type GCs in cluster II developed from intestinal-type GCs while those in cluster I from normal gastric epithelial cells.ConclusionmTOR inhibitors and checkpoint inhibitors might be useful for the treatment of a subset of diffuse-type GCs which may develop from intestinal-type GCs. More... »

PAGES

127

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  • Journal

    Author Affiliations

  • Department of Molecular Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
  • Personalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea
  • Department of Pathology, Seoul National University Bundang Hospital, Gyeonggi-do, Korea
  • Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
  • Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan
  • Present Address: Division of Cancer Biology and Therapeutics, Miyagi Cancer Center Research Institute, 981-1293, Miyagi, Japan
  • Department of Pathology, Seoul National University College of Medicine, Seoul, Korea
  • Genome Editing Research Center, Korea Research Institute of Bioscience & Biotechnology, Daejeon, Korea
  • Department of Gastrointestinal Surgery, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
  • Present Address: Department of Pathology, The Cancer Institute Hospital of the Japanese Foundation for Cancer Research, 135-8550, Tokyo, Japan
  • Department of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan
  • Center of Minimally Invasive Surgery, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
  • Department of Human Pathology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/s13046-019-1121-3

    DOI

    http://dx.doi.org/10.1186/s13046-019-1121-3

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112739185

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30866995


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