Novel activating KRAS mutation candidates in lung adenocarcinoma

Jiro Abe, Nobuhiro Tanuma, Miyuki Nomura, Shin Ito, Isao Kasugai, Ikuro Sato, Keiichi Tamai, Mai Mochizuki, Kazunori Yamaguchi, Hiroshi Shima, Yoshinori Okada, Jun Yasuda

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)


Lung adenocarcinoma (LUAC) is a unique lung cancer subtype that is responsive to several therapeutic agents. The KRAS gene is the second most frequently mutated gene in LUAC and the majority of KRAS mutations are one of three classical activating mutations (G12, G13, and Q61). Recently, other types of “minor” KRAS mutation have been identified among LUAC patients and some may have similar transforming activities to those of the classical KRAS mutations. Here we describe minor KRAS mutations in LUAC patients, some of which (A66T, A66V, and G75E) may have tumor-forming activity in mouse embryonic fibroblasts in an allograft model. RNA-Seq analysis revealed that mouse embryonic fibroblasts overexpressing these three minor KRAS mutations have distinct expression profiles compared with overexpression of the wild type but similar expression profiles compared with overexpression of the classical KRAS mutants. Our results indicate that some of the minor KRAS mutations cause varying tumor formation activity and are important targets for developing anti-RAS agents as chemotherapeutic agents.

Original languageEnglish
Pages (from-to)690-696
Number of pages7
JournalBiochemical and biophysical research communications
Issue number3
Publication statusPublished - 2020 Feb 12


  • Driver mutation
  • KRAS
  • Lung adenocarcinoma
  • RNA-Seq

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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