Aberrant chromatin remodeling in gynecological cancer (Review)

Ryuichiro Okawa, Kouji Banno, Miho Iida, Megumi Yanokura, Takashi Takeda, Moito Iijima, Haruko Kunitomi Irie, Kanako Nakamura, Masataka Adachi, Kiyoko Umene, Yuya Nogami, Kenta Masuda, Yusuke Kobayashi, Eiichiro Tominaga, Daisuke Aoki

Research output: Contribution to journalReview articlepeer-review

2 Citations (Scopus)

Abstract

Epigenetic regulatory mechanisms are a current focus in studies investigating cancer. Chromatin remodeling alters chromatin structure and regulates gene expression, and aberrant chromatin remodeling is involved in carcinogenesis. AT-rich interactive domain-containing protein 1A (ARID1A) and SWItch/sucrose non-fermentable-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 4 are remodeling factors that are mutated in numerous types of cancer. In gynecological cancer, ARID1A mutations have been identified in 46-57% of clear cell carcinoma and 30% of endometrioid carcinoma. Mutations of chromodomain helicase, DNA-binding protein 4 have been detected in 17-21% of endometrial serous cancer, and mutations of ARID1A and mixed-lineage leukemia 3 occur in 36 and 27% of uterine carcinosarcoma, respectively. These data suggest that aberrant chromatin remodeling is a potential cause of cancer, and have led to the development of novel proteins targeting these processes. Additional accumulation of information on the mechanisms of chromatin remodeling and markers for these events may promote personalized anticancer therapies.

Original languageEnglish
Pages (from-to)5107-5113
Number of pages7
JournalOncology Letters
Volume14
Issue number5
DOIs
Publication statusPublished - 2017 Nov

Keywords

  • AT-rich interaction domain 1A
  • Carcinogenesis
  • Chromatin remodeling
  • Gynecological cancer
  • Mutation
  • Switch/sucrose non-fermentable complex

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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