Homozygous loss of the cyclin-dependent kinase 4-inhibitor (p16) gene in human leukemias

Seishi Ogawa, Naoto Hirano, Naomi Sato, Tokiharu Takahashi, Akira Hangaishi, Kozo Tanaka, Mineo Kurokawa, Tomoyuki Tanaka, Kinuko Mitani, Yoshio Yazaki, Hisamaru Hirai

研究成果: Article査読

172 被引用数 (Scopus)

抄録

Recently, it has been shown that the homozygous deletion of the cyclin- dependent kinase-4 inhibitor (CDK4I; p16) gene, which is mapped to chromosome 9p21, is frequently observed in a wide spectrum of human cancers, including leukemias. Therefore, the CDK4I gene is thought to be a putative tumor- suppressor gene. We report here that both alleles of the CDK4I gene were completely or partially deleted in human leukemia cells derived from both patients and established cell lines. Thirty-seven hematopoietic cell lines and samples from 72 patients with leukemias were examined for homozygous loss of the CDK4I gene locus by Southern blot analysis. We found that a part or the whole of the CDK4I gene was homozygously deleted in 14 of the 37 (38%) cell lines and 4 of 72 (6%) samples from leukemia patients, including 45 with acute myelocytic leukemia, 14 with acute lymphocytic leukemia (ALL), and 13 with chronic myelocytic leukemia in blastic crisis. In the cell lines, the homozygous deletion of the CDK4I gene was detected in a variety of cell lineages, whereas all 4 cases showing the homozygous deletion were confined to ALL. It should be noted that 2 of them had no cytogenetic abnormalities of chromosome 9. Our results suggest that loss of the CDK4I function may contribute to immortalization of human leukemia cells and play a causative role at least in development of human lymphocytic leukemias.

本文言語English
ページ(範囲)2431-2435
ページ数5
ジャーナルBlood
84
8
DOI
出版ステータスPublished - 1994 10月 15
外部発表はい

ASJC Scopus subject areas

  • 生化学
  • 免疫学
  • 血液学
  • 細胞生物学

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