title: BMI-1 is highly expressed in M0-subtype acute myeloid leukemia.
abstract: Recent studies have suggested that one of the polycomb group genes, BMI-1, has an important role in the maintenance of normal and leukemic stem cells by repressing the INK4a/ARF locus. Here, we quantitatively examined BMI-1 expression level in samples from patients with acute myeloid leukemia (AML) and other hematologic malignancies. Moderate to high BMI-1 expression was detected in AML patients, and the BMI-1 expression levels in AML samples were significantly higher than in normal bone marrow controls (P = .0011). Specimens of French-American-British classification subtype M0 showed higher relative expression of the BMI-1 transcript (median, 390.2 3 10(-3)) than the other subtypes (median, 139.0 3 10(-3)) (P < .0001). Leukemia other than AML showed low to moderate expression. INK4a-ARF transcript expression tended to be inverse proportion to that of BMI-1. In an M0 patient with a high BMI-1 transcript level, the INK4a-ARF transcript level fell promptly and maintained a low value after the patient achieved complete remission. These results indicated that a subgroup of M0 patients has a high expression level of polycomb group gene BMI-1, which may contribute to leukemogenesis.
authors.affiliation: Department of Molecular Medicine and Hematology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Masashi
authors.initials: M
authors.lastname: Sawa
authors.forename: Kazuhito
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Toshiya
authors.initials: T
authors.lastname: Yokozawa
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Kiyoi
authors.forename: Asahi
authors.initials: A
authors.lastname: Hishida
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Kajiguchi
authors.forename: Masao
authors.initials: M
authors.lastname: Seto
authors.forename: Akio
authors.initials: A
authors.lastname: Kohno
authors.forename: Kunio
authors.initials: K
authors.lastname: Kitamura
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Itoh
authors.forename: Norio
authors.initials: N
authors.lastname: Asou
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Hamajima
authors.forename: Nobuhiko
authors.initials: N
authors.lastname: Emi
authors.forename: Tomoki
authors.initials: T
authors.lastname: Naoe
mesh_terms: D000208:Acute Disease; D001853:Bone Marrow; D016022:Case-Control Studies; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D020869:Gene Expression Profiling; D006801:Humans; D007951:Leukemia, Myeloid / Q000235:genetics*; D009687:Nuclear Proteins / Q000096:biosynthesis* / Q000145:classification / Q000235:genetics; D063150:Polycomb Repressive Complex 1; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis* / Q000145:classification / Q000235:genetics; D012097:Repressor Proteins / Q000096:biosynthesis* / Q000145:classification / Q000235:genetics
chemical_list: C069077:BMI1 protein, human; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D012097:Repressor Proteins; D063150:Polycomb Repressive Complex 1