title: [Expression of cell cycle control genes in myelodysplastic syndromes].
abstract: OBJECTIVE
  To study aberrant expression of cell cycle control genes in patients with myelodysplastic syndromes (MDS).
  
  
  METHODS
  Reverse transcription polymerase chain reaction (RT-PCR) was used to investigate the expression of cell cycle control genes (cyclin D2, cyclin D3, cyclin A1, cyclin E, CDK2, CDK4, CDK6, p21, p27, p57, Rb and E2F1) in bone marrow mononuclear cells (BMMNCs) from 29 normal control, 27 MDS and 19 de novo acute myeloid leukemia (AML).
  
  
  RESULTS
  The expression levels of cyclin D3 (0.65 +/- 0.17, P < 0.05) and cyclin A1 (0.48 +/- 0.04, P < 0.05) in MDS were higher than those in normal control and significantly lower than those in AML. The expression rates and levels of cyclin D2 (40.7% and 0.78 +/- 0.21) and cyclin E (51.9% and 0.52 +/- 0.10) in MDS were statistically higher than those in normal control and AML. The expression level of CDK2 in MDS (0.66 +/- 0.19, P < 0.01) was higher than that in normal control (0.42 +/- 0.04) and the expression rate of CDK6 in MDS (25.9%) higher than in normal control (3.4%, P < 0.05). There was no significant difference of the expression rates and levels of CDK4 in MDS, AML and normal control. The expression rates and levels of p21 (77.8% and 1.18 +/- 0.21) and p27 (48.1% and 1.14 +/- 0.40) in MDS were statistically higher than those in normal control and AML. The expression level of p57 in MDS (0.69 +/- 0.06) was higher than that (0.53 +/- 0.05, P < 0.01) in normal control but lower than in AML (0.96 +/- 0.16, P < 0.01). The expression rate (55.6%) and level (0.85 +/- 0.17) of Rb in MDS were significantly higher than those in normal control and AML. The expression rate (7.4%) and level (0.39 +/- 0.04) of E2F1 in MDS were comparable to those in normal control but lower than those in AML.
  
  
  CONCLUSIONS
  MDS clones have aberrant mechanism of cell cycle control: high expressions of cyclin family members, CDK2 and CDK6 may lead to high proliferation; high expression of p21 and p27 may cause the G1 phase arrest.
authors.affiliation: Institute of Hematology and Blood Diseases Hospital, CAMS and PUMC, Tianjin 300020, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Shi
authors.forename: Zong-hong
authors.initials: ZH
authors.lastname: Shao
authors.forename: Hong
authors.initials: H
authors.lastname: Liu
authors.forename: Hai-rong
authors.initials: HR
authors.lastname: Jia
authors.forename: Juan
authors.initials: J
authors.lastname: Sun
authors.forename: Jie
authors.initials: J
authors.lastname: Bai
authors.forename: Yan-ran
authors.initials: YR
authors.lastname: Cao
authors.forename: Xiu-li
authors.initials: XL
authors.lastname: Wang
authors.forename: Mei-feng
authors.initials: MF
authors.lastname: Tu
mesh_terms: D000293:Adolescent; D000328:Adult; D018797:Cell Cycle Proteins / Q000235:genetics*; D002648:Child; D050756:Cyclin-Dependent Kinase Inhibitor Proteins / Q000235:genetics*; D018844:Cyclin-Dependent Kinases / Q000235:genetics*; D050687:E2F1 Transcription Factor / Q000235:genetics; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D008297:Male; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000235:genetics* / Q000473:pathology; D016160:Retinoblastoma Protein / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D055815:Young Adult
chemical_list: D018797:Cell Cycle Proteins; D050756:Cyclin-Dependent Kinase Inhibitor Proteins; D050687:E2F1 Transcription Factor; D016160:Retinoblastoma Protein; D018844:Cyclin-Dependent Kinases