Disease relevance of CCNE2

• CONCLUSION: Our study shows that both CCNE1 and CCNE2 qualify as independent prognostic markers for lymph node-negative breast cancer patients, and that CCNE1 may provide additional information for specific subgroups of patients [1].
• Cyclin E2 may be used as a marker for examination of minimal residual disease [2].
• (4) positive rate of cyclin E2 expression (59.32%) in patients with acute myelocytic leukemia was lower than that (96%) in patients with acute lymphocytic leukemia, no correlation between cyclin E2 expression and white blood cell counts of patients was found [2].

High impact information on CCNE2

• Last, we found that cyclin E2 is overexpressed in approximately 24% of analyzed human mammary carcinomas [3].
• The catalytic activity associated with cyclin E2 complexes is cell cycle regulated and peaks at the G1/S transition [4].
• Cyclin A1, cyclin A2, and cyclin E2 expression levels did not have prognostic relevance for survival [5].
• The increased level of cyclin E2 in breast tumors suggests that, similar to cyclin E1, it may contribute to the pathogenesis of breast cancer [6].
• In primary solid tumors however, the expression and activity of cyclin E2, the newest member of the G(1) cyclin family, is largely unknown [6].

Biological context of CCNE2

• Cyclin E2 encodes a short lived protein whose turnover is most likely governed by the proteasome pathway and is regulated by phosphorylation on a conserved Thr-392 residue [7].
• Cyclin E2: a novel CDK2 partner in the late G1 and S phases of the mammalian cell cycle [8].
• Cyclin E2 mRNA expression is strongly suppressed by p53  [9]
• Both MM17 and U266 with complex cytogenetic aberrations demonstrated overexpression of cyclin E1 and E2, whereas IM-9 with a normal karyotype showed cyclin E2 but not E1 overexpression [10].
• Wild type Rb (RbWT) and to a lesser extent the low penetrance mutant Rb661W induced a G0/G1 arrest associated with induction of p27KIP1 and repression of cyclin E1 and cyclin E2 [11].
• Consistent with G1 arrest and cell growth inhibition, cyclin E2 and cyclin D1 messenger RNA expression in the cell was down-regulated with drug treatment [12].

Anatomical context of CCNE2

• Expression of the viral E6 oncoprotein in normal human fibroblasts increases the steady state level of cyclin E2, but not cyclin E1, while expression of the E7 oncoprotein upregulates both [7].
• Although cyclin E2 was abundantly expressed, histone H1 kinase activities of both E-type cyclins were virtually undetectable in this cell line [13].
• This study was aimed to investigate the expression of cyclin E2 and survivin gene in bone marrow cells from patients with acute leukemia and their relationship [2].

Associations of CCNE2 with chemical compounds

• In subgroup analyses of the tamoxifen-only treated patients, high CCNE1 levels predicted treatment resistance, while high levels of CCNE2 were associated with poor RFI in untreated patients [14].

Other interactions of CCNE2

• The expression of cyclin E2 mRNA oscillates periodically throughout the cell cycle, peaking at the G1/S transition, and exhibits a pattern of tissue specificity distinct from that of cyclin E1 [7].
• By univariate analysis, CCNE1, CCNE2, estrogen receptor and grade significantly predicted relapse free interval (RFI) [14].
• The second E-type cyclin, cyclin E2, has been shown to be overexpressed in breast cancers although the potential role as a diagnostic or prognostic marker is unknown [15].
• In addition, several genes were significantly (P < 0.025) down-regulated in OEA, including cyclin E2, Porcupine, c-Myc, and Axin 2 (4.8-, 3.6-, 2.9-, and 1.9-fold, respectively) [16].
• Reverse transcription polymerase chain reaction was used for detection of the expression of cyclin E2 and survivin mRNA in 84 adult patients with acute leukemia which included 16 cases of relapse, 60 cases of de novo acute leukemia, 8 cases of continuously complete remission, and 20 normal persons as controls [2].

References