Literature DB >> 29496308

Overexpression of CTNNB1: Clinical implication in Chinese de novo acute myeloid leukemia.

Xi-Xi Li1, Hong Guo2, Jing-Dong Zhou1, De-Hong Wu3, Ji-Chun Ma2, Xiang-Mei Wen2, Wei Zhang4, Zi-Jun Xu5, Jiang Lin2, Qian Jun6.   

Abstract

Activation of Wnt/β-catenin signaling played a crucial role in tumorigenesis, and β-catenin (CTNNB1) overexpression has been identified in numerous solid tumors. The present study was designed to determine CTNNB1 expression and its clinical significance in Chinese de novo acute myeloid leukemia (AML) patients. Real-time quantitative PCR was carried out to detect the pattern of CTNNB1 expression in 140 AML patients and 46 controls. The level of CTNNB1 transcript in AML patients was significantly up-regulated compared with controls (P < 0.001). CTNNB1high patients showed significantly older age than CTNNB1low patients (P < 0.05). The frequency of high CTNNB1 expression was significantly observed in patients with intermediate/poor karyotypes. CTNNB1high patients had a significantly lower complete remission (CR) rate than CTNNB1low patients (P = 0.004). Among cytogenetically normal AML (CN-AML), CTNNB1high patients presented significantly shorter overall survival (OS, P = 0.004) and leukemia-free survival (LFS, P = 0.038) than CTNNB1low patients. Multivariate analysis confirmed that CTNNB1 expression was an independent prognostic factor for OS among CN-AML. Moreover, CTNNB1 expression level significantly decreased after CR stage (P = 0.032) and increased in relapsed stage (P = 0.015). Our findings suggest that CTNNB1 is overexpressed and confers a poor prognosis in AML, and could be used as a biomarker in monitoring disease recurrence.
Copyright © 2018. Published by Elsevier GmbH.

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Keywords:  Acute myeloid leukemia; CTNNB1; Expression; Prognosis

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Year:  2018        PMID: 29496308     DOI: 10.1016/j.prp.2018.01.003

Source DB:  PubMed          Journal:  Pathol Res Pract        ISSN: 0344-0338            Impact factor:   3.250


  1 in total

1.  Casein kinase 1α inhibits p53 downstream of MDM2‑mediated autophagy and apoptosis in acute myeloid leukemia.

Authors:  Wanling Xu; Ziyang Huang; Yifeng Gan; Rongrong Chen; Yisha Huang; Bin Xue; Songfu Jiang; Zhijie Yu; Kang Yu; Shenghui Zhang
Journal:  Oncol Rep       Date:  2020-09-09       Impact factor: 3.906

  1 in total

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