Publication

Enhanced expressions of FHL2 and iASPP predict poor prognosis in acute myeloid leukemia

Cheng, Z., Dai, Y., Pang, Y., Jiao, Y., Zhao, H., Zhang, Z., Qin, T., Hu, N., Zhang, Y., Ke, X., Chen, Y., Wu, D., Shi, J. & Fu, L., 18-Jun-2019, In : Cancer Gene Therapy. 26, 1-2, p. 17-25 9 p.

Research output: Contribution to journalArticleAcademicpeer-review

  • Zhiheng Cheng
  • Yifeng Dai
  • Yifan Pang
  • Yang Jiao
  • Hongmian Zhao
  • Zhihui Zhang
  • Tong Qin
  • Ning Hu
  • Yijie Zhang
  • Xiaoyan Ke
  • Yang Chen
  • Depei Wu
  • Jinlong Shi
  • Lin Fu

iASPP is a negative regulator of the apoptotic function of p53, and it can enhance the ability of hematopoietic stem cells to self-renew and resist chemo- and radiation therapy. Recent study showed that iASPP could impact the proliferation and apoptosis of leukemia cells by interacting with FHL2. However, whether they have prognostic significance in acute myeloid leukemia (AML) is unknown. Eighty-four AML patients with FHL2 and iASPP expression data from The Cancer Genome Atlas database were enrolled in the study. Patients with high expressions of FHL2 and iASPP had significantly shorter event-free survival (EFS) and overall survival (OS) than patients with low expressions (P = 0.005, P = 0.003, respectively). Univariate analysis indicated that high expressions of FHL2 or iASPP were unfavorable for EFS and OS (all P <0.05), while multivariate analysis confirmed that high FHL2 expression was an independent risk factor for EFS and OS (all P <0.05). In patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT), however, EFS and OS were not significantly different between FHL2 or iASPP high- and low-expression groups. Our results suggested that high expressions of FHL2 and iASPP were poor prognostic factors for AML, but the prognostic effect might be overcome by allo-HSCT.

Original languageEnglish
Pages (from-to)17-25
Number of pages9
JournalCancer Gene Therapy
Volume26
Issue number1-2
Publication statusPublished - 18-Jun-2019

    Keywords

  • HEMATOPOIETIC STEM-CELLS, APOPTOSIS, MUTATIONS, INTERACTS, IMPACT, CANCER, RISK

ID: 91673750