High IFITM3 expression predicts adverse prognosis in acute myeloid leukemia

Yan Liu, Rongjian Lu, Wei Cui, Yifan Pang, Chaojun Liu, Longzhen Cui, Tingting Qian, Liang Quan, Yifeng Dai, Yang Jiao, Yue Pan, Xu Ye, Jinlong Shi, Zhiheng Cheng, Lin Fu*

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

    30 Citations (Scopus)
    149 Downloads (Pure)

    Abstract

    Acute myeloid leukemia (AML) is a malignancy caused by the uncontrolled and dysregulated clonal expansion of abnormal myeloid primordial cells. In general, the prognosis of AML remains poor despite new discoveries in its pathogenesis and treatment. It is crucial to find early and sensitive biomarkers and continue to explore active targeted treatments. Interferon-induced transmembrane protein (IFITM) family is an important part of the interferon signaling pathway and participate in the regulation of immune cell signaling, adhesion, cancer, and liver cell migration. However, the clinical and prognostic value of the IFITM family in AML has rarely been studied. We screened The Cancer Genome Atlas database and found 155 AML patients with IFITM family (IFITM1-5) expression data. In patients who only received chemotherapy, those with high IFITM3 expression had significantly shorter event-free survival (EFS) and overall survival (OS) than patients with low expression (all P <0.05). Multivariate analysis demonstrated that high IFITM3 expression was an independent risk factor for EFS and OS in patients only received chemotherapy (all P <0.05). In patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT), however, all IFITM members had no impact on either EFS or OS. In conclusion, our study elucidated that high IFITM3 expression could be an adverse prognostic factor for AML, whose effect might be overcome by allo-HSCT.

    Original languageEnglish
    Pages (from-to)38-44
    Number of pages7
    JournalCancer Gene Therapy
    Volume27
    Issue number1-2
    DOIs
    Publication statusPublished - Feb-2020

    Keywords

    • DNMT3A MUTATIONS
    • GENE
    • OVEREXPRESSION
    • IMPACT
    • STAGE

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