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 voor dit werk

    OnderzoeksoutputAcademicpeer review

    28 Citaten (Scopus)
    114 Downloads (Pure)

    Samenvatting

    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.

    Originele taal-2English
    Pagina's (van-tot)38-44
    Aantal pagina's7
    TijdschriftCancer Gene Therapy
    Volume27
    Nummer van het tijdschrift1-2
    DOI's
    StatusPublished - feb.-2020

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