ALL-017 Adult T-Cell Acute Lymphoblastic Leukemia With Transducin-Like Enhancer Gene Expression

Abstract

Transducin-like enhancer of split 1 (TLE1) is a member of the TLE family of transcriptional co-repressors that control the transcription of a wide range of genes. The aim of this study was to evaluate the prognostic role of TLE1 gene expression in patients with T-cell acute lymphoblastic leukemia (T-ALL). This study was conducted on 97 newly diagnosed T-ALL patients admitted to the Mansoura University oncology center (59 males and 38 females) with median age 33 years, in addition to 102 apparently healthy individuals who served as a control group. TLE1 gene expression was measured in both patients and control groups by real time - PCR. The calculation of relative gene expression was done using the AACt method. TEL1 gene expression was significantly down regulated in T-ALL cases (median 2.83) as compared to controls (median 84.65) (p < 0.001). Low TEL1 gene expression was significantly associated with CNS infiltration, failure to achieve 1st complete remission and higher relapse rate (p< 0.001, 0.001 and 0.023, respectively). Early T-cell precursor (ETP)-ALL/LBL subtype was found to be significantly associated with low TEL1 gene expression (P 0.04), however there was no relation between TEL1 gene expression and TCR rearrangement or other available molecular abnormalities. Likewise, low TEL1 gene expression was significantly associated with shorter overall survival (OS) and disease-free survival (DFS) (P= 0.012 and 0.011, respectively). Furthermore, Low TEL1 gene expression was considered a risk predictor of relapse with OR 3.636(CI.1.422-9.295) (P =0.007); and OR 0.803(CI. 0.609-0.96) (P=0.021) and an independent predictor of T-ALL patients' outcomes with OR 0.619 (CI. 0.44-0.872) (P=0.006). TLE1 gene expression was significantly down regulated in T-ALL as compared with controls. Low TLE1 expression is an independent predictor of the T-ALL patient's outcome and could open the way for further risk stratification and targeted therapy in T-ALL.