PTEN abnormalities predict poor outcome in children with T‐cell acute lymphoblastic leukemia treated according to ALL IC‐BFM protocols

Abstract

CORRESPONDENCE E93 CORRESPONDENCE E95 data; ŁS and TS provided FC-MRD data; KZ and PB performed statistical analyses; JK and TS coordinated acquisition of samples and clinical data; BSZ and RJ designed and created figures; PVV supervised sWGS analyses; AEK supervised MLPA analyses; MD supervised the study and MW was in charge of overall direction; BSZ and MD wrote the manuscript; all authors approved the manuscript.

Identification of prognostic factors in childhood T‐cell acute lymphoblastic leukemia: Results from DFCI ALL Consortium Protocols 05‐001 and 11‐001

“…[28][29][30] Additionally, mutational dysregulation of PI3K and Ras pathways have been associated with poor outcomes in childhood T-ALL. [31][32][33][34][35] In a study of adult patients with T-ALL published by the Group for Research in Adult Acute Lymphoblastic Leukemia (GRAALL), the presence of a NOTCH1 activating mutation combined with the absence of PTEN/RAS alterations predicted a favorable outcome. 36 The French Acute Lymphoblastic Leukaemia (FRALLE) Study Group proposed a new pediatric T-ALL risk-stratification paradigm that combined MRD assessment and genetic analysis of NOTCH1, FBXW7, PTEN, KRAS, NRAS.…”

hsa-miR-20b-5p and hsa-miR-363-3p Affect Expression of PTEN and BIM Tumor Suppressor Genes and Modulate Survival of T-ALL Cells In Vitro

“…In pediatric T-ALL, PTEN abnormalities are found in approx. 15% of pediatric T-ALL cases and have been shown, also by our group, to be related to therapy resistance and poor prognosis [26][27][28][29]. BIM (alias BCL2L11) encodes a protein from BCL-2 family of apoptosis-related proteins acting as apoptotic activator [21].…”

lncRNA F11-AS1 Suppresses Glioma by Regulation miRNA-3146/PTEN

“…PTEN is intervened by gene or small-molecule inhibitor. Some good laboratory results on the inhibition of the proliferation of tumor cells by P13K/AKT pathway have been obtained [18][19][20][21][22][23]. The results of this study proved that the overexpression of F11-AS1 causes the decrease of the expression of miRNA-3146, so as to inhibit the PI3K/AKT signaling pathway after the activation of PTEN and inhibit the bioactivity of glioma cells.…”