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Background  Knowledge of the oncogenic signaling pathways of T-cell acute lymphoblastic leukemia (T-ALL) remains limited. Constitutive aberrant activation of the nuclear factor kappa B (NF-κB) signaling pathway has been detected in various lymphoid malignancies and plays a key role in the development of these carcinomas. The zinc finger-containing protein, A20, is a central regulator of multiple NF-κB-activating signaling cascades. A20 is frequently inactivated by deletions and/or mutations in several B-and T-cell lymphoma subtypes. However, few  A20  mutations and polymorphisms have been reported in T-ALL. Thus, it is of interest to analyze the expression characteristics of  A20  and its regulating factors, including upstream regulators and the CBM complex, which includes  CARMA1 ,  BCL10 , and  MALT1 .    Methods  The expression levels of  CARMA1 ,  BCL10 ,  MALT1 ,  A20 , and  NF-κB  were detected in peripheral blood mononuclear cells (PBMCs) from 21 patients with newly diagnosed T-ALL using real-time PCR, and correlations between the aberrant expression of these genes in T-ALL was analyzed. Sixteen healthy individuals, including 10 males and 6 females, served as controls.    Results  Significantly lower  A20  expression was found in T-ALL patients (median: 4.853) compared with healthy individuals (median: 8.748;  P  = 0.017), and significantly increased expression levels of  CARMA1  (median: 2.916;  P  = 0.034),  BCL10  (median: 0.285;  P  = 0.033), and  MALT1  (median: 1.201;  P  = 0.010) were found in T-ALL compared with the healthy individuals (median: 1.379, 0.169, and 0.677, respectively). In contrast, overexpression of  NF-κB  (median: 0.714) was found in T-ALL compared with healthy individuals (median: 0.335;  P  = 0.001). A negative correlation between the  MALT1  and  A20  expression levels and a positive correlation between  CARMA1  and  BCL10  were found in T-ALL and healthy individuals. However, no negative correlation was found between  A20  and  NF-κB  and the  MALT1  and  NF-κB  expression level in the T-ALL group.    Conclusions  We characterized the expression of the  CARMA-BCL10-MALT1-A20-NF-κB  pathway genes in T-ALL. Overexpression of  CARMA-BCL10-MALT  in T-ALL may contribute to the constitutive cleavage and inactivation of  A20 , which enhances  NF-κB  signaling and may be related to T-ALL pathogenesis.

Characteristics of CARMA1-BCL10-MALT1-A20-NF-κB expression in T cell-acute lymphocytic leukemia