AID expression is correlated with Bcr-Abl expression in CML-LBC and can be down-regulated by As2O3 and/or imatinib

Liu, Zi-Jie; Wu, Xia; Duan, Yong; Wang, Yuming; Shan, Bin; Kong, J. H.; Ma, Xiao-Bo; Bao, Yun

doi:10.1016/j.leukres.2011.04.020

Cited by 5 publications

(4 citation statements)

References 20 publications

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“…Ectopic or constitutive expression of AID in neoplastic cells is thought to contribute to a tumor-promoting mutator phenotype because of its widespread and promiscuous mutational and DNA breakage activities (Okazaki et al, 2003;Heintel et al, 2004;Pasqualucci et al, 2008;Klemm et al, 2009;Robbiani et al, 2009;Shinmura et al, 2011). Although the functional significance of AID expression in tumors is not yet fully understood, it appears to have prooncogenic activities relating to tumor initiation, progression, or acquisition of therapy resistance in some cancers (Kou et al, 2007;Klemm et al, 2009;Liu et al, 2011;Shimizu et al, 2012).…”

mentioning

confidence: 99%

Attenuating homologous recombination stimulates an AID-induced antileukemic effect

Lamont

Hasham

Donghia

et al. 2013

Journal of Experimental Medicine

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confidence: 99%

Attenuating homologous recombination stimulates an AID-induced antileukemic effect

Lamont

Hasham

Donghia

et al. 2013

Journal of Experimental Medicine

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“…Whereas the activation of MYC in lymphomas is partially caused by an elevated mutation frequency in several cases, B-cell precursor leukemia has an almost negligible mutation rate [46]. However, BCR-ABL rearranged pre-B-acute lymphoblastic leukemia (ALL) is driven by an aberrant expression of AID [47], which is expressed at such an early stage of B lymphocyte development [48], as a consequence of the enhanced kinase activity of BCR-ABL1 fusion protein (i.e., tyrosine kinase P210) [47,49]. Nevertheless, the proportion of patients harboring mutations at the MYC gene itself among Ph + ALL cases remains low and stable compared with that of Phpatients [47].…”

Section: B Lymphoblastic Leukemia With T(9;22) Bcr-abl1 Rearrangementmentioning

confidence: 99%

MYC’s Fine Line Between B Cell Development and Malignancy

Barrios

Meler

Parra

2020

Cells

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The transcription factor MYC is transiently expressed during B lymphocyte development, and its correct modulation is essential in defined developmental transitions. Although temporary downregulation of MYC is essential at specific points, basal levels of expression are maintained, and its protein levels are not completely silenced until the B cell becomes fully differentiated into a plasma cell or a memory B cell. MYC has been described as a proto-oncogene that is closely involved in many cancers, including leukemia and lymphoma. Aberrant expression of MYC protein in these hematological malignancies results in an uncontrolled rate of proliferation and, thereby, a blockade of the differentiation process. MYC is not activated by mutations in the coding sequence, and, as reviewed here, its overexpression in leukemia and lymphoma is mainly caused by gene amplification, chromosomal translocations, and aberrant regulation of its transcription. This review provides a thorough overview of the role of MYC in the developmental steps of B cells, and of how it performs its essential function in an oncogenic context, highlighting the importance of appropriate MYC regulation circuitry.

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“…ATO combined with all‐trans retinoic acid (ATRA) increases the 50‐month overall survival rate of acute promyelocytic leukaemia (APL) patients to 99%, a result which is superior to ATRA combined with chemotherapy . In addition, ATO combined with TKI showed synergistic anti‐leukaemia effect on chronic myelogenous leukaemia (CML), which is also caused by BCR‐ABL1 . Recently, we found that ATO was able to rewire the response of mantle cell lymphoma (MCL) to the proteasome inhibitor bortezomib .…”

Section: Introductionmentioning

confidence: 99%

Combination of arsenic trioxide and Dasatinib: a new strategy to treat Philadelphia chromosome‐positive acute lymphoblastic leukaemia

Wang

Cheng

Peng

et al. 2017

J Cellular Molecular Medi

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Tyrosine kinase inhibitors (TKIs) have significantly improved the prognosis of Philadelphia chromosome‐positive acute lymphoblastic leukaemia (Ph+ ALL), one of the most common and aggressive forms of haematological malignancies. However, TKI resistance has remained an unsolved issue. In this study, we investigate the impact of adding arsenic trioxide (ATO) on the action of Dasatinib, a second‐generation TKI, in Ph+ ALL. We show that ATO cooperates with Dasatinib in both TKI‐sensitive and resistant Ph+ ALL cell lines to increase apoptosis and we unravel the underlying mechanisms. Indeed, combining ATO and Dasatinib leads to severe cell apoptosis by activating the UPR apoptotic IRE1/JNK/PUMA axis, while neutralizing the UPR ATF4‐dependent anti‐apoptotic axis, activated by ATO alone. Additionally, ATO and Dasatinib in combination repress the expression of several genes, which we previously showed to be associated with shorter survival probability in ALL patients. Overall these data support the use of ATO in combination with Dasatinib as a novel therapeutic regimen for Ph+ ALL patients.

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AID expression is correlated with Bcr-Abl expression in CML-LBC and can be down-regulated by As2O3 and/or imatinib

Cited by 5 publications

References 20 publications

Attenuating homologous recombination stimulates an AID-induced antileukemic effect

Attenuating homologous recombination stimulates an AID-induced antileukemic effect

MYC’s Fine Line Between B Cell Development and Malignancy

Combination of arsenic trioxide and Dasatinib: a new strategy to treat Philadelphia chromosome‐positive acute lymphoblastic leukaemia

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