C-myc protein expression in B-cell acute lymphoblastic leukemia, prognostic significance?

Allen, Ashleigh; Gill, Kamraan Z.; Hoehn, Daniela; Sulis, Maria Luisa; Bhagat, Govind; Alobeid, Bachir

doi:10.1016/j.leukres.2014.06.022

Cited by 20 publications

(19 citation statements)

References 28 publications

(30 reference statements)

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“…Aberrations that can alter the expression of c‐Myc are involved in many hematological malignancies, especially in Burkitt's lymphoma and diffuse large B‐cell lymphoma . However, so far, only a single previous work by Allen et al suggested a possible association of c‐Myc with a higher risk of relapse in BCP‐ALL.…”

Section: Discussionmentioning

confidence: 99%

Che‐1 is targeted by c‐Myc to sustain proliferation in pre‐B‐cell acute lymphoblastic leukemia

Folgiero

Socolovschi²,

Pallocca³

et al. 2018

EMBO Reports

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Despite progress in treating B-cell precursor acute lymphoblastic leukemia (BCP-ALL), disease recurrence remains the main cause of treatment failure. New strategies to improve therapeutic outcomes are needed, particularly in high-risk relapsed patients. Che-1/AATF (Che-1) is an RNA polymerase II-binding protein involved in proliferation and tumor survival, but its role in hematological malignancies has not been clarified. Here, we show that Che-1 is overexpressed in pediatric BCP-ALL during disease onset and at relapse, and that its depletion inhibits the proliferation of BCP-ALL cells. Furthermore, we report that c-Myc regulates Che-1 expression by direct binding to its promoter and describe a strict correlation between Che-1 expression and c-Myc expression. RNA-seq analyses upon Che-1 or c-Myc depletion reveal a strong overlap of the respective controlled pathways. Genomewide ChIP-seq experiments suggest that Che-1 acts as a downstream effector of c-Myc. These results identify the pivotal role of Che-1 in the control of BCP-ALL proliferation and present the protein as a possible therapeutic target in children with relapsed BCP-ALL.

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Section: Discussionmentioning

confidence: 99%

Che‐1 is targeted by c‐Myc to sustain proliferation in pre‐B‐cell acute lymphoblastic leukemia

Folgiero

Socolovschi²,

Pallocca³

et al. 2018

EMBO Reports

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“…MondoA has been proposed to function as an oncogene in B-cell acute lymphoblastic leukaemia ( Wernicke et al , 2012 ). The function of c-Myc in B-ALL is not well studied, but elevated c-Myc levels do associate with increased risk of persistent disease ( Allen et al , 2014 ). Whether MondoA is required for B-ALL growth and tumourigenesis or is required to support other c-Myc-driven B-cell lymphomas such as Burkitt's and diffuse large B-cell should be investigated ( Slack and Gascoyne, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis

Wilde

Ayer

2015

Br J Cancer

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Metabolic reprogramming towards aerobic glycolysis is a common feature of transformed cells and can be driven by a network of transcription factors. It is well established that c-Myc and hypoxia-inducible factor-1α (HIF-1α) contribute to metabolic reprogramming by driving the expression of glycolytic target genes. More recently, the c-Myc-related transcription factor MondoA has been shown to restrict glucose uptake and aerobic glycolysis via its induction of thioredoxin-interacting protein (TXNIP). Three recent studies demonstrate that complex and cancer type-specific interactions between c-Myc, MondoA and HIF-1α underlie metabolism, tumourigenesis and drug response. In triple-negative breast cancer, c-Myc blocks MondoA-dependent activation of TXNIP to stimulate aerobic glycolysis. In contrast, in neuroblastoma, N-Myc requires MondoA for metabolic reprogramming and tumourigenesis. Finally, the therapeutic response of BRAFV600E melanoma cells to vemurafenib requires downregulation of c-Myc and HIF-1α and upregulation of MondoA-TXNIP, and the subsequent reprogramming away from aerobic glycolysis. In this minireview we highlight the findings in these three studies and present a working model to explain why c-Myc and MondoA function cooperatively in some cancers and antagonistically in others.

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“…All samples were collected at the Affiliated hospital of Guangdong Medical University (Zhanjiang, China). Diagnosis of B-ALL was determined according to the accepted WhO criteria (24)(25)(26). Control samples were obtained from 10 patients with unexplained fever or anemia whose bone marrow aspirates was demonstrated to be normal bone marrow morphology.…”

Section: Methodsmentioning

confidence: 99%

Integrated analysis of microRNA and transcription factor reveals important regulators and regulatory motifs in adult B-cell acute lymphoblastic leukemia

Lin

Liu

Zhang

et al. 2016

International Journal of Oncology

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B-cell acute lymphoblastic leukemia (B‑ALL) is an aggressive hematological malignancy and a leading cause of cancer-related mortality in children and young adults. The molecular mechanisms involved in the regulation of its gene expression has yet to be fully elucidated. In the present study, we performed large scale expression profiling of microRNA (miRNA) and transcription factor (TF) by Illumina deep‑sequencing and TF array technology, respectively, and identified 291 differentially expressed miRNAs and 201 differentially expressed TFs in adult B‑ALL samples relative to their controls. After integrating expression profile data with computational prediction of miRNA and TF targets from different databases, we construct a comprehensive miRNA‑TF regulatory network specifically for adult B‑ALL. Network function analysis revealed 25 significantly enriched pathways, four pathways are well‑known to be involved in B‑ALL, such as PI3K‑Akt signaling pathway, Jak‑STAT signaling pathway, Ras signaling pathway and cell cycle pathway. By analyzing the network topology, we identified 28 hub miRNAs and 19 hub TFs in the network, and found nine potential B‑ALL regulators among these hub nodes. We also constructed a Jak‑STAT signaling sub‑network for B‑ALL. Based on the sub‑network analysis and literature survey, we proposed a cellular model to discuss MYC/miR‑15a‑5p/FLT3 feed-forward loop (FFL) with Jak‑STAT signaling pathway in B‑ALL. These findings enhance our understanding of this disease at the molecular level, as well as provide putative therapeutic targets for B-ALL.

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C-myc protein expression in B-cell acute lymphoblastic leukemia, prognostic significance?

Cited by 20 publications

References 28 publications

Che‐1 is targeted by c‐Myc to sustain proliferation in pre‐B‐cell acute lymphoblastic leukemia

Che‐1 is targeted by c‐Myc to sustain proliferation in pre‐B‐cell acute lymphoblastic leukemia

Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis

Integrated analysis of microRNA and transcription factor reveals important regulators and regulatory motifs in adult B-cell acute lymphoblastic leukemia

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