BCL3 rearrangement, amplification and expression in diffuse large B-cell lymphoma

Ibrahim, Hazem; Amen, Furrat; Reid, Alistair; Naresh, Kikkeri N.

doi:10.1111/j.1600-0609.2011.01684.x

Cited by 7 publications

(6 citation statements)

References 21 publications

(38 reference statements)

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“…The arrest in cell cycle at G2 phase was accompanied by decreased expression of PLK‐1 and cytoplasmic restriction of BCL3 protein. Several evidences have linked down‐regulation of PLK‐1 gene expression coupled with defective nuclear translocation of BCL3 protein to the initiation of B‐cell lymphoblastic leukemia . In contrast to our previous results , pediatric subjects with B‐ALL included in the present study did not show any degradation of CYLD by MALT1.…”

Section: Discussioncontrasting

confidence: 99%

Functional nature of a novel mutant CYLD observed in pediatric lymphoblastic B‐cell leukemia

Arora

Kaul

Varma

2015

Pediatric Blood & Cancer

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The Deubiquitinating enzyme, Cylindromatosis (CYLD), has been established as a crucial regulator of B-cells. The present study was addressed to identify the nature of CYLD-dependent RNomics in patients of pediatric age group with B-ALL. The study revealed the presence of a novel mutant CYLD of 55 kDa in these patients. The mutant CYLD displayed its ability to restrict the cells in G2 phase of cell cycle, down-regulate PLK-1 and block the nuclear translocation of BCL3. Based upon these results, we propose that this mutant CYLD has the capacity to act as a differential marker characteristic of B-cell lymphoblastic leukemia. Pediatr Blood Cancer 2015;62:1066-1069. © 2015 Wiley Periodicals, Inc.

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Section: Discussioncontrasting

confidence: 99%

Functional nature of a novel mutant CYLD observed in pediatric lymphoblastic B‐cell leukemia

Arora

Kaul

Varma

2015

Pediatric Blood & Cancer

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“…BCL3 was statistically significant lower expression levels in bone marrow mononuclear cells of pediatric AML patients, and confirmed using ROC curve analysis revealing that BCL3 was a promising candidate biomarker for pediatric AML at prognosis. This is consistent with findings of previously studies reporting dysregulation of BCL3 expression in T/B cell leukemia [ 16 – 18 ], Hodgkin lymphoma [ 19 , 20 ], T/B cell lymphoma [ 21 , 22 ]. Apart from hematology malignancies, BCL3 has been shown to be participated in progression of diverse solid tumors, such as breast cancer [ 15 ], renal-cell carcinoma [ 13 ], non-small-cell lung cancer [ 12 ], cervical cancer [ 11 ], colorectal cancer [ 23 ].…”

Section: Discussionsupporting

confidence: 93%

BCL3 Expression Is a Potential Prognostic and Predictive Biomarker in Acute Myeloid Leukemia of FAB Subtype M2

Niu

Yang

Chen

et al. 2018

Pathol. Oncol. Res.

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Although the implication of BCL3 has been disclosed in human chronic lymphocytic leukemia as well as other solid tumors, the diagnostic and prognostic of BCL3 expression in acute myeloid leukemia (AML) remains largely unclear. In this study, we isolated total RNA from bone marrow mononuclear cells collected from 101 de novo AML patients and 27 healthy donors. After reverse transcription, quantitative real-time PCR was performed to detect BCL3 expression level. BCL3 mRNA level was significantly down-regulated in BMMCs of AML patients compared with healthy controls ( P = 0.0015). BCL3 was showed a higher level in AML patients with poor-risk karyotypes than that of in patients with favorable/intermediate-risk karyotypes ( P = 0.014). ROC analysis demonstrated that BCL3 could effectively differentiate AML patients from normal controls. Among the French-American-British (FAB) subtypes, the frequency of low BCL3 expression in M2 subtypes is significantly higher than that of in the other subtypes M1/M4/M5/M6/M7 ( P = 0.006), and mildly lower in myelomonocytic/monocytic subtypes M4/M5 ( P = 0.064) than those in M1/M2/M6/M7 subtypes. Chromosome analysis revealed that BCL3 low patients had a remarkably higher frequency of t (8;21) abnormality ( P = 0.0047) and lower frequency of normal karyotype ( P = 0.0059) than BCL3 high patients. BCL3 high patients showed a significantly higher frequency of FLT3-ITD mutation ( P = 0.028) and lower frequency of C-Kit mutation ( P = 0.0232) than BCL3 low patients. Although there were no significant differences in complete remission and overall survival between BCL3 low and BCL3 high groups, patients with high BCL3 expression markedly shorter overall survival (OS, P = 0.049), relapse-free survival (RFS, P = 0.027) and disease-free survival (DFS, P = 0.042) in M2 AML than low BCL3 expression patients. Additionally, in AMLs of M2 subtype, high BCL3 expression patients had markedly lower complete remission (CR) rate ( P = 0.0317) after the second induction treatment than patients with BCL3 low expression. Thus, these findings indicated that BCL3 appeared as a promising molecular biomarker of pediatric acute myeloid leukemia with unfavorable prognosis.

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“…In addition, several other miRNAs located on chromosome 19q13.42, such as miR-520g, miR-520h, and miR-520b, have been found to be downregulated in multiple myeloma [53]. Although recurrent translocations involving chromosome 19q13 such as t(14;19)(q32.3;q13.2) have been reported in B-cell malignancies, they are extremely rare [54], [55]. Given that epigenetics has a profound effect on the regulation of miRNA expression and DNA hypermethylation has been shown to be involved in the decrease of miRNA in lymphomas, we examined if the decreased expression of miR-520c in DLBCLs as compared to normal B cells could be due to hypermethylation of the genomic locus (Text S1, Figure S8, Table S4).…”

Section: Discussionmentioning

confidence: 99%

Down-Regulation of eIF4GII by miR-520c-3p Represses Diffuse Large B Cell Lymphoma Development

et al. 2014

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Deregulation of the translational machinery is emerging as a critical contributor to cancer development. The contribution of microRNAs in translational gene control has been established however; the role of microRNAs in disrupting the cap-dependent translation regulation complex has not been previously described. Here, we established that elevated miR-520c-3p represses global translation, cell proliferation and initiates premature senescence in HeLa and DLBCL cells. Moreover, we demonstrate that miR-520c-3p directly targets translation initiation factor, eIF4GII mRNA and negatively regulates eIF4GII protein synthesis. miR-520c-3p overexpression diminishes cells colony formation and reduces tumor growth in a human xenograft mouse model. Consequently, downregulation of eIF4GII by siRNA decreases translation, cell proliferation and ability to form colonies, as well as induces cellular senescence. In vitro and in vivo findings were further validated in patient samples; DLBCL primary cells demonstrated low miR-520c-3p levels with reciprocally up-regulated eIF4GII protein expression. Our results provide evidence that the tumor suppressor effect of miR-520c-3p is mediated through repression of translation while inducing senescence and that eIF4GII is a key effector of this anti-tumor activity.

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BCL3 rearrangement, amplification and expression in diffuse large B-cell lymphoma

Cited by 7 publications

References 21 publications

Functional nature of a novel mutant CYLD observed in pediatric lymphoblastic B‐cell leukemia

Functional nature of a novel mutant CYLD observed in pediatric lymphoblastic B‐cell leukemia

BCL3 Expression Is a Potential Prognostic and Predictive Biomarker in Acute Myeloid Leukemia of FAB Subtype M2

Down-Regulation of eIF4GII by miR-520c-3p Represses Diffuse Large B Cell Lymphoma Development

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