The combined expression of VPREB3 and ID3 represents a new helpful tool for the routine diagnosis of mature aggressive B‐cell lymphomas

Soldini, Davide; Georgis, Antoin; Montagna, Chiara; Schüffler, Peter J.; Martin, Vittoria; Curioni-Fontecedro, Alessandra; Martinez, Antonio; Tinguely, Marianne

doi:10.1002/hon.2094

Cited by 6 publications

(6 citation statements)

References 20 publications

(47 reference statements)

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“…The expression of Vpreb3/ pre B-lymphocyte protein 3 was found to be decreased in MMP-9 −/− mice compared to WT mice in both control and DSS conditions. Vpreb3 is expressed during B-cell differentiation in subsets of mature B lymphocytes and is linked to formation of B-cell lymphomas31. Many genes ( n =249) were found to be uniquely expressed by MMP-9 −/− mice after DSS administration.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of gelatinase B/MMP-9 does not attenuate colitis in murine models of inflammatory bowel disease

et al. 2017

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One third of patients with inflammatory bowel disease (IBD) inadequately respond to anti-TNF treatment and preclinical data suggest that matrix metalloproteinase-9 (MMP-9) is a novel therapeutic target. Here we show that IBD clinical and histopathological parameters found in wild type mice challenged with three different models of colitis, acute and chronic dextran sodium sulphate (DSS), and acute 2,4,6-trinitrobenzenesulfonic acid-induced colitis are not attenuated in MMP-9 knockout mice. We find similar colonic gene expression profiles in wild type and MMP-9 knockout mice in control and acute DSS conditions with the exception of eleven genes involved in antimicrobial response during colitis. Parameters of chronic colitis are similar in wild type and MMP-9 knockout mice. Pharmacological inhibition of MMP-9 with bio-active peptides does not improve DSS colitis. We suggest that MMP-9 upregulation is a consequence rather than a cause of intestinal inflammation and we question whether MMP-9 represents a disease target in IBD.

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Section: Discussionmentioning

confidence: 99%

Inhibition of gelatinase B/MMP-9 does not attenuate colitis in murine models of inflammatory bowel disease

et al. 2017

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“…Similarly, we found CCN2 upregulated in B-ALL compared to T-ALL ( Table 3 ). It is worth highlighting that VPREB3 is a B-cell receptor component [100], which explains its upregulation in B-ALL compared to T-ALL ( Table 3 ). Increased gene expression of this gene can activate the pro-survival phosphatidylinositol-3-OH kinase pathway [100].…”

Section: Resultsmentioning

confidence: 99%

“…It is worth highlighting that VPREB3 is a B-cell receptor component [100], which explains its upregulation in B-ALL compared to T-ALL ( Table 3 ). Increased gene expression of this gene can activate the pro-survival phosphatidylinositol-3-OH kinase pathway [100]. Recently, another study also analyzed molecular differences between B-ALL and T-ALL and found VPREB3 as a methylation and expression signature gene [101].…”

Section: Resultsmentioning

confidence: 99%

Data-driven discovery of gene expression markers distinguishing pediatric acute lymphoblastic leukemia subtypes

Nourbakhsh,

Tom,

Schrøder Lassen

et al. 2024

Preprint

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Acute lymphoblastic leukemia (ALL), the most common cancer in children, is overall divided into two subtypes, B-cell precursor ALL (B-ALL) and T-cell ALL (T-ALL), which have different molecular characteristics. Despite massive progress in understanding the disease trajectories of ALL, ALL remains a major cause of death in children. Thus, further research exploring the biological foundations of ALL is essential. Here, we examined the diagnostic, prognostic, and therapeutic potential of gene expression data in pediatric patients with ALL. We discovered a subset of expression markers differentiating B- and T-ALL:CCN2,VPREB3,NDST3,EBF1, RN7SKP185, RN7SKP291, SNORA73B, RN7SKP255, SNORA74A, RN7SKP48, RN7SKP80, LINC00114, a novel gene (ENSG00000227706), and 7SK. The expression level of these markers all demonstrated significant effects on survival of the patients, comparing the two subtypes. We also discovered four expression subgroups in the expression data with eight genes driving separation between two of these predicted subgroups. A subset of the 14 markers could separate B- and T-ALL in an independent cohort of patients with ALL. This study can enhance our knowledge of the transcriptomic profile of different ALL subtypes.

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“…Additionally, ID1 and ID3 coexpression was correlated with a poor clinical outcome in patients with locally advanced non-small cell lung cancer treated with definitive chemoradiotherapy [ 39 ]. The combined expression of VPREB3 and ID3 was used to develop a new helpful tool for the routine diagnosis of mature aggressive B-cell lymphomas [ 40 ]. All these results suggested the prognostic value of ID3 expression in diverse human cancers.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of ID genes reveals the clinical and prognostic value of ID3 expression in acute myeloid leukemia using bioinformatics identification and experimental validation

Zhao

Wang

et al. 2022

BMC Cancer

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Background Dysregulation of inhibitor of differentiation/DNA binding (ID) genes is linked to cancer growth, angiogenesis, invasiveness, metastasis and patient survival. Nevertheless, few investigations have systematically determined the expression and prognostic value of ID genes in acute myeloid leukemia (AML). Methods The expression and clinical prognostic value of ID genes in AML were first identified by public databases and further validated by our research cohort. Results Using public data, the expression of ID1/ID3 was markedly downregulated in AML, and the expression of ID2 was greatly upregulated in AML, whereas ID4 showed no significant difference. Among the ID genes, only ID3 expression may be the most valuable prognostic biomarker in both total AML and cytogenetically normal AML (CN-AML) and especially in CN-AML. Clinically, reduced ID3 expression was greatly associated with higher white blood cell counts, peripheral blood/bone marrow blasts, normal karyotypes and intermediate cytogenetic risk. In addition, low ID3 expression was markedly related to FLT3 and NPM1 mutations as well as wild-type TP53. Despite these associations, multivariate Cox regression analysis revealed that ID3 expression was an independent risk factor affecting overall survival (OS) and disease free survival (DFS) in CN-AML patients. Biologically, a total of 839 mRNAs/lncRNAs and 72 microRNAs were found to be associated with ID3 expression in AML. Importantly, the expression of ID3 with discriminative value in AML was further confirmed in our research cohort. Conclusion The bioinformatics analysis and experimental verification demonstrate that low ID3 expression independently affects OS and DFS in patients with CN-AML, which might be seen as a potential prognostic indicator in CN-AML.

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The combined expression of VPREB3 and ID3 represents a new helpful tool for the routine diagnosis of mature aggressive B‐cell lymphomas

Cited by 6 publications

References 20 publications

Inhibition of gelatinase B/MMP-9 does not attenuate colitis in murine models of inflammatory bowel disease

Inhibition of gelatinase B/MMP-9 does not attenuate colitis in murine models of inflammatory bowel disease

Data-driven discovery of gene expression markers distinguishing pediatric acute lymphoblastic leukemia subtypes

Comprehensive analysis of ID genes reveals the clinical and prognostic value of ID3 expression in acute myeloid leukemia using bioinformatics identification and experimental validation

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