scholarly journals Mechanisms of resistance to EZH2 inhibitors in diffuse large B-cell lymphomas

Blood ◽  
2018 ◽  
Vol 131 (19) ◽  
pp. 2125-2137 ◽  
Author(s):  
Malik Bisserier ◽  
Narendra Wajapeyee
Keyword(s):  
B Cell ◽  
Resistance Mechanisms ◽  
Drug Binding ◽  
Mechanisms Of Resistance ◽  
B Cell Lymphomas ◽  
Survival Pathways ◽  
Key Points ◽  
Large B Cell

Key Points Resistance to EZH2 inhibitors occurs due to the activation of survival pathways and acquired EZH2 mutations that prevent drug binding. Resistance mechanisms for different EZH2 inhibitors varies. Thus, cells resistant to 1 EZH2 inhibitor are sensitive to other inhibitors.

scholarly journals SYK Inhibition Modulates Distinct PI3K/AKT- Dependent Survival Pathways and Cholesterol Biosynthesis in Diffuse Large B Cell Lymphomas

Cancer Cell ◽  
2013 ◽  
Vol 23 (6) ◽  
pp. 826-838 ◽  
Author(s):  
Linfeng Chen ◽  
Stefano Monti ◽  
Przemyslaw Juszczynski ◽  
Jing Ouyang ◽  
Bjoern Chapuy ◽  
...  
Keyword(s):  
B Cell ◽  
Cholesterol Biosynthesis ◽  
B Cell Lymphomas ◽  
Survival Pathways ◽  
Large B Cell

scholarly journals FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas

Blood ◽  
2016 ◽  
Vol 127 (6) ◽  
pp. 739-748 ◽  
Author(s):  
Maciej Szydlowski ◽  
Przemyslaw Kiliszek ◽  
Tomasz Sewastianik ◽  
Ewa Jablonska ◽  
Emilia Bialopiotrowicz ◽  
...  
Keyword(s):  
B Cell ◽  
B Cell Lymphomas ◽  
Akt Inhibitor ◽  
Key Points ◽  
Large B Cell

Key Points In tonic BCR signal-dependent DLBCLs, FOXO1 is required for SYK and AKT inhibitor-induced toxicity.

scholarly journals T-cell defect in diffuse large B-cell lymphomas involves expansion of myeloid-derived suppressor cells

Blood ◽  
2016 ◽  
Vol 128 (8) ◽  
pp. 1081-1092 ◽  
Author(s):  
Imane Azzaoui ◽  
Fabrice Uhel ◽  
Delphine Rossille ◽  
Celine Pangault ◽  
Joelle Dulong ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Clinical Outcomes ◽  
Suppressor Cells ◽  
Myeloid Derived Suppressor Cells ◽  
B Cell Lymphomas ◽  
Key Points ◽  
Cell Inhibition ◽  
Large B Cell ◽  
Cell Defect

Key Points Expansion of circulating monocytic myeloid-derived suppressor cells (MDSCs) correlates with clinical outcomes in patients with DLBCL. Mechanisms of MDSC-dependent T-cell inhibition in DLBCL are related to IL-10, PD-L1, and S100A12.

scholarly journals ATM deficiency promotes development of murine B-cell lymphomas that resemble diffuse large B-cell lymphoma in humans

Blood ◽  
2015 ◽  
Vol 126 (20) ◽  
pp. 2291-2301 ◽  
Author(s):  
Karen S. Hathcock ◽  
Hesed M. Padilla-Nash ◽  
Jordi Camps ◽  
Dong-Mi Shin ◽  
Daniel Triner ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Cell Lymphoma ◽  
Immune Surveillance ◽  
B Cell Lymphoma ◽  
B Cell Lymphomas ◽  
Large B Cell Lymphoma ◽  
Key Points ◽  
Large B Cell

Key Points ATM deficiency promotes the development of murine B-cell lymphomas that model human ABC DLBCL. T cell–dependent immune surveillance may be important to prevent emergence of ATM-deficient B-cell lymphomas.

scholarly journals CARMA1- and MyD88-dependent activation of Jun/ATF-type AP-1 complexes is a hallmark of ABC diffuse large B-cell lymphomas

Blood ◽  
2016 ◽  
Vol 127 (14) ◽  
pp. 1780-1789 ◽  
Author(s):  
Mélanie Juilland ◽  
Montserrat Gonzalez ◽  
Tabea Erdmann ◽  
Yara Banz ◽  
Zala Jevnikar ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Lines ◽  
High Expression ◽  
B Cell Lymphomas ◽  
Key Points ◽  
Large B Cell

Key Points AP-1 complexes of the Jun/ATF type promote growth of ABC DLBCL cell lines. High expression of ATF3 is a hallmark of samples from patients with non-GC/ABC DLBCL.

scholarly journals Genetic basis of PD-L1 overexpression in diffuse large B-cell lymphomas

Blood ◽  
2016 ◽  
Vol 127 (24) ◽  
pp. 3026-3034 ◽  
Author(s):  
Konstantinos Georgiou ◽  
Longyun Chen ◽  
Mattias Berglund ◽  
Weicheng Ren ◽  
Noel F. C. C. de Miranda ◽  
...  
Keyword(s):  
B Cell ◽  
Genetic Basis ◽  
Genetic Alterations ◽  
Genetic Mechanism ◽  
B Cell Lymphomas ◽  
Igh Locus ◽  
Key Points ◽  
Large B Cell

Key Points Translocations between PD-L1 and the IGH locus represent a genetic mechanism of PD-L1 overexpression in DLBCL. Genetic alterations in the PD-L1/PDL-2 locus are mainly associated with the non-GCB subtype of DLBCL.

scholarly journals Exome sequencing reveals novel mutation targets in diffuse large B-cell lymphomas derived from Chinese patients

Blood ◽  
2014 ◽  
Vol 124 (16) ◽  
pp. 2544-2553 ◽  
Author(s):  
Noel F. C. C. de Miranda ◽  
Konstantinos Georgiou ◽  
Longyun Chen ◽  
Chenglin Wu ◽  
Zhibo Gao ◽  
...  
Keyword(s):  
B Cell ◽  
Exome Sequencing ◽  
Novel Mutation ◽  
Notch Pathway ◽  
Chinese Patients ◽  
Deleterious Mutations ◽  
B Cell Lymphomas ◽  
Key Points ◽  
Large B Cell

Key PointsSequencing of Chinese DLBCL reveals novel mutation targets and highlights additional/alternative tumorigenic pathways in these tumors. DTX1 is frequently mutated in Chinese DLBCL and deleterious mutations in this gene contribute to the activation of the Notch pathway.

Molecular Signatures Define New Rational Treatment Targets in Large B-Cell Lymphomas

Hematology ◽  
2007 ◽  
Vol 2007 (1) ◽  
pp. 265-269 ◽  
Author(s):  
Margaret A. Shipp
Keyword(s):  
B Cell ◽  
Clinical Investigation ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Molecular Signatures ◽  
B Cell Lymphomas ◽  
Treatment Regimens ◽  
Lymphoid Malignancies ◽  
Survival Pathways ◽  
Large B Cell

Abstract Diffuse large B-cell lymphomas (DLBCLs), the most common lymphoid malignancies, are clinically and genetically heterogeneous disorders. Although DLBCL is a chemo-responsive tumor, many patients will not be cured with conventional empiric treatment regimens. Gene expression profiles, analyses of specific genetic abnormalities and functional assays have been used to develop comprehensive molecular signatures of tumors that share similar features and rely upon common survival pathways. These studies are leading to the identification of subtype-specific rational therapeutic targets and associated inhibitors for clinical investigation.

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