Relevant bibliographies by topics / B cell lymphoma, Chronic Lymphocytic Leukemia, B lymphocytes, mouse models

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'B cell lymphoma, Chronic Lymphocytic Leukemia, B lymphocytes, mouse models'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "B cell lymphoma, Chronic Lymphocytic Leukemia, B lymphocytes, mouse models"

1

Collins, Ryan, Prabhjot Kaur, Olga Danilova, James Direnzo, and Alexey V. Danilov. "p53 Homolog TAp63 elicits apoptosis in Chronic Lymphocytic Leukemia (CLL) B-Cells,." Blood 118, no. 21 (2011): 3894. http://dx.doi.org/10.1182/blood.v118.21.3894.3894.

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Abstract Abstract 3894 p63 is a p53 homolog whose function depends on the cellular context. The full-length TAp63 variant may carry an anti-oncogenic potential in solid tumor models, where it mediates Ras-induced cellular senescence, antagonizes tumorigenesis and suppresses the development of metastases. In hepatoma cells TAp63 is involved in activation of both extrinsic and intrinsic apoptosis pathways. By contrast, ΔNp63, an amino-terminally truncated p63 variant, is oncogenic in tumors of squamous cell origin. TAp63 is the predominantly expressed p63 isoform in lymphoid malignancies. Increa
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Paoluzzi, Luca, Mithat Gonen, Govind Bhagat, et al. "The BH3-only mimetic ABT-737 synergizes the antineoplastic activity of proteasome inhibitors in lymphoid malignancies." Blood 112, no. 7 (2008): 2906–16. http://dx.doi.org/10.1182/blood-2007-12-130781.

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Abstract Overexpression of antiapoptotic members of the Bcl-2 family is observed in approximately 80% of B-cell lymphomas, contributing to intrinsic and acquired drug resistance. Nullifying the antiapoptotic influence of these proteins can potentially overcome this resistance, and may complement conventional chemotherapy. ABT-737 is a BH3-only mimetic and potent inhibitor of the antiapoptotic Bcl-2 family members Bcl-2, Bcl-XL, and Bcl-w. In vitro, ABT-737 exhibited concentration-dependent cytotoxicity against a broad panel of lymphoma cell lines including mantle cell lymphoma (MCL) and diffus
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Byrd, John C. "Therapeutic Targeting of B-Cell Receptor Signaling Pathways." Blood 120, no. 21 (2012): SCI—27—SCI—27. http://dx.doi.org/10.1182/blood.v120.21.sci-27.sci-27.

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Abstract Abstract SCI-27 Targeted therapy in hematologic malignancies has achieved significant therapeutic success when relatively selective inhibition is attainable to a target dispensable to the majority of normal cells. The best appreciated example of this is imatinib in chronic myeloid leukemia (CML), in which a single translocation forms a fusion protein involving the tyrosine kinase ABL that molecularly defines the disease. Kinase inhibition of ABL in this setting by imatinib (or other second- and third-generation kinase inhibitors) promotes durable, long-term remission in CML patients.
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ElGamal, Dalia, Yiming Zhong, Katie Williams, et al. "PKC Inhibitor AEB071 Demonstrates Pre-Clinical Activity In Chronic Lymphocytic Leukemia." Blood 122, no. 21 (2013): 4187. http://dx.doi.org/10.1182/blood.v122.21.4187.4187.

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Abstract Targeting B-cell receptor (BCR) downstream pathways is of therapeutic importance in eradicating chronic lymphocytic leukemia (CLL) cells. Members of the protein kinase C (PKC) family play an important role in B-cell activation. PKC-β has recently been shown to be over-expressed in CLL and essential to CLL development in the TCL1 mouse model. Mice deficient in PKC-β exhibit a survival defect in response to BCR stimulation, correlating with an inability to induce the NF-κB-dependent anti-apoptotic proteins as Bcl-xL and A1. Moreover, PKC-β-dependent activation of NF-κB in stromal cells
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5

Ghia, Paolo, Maria TS Bertilaccio, Cristina Scielzo, et al. "Novel Mouse Models of Chronic Lymphocytic Leukemia (CLL) Unravel the Molecular Mechanisms Controlling Bone Marrow Involvement by Leukemic B Cells." Blood 114, no. 22 (2009): 360. http://dx.doi.org/10.1182/blood.v114.22.360.360.

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Abstract Abstract 360 In CLL, the bone marrow (BM) represents a typical site of involvement and relapse, suggesting a preferential homing of leukemic cells to this anatomical site compared to other lymphoid organs, though the mechanisms controlling CLL cell migration and accumulation within the BM are unclear. In order to define the rules driving in vivo CLL cell re-circulation between the blood and tissutal compartments, we specifically generated two different mouse models and investigated the role played by HS1; this molecule, other than being a putative prognostic factor in CLL, is also inv
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Walker, Janek S., Casey B. Cempre, Jordan N. Skinner, Brandi R. Walker, John C. Byrd, and Rosa Lapalombella. "Simultaneous Disruption of XPO1 and A20 in Murine B Cells Influences Both B and T Cell Repertoire." Blood 138, Supplement 1 (2021): 1542. http://dx.doi.org/10.1182/blood-2021-152777.

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Abstract Introduction & Objectives: Efforts to characterize the heterogeneity of advanced hematologic malignancies using large-scale genomic studies have identified recurrent monoallelic mutations affecting the E571 residue of the essential nuclear exporter, Exportin-1 (XPO1; E571K in ~80% of cases, E571G in ~15% of cases). E571-XPO1 mutations alter the charge and structural basis of the cargo-binding region, disrupting critical biophysical interactions between XPO1 and its' cargos. Enriched in hematologic malignancies, E571-XPO1 mutations are predominantly reported in chronic lymphocytic
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7

Qin, Hong, Guowei Wei, Ippei Sakamaki, et al. "Novel BAFF-Receptor Antibody to Natively Folded and Glycosylated Recombinant Protein Eliminates Drug Resistant B Cell Malignancies In Vivo." Blood 128, no. 22 (2016): 468. http://dx.doi.org/10.1182/blood.v128.22.468.468.

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Abstract Background: Targeted monoclonal antibodies (mAbs) such as the anti-CD20 rituximab, are proven therapies in lymphoma, yet these diseases remain incurable because of primary or acquired resistance. Using a eukaryotic expression system to produce antigen closely representing endogenous protein, we developed a new therapeutic antibody against an alternative lymphoma target. B cell activating factor receptor (BAFF-R/TNFRSF13C) is a tumor-necrosis factor receptor superfamily member specifically involved in B lymphocyte development and mature B cell survival. Although earlier attempts to tar
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8

Rogers, Kerry A., Dalia El-Gamal, Harrington K. Bonnie, et al. "The Eµ-Myc/TCL1 Transgenic Mouse As a New Aggressive B-Cell Malignancy Model Suitable for Preclinical Therapeutics Testing." Blood 126, no. 23 (2015): 2752. http://dx.doi.org/10.1182/blood.v126.23.2752.2752.

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Abstract Background: Aggressive B-cell lymphomas occurring in the setting of Chronic Lymphocytic Leukemia (CLL) as a large cell transformation are an important clinical problem, and improved mouse models to test novel and targeted therapeutics are needed. The Eµ-Myc mouse overexpresses c-Myc gene which is placed under control of the Myc promoter and lymphoid-specific IgH enhancer (Eµ), resulting in c-Myc overexpression and spontaneous B-cell lymphoma development. The Eµ-Myc mice have been used in drug development, however malignancy develops at variable ages and with differing genetics and res
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9

Schrage, Matthew I., David Kim, Jeffrey Calimlim, et al. "The PIM1 Oncogene Accelerates TCL1 Driven Lymphomagenesis in a Double-Transgenic Murine Model." Blood 112, no. 11 (2008): 1806. http://dx.doi.org/10.1182/blood.v112.11.1806.1806.

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Abstract Previously, we identified and validated PIM-1 as a differentially expressed gene in mantle cell lymphoma (MCL) patient samples. Further, we have shown PIM-1 to be a significant prognostic biomarker in MCL. PIM-1 is an oncogenic serine/threonine kinase that is transcriptionally regulated by cytokines, mitogens, and numerous growth factors. It cooperates with other oncogenes in tumorigenesis and has been implicated in the development of leukemias, lymphomas, late progression events, and most recently in prostate cancer. PIM-1 is overexpressed in aggressive lymphomas, such as the blastoi
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10

Kuo, Hsu-Ping, Sidney Hsieh, Jennifer Whang, Yujun Huang, Mint Sirisawad, and Betty Y. Chang. "Ibrutinib Potentiated NK Cell-Mediated Cytotoxicity in Mouse Models of B-Cell Lymphomas." Blood 128, no. 22 (2016): 4140. http://dx.doi.org/10.1182/blood.v128.22.4140.4140.

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Abstract Background: Ibrutinib, a first-in-class, once-daily oral inhibitor of Bruton's tyrosine kinase (BTK), is indicated by the US FDA for the treatment of patients with chronic lymphocytic leukemia/small lymphocytic lymphoma, including patients with deletion 17p, patients with mantle cell lymphoma who have received at least 1 prior therapy, and patients with Waldenström's macroglobulinemia. In addition to blocking B-cell activation via inhibition of BTK signaling, ibrutinib was reported to modulate immune function by driving TH1 response through IL-2-inducible T-cell kinase (Dubovsky, Bloo
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Dissertations / Theses on the topic "B cell lymphoma, Chronic Lymphocytic Leukemia, B lymphocytes, mouse models"

1

SIMONETTI, GIORGIA. "B lymphoid malignancies: insights from mouse models." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/30033.

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Despite several recent advancements in the treatment of B lymphoproliferative disorders, still a considerable number of lymphoma cases either cannot be cured or become incurable when relapsing. This issue reflects the need for better and more effective therapies that can be designed once novel pathogenic mechanisms have been designed and suitable preclinical models have been established. Therefore, aim of this thesis was to understand the molecular mechanisms leading to mature B lymphoid malignancies by using different mouse models, in order to identify novel potential therapeutic targets and
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You might also be interested in the extended bibliographies on the topic 'B cell lymphoma, Chronic Lymphocytic Leukemia, B lymphocytes, mouse models' for particular source types:
Journal articles
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