Relevant bibliographies by topics / Eμ-TCL1 mice

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Academic literature on the topic 'Eμ-TCL1 mice'

Author: Grafiati
Published: 14 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Eμ-TCL1 mice"

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Gobessi, Stefania, Francesca Belfiore, Sara Bennardo, Brendan Doe, Luca Laurenti та Dimitar G. Efremov. "Expression of ZAP-70 Does Not Accelerate Leukemia Development and Progression in the Eμ-TCL1 Transgenic Mouse Model of Chronic Lymphocytic Leukemia". Blood 120, № 21 (2012): 925. http://dx.doi.org/10.1182/blood.v120.21.925.925.

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Abstract Abstract 925 One of the most relevant prognostic factors in chronic lymphocytic leukemia (CLL) is expression of the protein tyrosine kinase ZAP-70. Typically, patients whose leukemic cells express ZAP-70 at 30–100% of the levels in normal T cells have aggressive disease, whereas patients whose leukemic cells do not express ZAP-70 or express only low levels of this protein have indolent disease. Previously, we and others demonstrated that ZAP-70 modulates B-cell receptor signaling and thus affects the capacity of the leukemic cells to respond to antigen stimulation. However, a direct l
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Larsson, Connie A., Kensuke Kojima, Yong Wang та ін. "BET Bromodomain Inhibition Reduces Leukemic Burden and Prolongs Survival In The Eμ-TCL1 Transgenic Mouse Model Of Chronic Lymphocytic Leukemia (CLL) Independent Of TP53 Mutation Status". Blood 122, № 21 (2013): 876. http://dx.doi.org/10.1182/blood.v122.21.876.876.

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Abstract Introduction Inhibition of Brd4, a bromodomain and extra-terminal (BET) protein, results in antiproliferative effects and terminal differentiation in the MYC-driven B-cell malignancies multiple myeloma and Burkitt's lymphoma by selectively repressing MYC. Elevated MYC expression correlates with progression of B-cell chronic lymphocytic leukemia (B-CLL) marking Brd4 as a potential therapeutic target. 17p deletion or somatic TP53 mutations are the poorest prognostic factors in B-CLL, resulting refractoriness to conventional therapy. The recent identification of a Brd4-interacting protei
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Bennardo, Sara, Stefano Iacovelli, Stefania Gobessi та ін. "The Nature of the Antigen Determines Leukemia Development and Behavior in the Eμ-TCL1 Transgenic Mouse Model of CLL". Blood 120, № 21 (2012): 181. http://dx.doi.org/10.1182/blood.v120.21.181.181.

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Abstract Abstract 181 Studies conducted over the past decade have revealed a strong association between the mutational status of the immunoglobulin heavy-chain variable region (IGHV) genes and clinical course in patients with chronic lymphocytic leukemia (CLL). In patients with aggressive CLL, the leukemic cells typically express B cell receptors (BCRs) encoded by unmutated IGHV genes, whereas these genes are most often mutated in leukemic cells from patients with indolent disease. The mutational status of the IGHV genes reflects features of the antigen, such as antigen structure, form, presen
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Wu, Qingli, Zierold Claudia, and Erik A. Ranheim. "Dysregulation of Frizzled 6 Is a Critical Component of B Cell Leukemogenesis in a Mouse Model of Chronic Lymphocytic Leukemia." Blood 110, no. 11 (2007): 347. http://dx.doi.org/10.1182/blood.v110.11.347.347.

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Abstract Wnt/Fzd signaling is known to play a key role in development, tissue specific stem cell maintenance, and tumorigenesis, particularly through the canonical pathway involving stabilization of β-catenin. We have previously shown that Fzd9−/− mice exhibit a decrease in pre-B cells at a stage when self-renewing division is occurring in preference to further differentiation, prior to light chain immunoglobulin recombination. To determine whether pathologic usurpation of this pathway plays a role in B cell leukemogenesis, we examined the expression of Wnt/Fzd pathway genes in the Eμ-TCL1 mou
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Bellone, Matteo, Paolo Dellabona, Arianna Calcinotto, et al. "CD4+ T Cells Sustain Aggressive Chronic Lymphocytic Leukemia through a CD40L-Independent Mechanism." Blood 134, Supplement_1 (2019): 683. http://dx.doi.org/10.1182/blood-2019-128246.

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In Chronic Lymphocytic Leukemia (CLL), mature CD5+ B cells accumulate in lymphoid organs such as bone marrow and lymph nodes where they proliferate and expand within localized proliferation centers. In vitro and in vivo data suggest that survival and proliferation of CLL cells within proliferation centers may be also dependent on microenvironmental interactions originating from the surrounding cellular elements (e.g. monocyte-derived nurse-like cells, mesenchymal stromal cells, or CD4+ T lymphocytes), that deliver both membrane-bound and soluble signals to CLL cells. In particular, the role of
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Alhakeem, Sara S., Mary K. McKenna, Sunil K. Nooti, et al. "Suppression of Anti-Tumor Immunity in Chronic Lymphocytic Leukemia Via Interleukin-10 Production." Blood 128, no. 22 (2016): 3215. http://dx.doi.org/10.1182/blood.v128.22.3215.3215.

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Abstract The most common human leukemia is B-cell chronic lymphocytic leukemia (B-CLL), which is characterized by a progressive accumulation of abnormal B-lymphocytes in blood, bone marrow and secondary lymphoid organs. Typically disease progression is slow, but as the number of leukemic cells increases, they interfere with the production of other important blood cells, causing the patients to be in an immunosuppressive state. To study the basis of this immunoregulation, we used cells from the transgenic Eμ-Tcl1 mouse, which spontaneously develop B-CLL due to a B-cell specific expression of th
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McKenna, Mary Kathryn, Sunil K. Nooti, Sara Samir Alhakeem, et al. "Role of Prostate apoptosis response-4 tumor suppressor in the survival and growth of Chronic Lymphocytic Leukemia." Journal of Immunology 196, no. 1_Supplement (2016): 72.15. http://dx.doi.org/10.4049/jimmunol.196.supp.72.15.

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Abstract Chronic Lymphocytic Leukemia (CLL), the most common adult leukemia in the western world, is characterized by accumulation of clonally expanded CD5+CD19+ B lymphocytes in blood and secondary lymphoid organs with impaired apoptotic mechanisms. Prostate apoptosis response-4 (Par-4) is a pro-apoptotic tumor suppressor protein, which is silenced by promoter methylation in more than 30% of all cancers. It is also secreted and induces apoptosis selectively in many types of cancer cells but not in normal cells. Here we characterized the role of Par-4 in CLL cells using a murine model. The Eμ-
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McClanahan, Fabienne, Cristina Ghirelli, Paul Greaves та ін. "Inhibitory Ligands CD200, CD270, CD274 and CD276 Are Expressed On Eμ-TCL1 Transgenic Mouse Splenocytes and Are of Potential Relevance to Impaired T-Cell Function in Vivo". Blood 120, № 21 (2012): 313. http://dx.doi.org/10.1182/blood.v120.21.313.313.

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Abstract Abstract 313 Background: We have previously demonstrated that CD4 and CD8 T-cells from CLL patients show profound dysfunctions in multiple gene pathways, including the actin cytoskeleton, which impairs the formation of functional immunologic synapses between T cells and APCs. Functional screening assays on Mec-1 cells have identified CD200, CD270, CD274, and CD276 as inhibitory ligands which induce impaired actin synapse formation in both allogeneic and autologous T cells. We also demonstrated that the Eμ-TCL1 transgenic mouse model of CLL closely resembles the T-cell defects observed
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Kriss, Crystina L., Javier A. Pinilla-Ibarz, Adam W. Mailloux, et al. "Overexpression of TCL1 activates the endoplasmic reticulum stress response: a novel mechanism of leukemic progression in mice." Blood 120, no. 5 (2012): 1027–38. http://dx.doi.org/10.1182/blood-2011-11-394346.

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Abstract Chronic lymphocytic leukemia (CLL) represents 30% of adult leukemia. TCL1 is expressed in ∼ 90% of human CLL. Transgenic expression of TCL1 in murine B cells (Eμ-TCL1) results in mouse CLL. Here we show for the first time that the previously unexplored endoplasmic reticulum (ER) stress response is aberrantly activated in Eμ-TCL1 mouse and human CLL. This includes activation of the IRE-1/XBP-1 pathway and the transcriptionally up-regulated expression of Derlin-1, Derlin-2, BiP, GRP94, and PDI. TCL1 associates with the XBP-1 transcription factor, and causes the dysregulated expression o
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Enzler, Thomas, Arnon P. Kater, Weizhou Zhang та ін. "Chronic lymphocytic leukemia of Eμ-TCL1 transgenic mice undergoes rapid cell turnover that can be offset by extrinsic CD257 to accelerate disease progression". Blood 114, № 20 (2009): 4469–76. http://dx.doi.org/10.1182/blood-2009-06-230169.

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AbstractResults of heavy-water labeling studies have challenged the notion that chronic lymphocytic leukemia (CLL) represents an accumulation of noncycling B cells. We examined leukemia cell turnover in Eμ-TCL1 transgenic (TCL1-Tg) mice, which develop a CLL-like disease at 8 to 12 months of age. We found that leukemia cells in these mice not only had higher proportions of proliferating cells but also apoptotic cells than did nonleukemic lymphocytes. We crossed TCL1-Tg with BAFF-Tg mice, which express high levels of CD257. TCL1×BAFF-Tg mice developed CLL-like disease at a significantly younger
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Dissertations / Theses on the topic "Eμ-TCL1 mice"

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Vanni, Francesca. "A novel class of anti-tumoral compounds, pyrrolonaphtoxazepines (PNOXs), targets the p66Shc/STAT4 axis in CLL prymary cells and reduces tumor burden in Eμ-TCL1 mice". Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1140697.

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Chronic lymphocytic leukemia is an haematological malignancy characterized by the accumulation of CD5+CD19+ mature B cell clones in peripheral blood, spleen, lymph nodes and bone marrow (B-CLL). Leukemic cells accumulation is both dependent upon enhanced B cell receptor (BCR)-driven proliferation and defects in the apoptotic machinery. Additionally, alterations of surface chemokine receptors have been accounted for the enhanced accumulation and survival of CLL cells within the secondary lymphoid organs (SLOs). At present, treatment options for CLL patients include drugs targeting proteins part
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