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Статті в журналах з теми "Eμ-TCL1 mice"

Автор: Grafiati

Опубліковано: 14 березня 2023

Оновлено: 31 липня 2025

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Nganga, Vincent K., Victoria L. Palmer, Hina Naushad та ін. "Accelerated progression of chronic lymphocytic leukemia in Eμ-TCL1 mice expressing catalytically inactive RAG1". Blood 121, № 19 (2013): 3855–66. http://dx.doi.org/10.1182/blood-2012-08-446732.

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Key Points Expressing dominant-negative RAG1 to inhibit BCR editing of autoreactivity in CLL-prone Eμ-TCL1 mice accelerates disease onset. Gene expression profiling studies provide evidence of distinct but convergent pathways for CLL development.

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12

Wu, Qingli, and Erik A. Ranheim. "Upregulation of Genes Involved in the Beta-Catenin Signaling Pathway in a Mouse Model of Chronic Lymphocytic Leukemia." Blood 104, no. 11 (2004): 1121. http://dx.doi.org/10.1182/blood.v104.11.1121.1121.

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Abstract Binding of Wnt ligands to Frizzled (Fzd) family and LRP5/6 receptors results in stabilization of beta-catenin protein, its translocation to the nucleus, and in association with LEF/TCF family transcription factors, expression of target genes. This canonical Wnt signaling pathway plays a critical role in development and in the maintenance of tissue specific stem cell populations in the skin, gut, and bone marrow. Dysregulation of the beta-catenin signaling pathway has been described in numerous human malignancies, including chronic lymphocytic leukemia (CLL). Using the Eμ-TCL1 transgen

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13

Grioni, Matteo, Arianna Brevi, Elena Cattaneo та ін. "CD4+ T cells sustain aggressive chronic lymphocytic leukemia in Eμ-TCL1 mice through a CD40L-independent mechanism". Blood Advances 5, № 14 (2021): 2817–28. http://dx.doi.org/10.1182/bloodadvances.2020003795.

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Abstract Chronic lymphocytic leukemia (CLL) is caused by the progressive accumulation of mature CD5+ B cells in secondary lymphoid organs. In vitro data suggest that CD4+ T lymphocytes also sustain survival and proliferation of CLL clones through CD40L/CD40 interactions. In vivo data in animal models are conflicting. To clarify this clinically relevant biological issue, we generated genetically modified Eμ-TCL1 mice lacking CD4+ T cells (TCL1+/+AB0), CD40 (TCL1+/+CD40−/−), or CD8+ T cells (TCL1+/+TAP−/−), and we monitored the appearance and progression of a disease that mimics aggressive human

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14

Ramsay, Alan G., Gullu Gorgun, Tobias A. W. Holderried, et al. "A Mouse Model for Immunotherapeutic Reversal of Leukemia-Induced T Cell Dysfunction." Blood 112, no. 11 (2008): 30. http://dx.doi.org/10.1182/blood.v112.11.30.30.

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Abstract Understanding the elusive mechanisms of tumor-driven immune evasion will aid the refinement of existing cancer immunotherapy strategies and identify novel treatments. To date, pre-clinical animal models that closely model human cancer, including the immune suppressive mechanisms utilized by cancer cells, have been under-characterized. The identification and use of such models should allow better predictions of successful human responses to immunotherapy. As a model for changes induced in non-malignant cells by cancer, we examined T cell function in Eμ-TCL1 transgenic mice as they deve

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15

Reinart, Nina, Malgorzata Ciesla, Cornelia Rudolph, et al. "Macrophage Migration Inhibitory Factor (MIF) Promotes the Development of Murine Chronic Lymphocytic Leukemia (CLL)." Blood 112, no. 11 (2008): 27. http://dx.doi.org/10.1182/blood.v112.11.27.27.

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Abstract Introduction: Tumor formation results from a complex interplay between genetic/epigenetic alterations, cell cycle dysregulation and promotion by the tumor environment. Stimulation by extracellular survival factors is important for chronic lymphocytic leukemia (CLL), since the leukemic cells undergo spontaneous apoptosis when removed from their normal milieu. Since preliminary experiments demonstrated that macrophage migration inhibitory factor (MIF), a chemokine-like proinflammatory mediator and an intracellular regulator of growth and apoptosis, is overexpressed in human CLL, we inve

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16

Gamal, Wael, Nienke B. Goedhart, Helga Simon-Molas, et al. "Reprogramming CLL T-Cell Mitochondrial Fitness Using PI3K Inhibition for Enhancing CAR T-Cell Therapy." Blood 144, Supplement 1 (2024): 4803. https://doi.org/10.1182/blood-2024-210992.

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Chronic lymphocytic leukemia (CLL) presents a significant clinical shortfall, as the number of patients developing resistance to both BTK inhibitors and Bcl2-targeted therapies is rapidly increasing. To date, chimeric antigen receptor (CAR) T cells have shown restricted success in CLL, attributed to CLL-induced T-cell dysfunction and a shift toward terminally differentiated cell subsets. The mechanisms behind these T-cell changes are still not well-understood. T-cell activation and differentiation are metabolically demanding processes. Previously, we identified abnormal T-cell metabolic proper

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17

Scielzo, Cristina, Maria T. S. Bertilaccio, Giorgia Simonetti, et al. "HS1 has a central role in the trafficking and homing of leukemic B cells." Blood 116, no. 18 (2010): 3537–46. http://dx.doi.org/10.1182/blood-2009-12-258814.

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Abstract The function of the intracellular protein hematopoietic cell–specific Lyn substrate-1 (HS1) in B lymphocytes is poorly defined. To investigate its role in migration, trafficking, and homing of leukemic B lymphocytes we have used B cells from HS1−/− mice, the HS1-silenced human chronic lymphocytic leukemia (CLL) MEC1 cell line and primary leukemic B cells from patients with CLL. We have used both in vitro and in vivo models and found that the lack of expression of HS1 causes several important functional effects. In vitro, we observed an impaired cytoskeletal remodeling that resulted in

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18

Gamal, Wael, Melanie Mediavilla Varela, Angimar Uriepero Palma, et al. "Identifying the Role of Endoplasmic Reticulum Stress in CLL T-Cell Dysfunction." Blood 144, Supplement 1 (2024): 1848. https://doi.org/10.1182/blood-2024-210608.

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Chronic lymphocytic leukemia (CLL) presents a significant clinical challenge due to the increasing incidence of resistance to targeted therapies. Despite the potential of adoptive T-cell therapy (ACT), its efficacy in CLL has been limited, mainly due to CLL-induced T-cell dysfunction and a skewed differentiation toward terminal subsets. The underlying mechanisms of these T-cell alterations remain poorly understood. Given that T-cell activation and differentiation are metabolically intensive processes, previous research (van Bruggen et al, Blood 2019) has highlighted aberrant mitochondrial prop

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19

Ferrer, Gerardo, Xiao-Jie Yan, Brendan Franca, et al. "Chronic Lymphocytic Leukemia Patients and Eµ-TCL1 Mice Share a Phenotype of Functional Granulocyte-like and Dysfunctional Monocyte-like Myeloid Derived Suppressor Cells." Blood 126, no. 23 (2015): 614. http://dx.doi.org/10.1182/blood.v126.23.614.614.

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Abstract Immune imbalance is a common characteristic of patients with chronic lymphocytic leukemia (CLL). This feature is shared with Eμ-TCL1 transgenic mice that, like CLL patients, exhibit an expansion of CD5+ B cells with associated non-B-cell defects. In patients and in mice, T-cell responses are often ineffective. This alteration is generally considered due to the direct effects of the leukemic cells. The expansion of myeloid derived suppressor cells (MDSCs), which play a major role in helping tumor cells escape immune surveillance by inhibiting T-cell responses, is promoted by many cance

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20

Alhakeem, Sara Samir, Mary Kathryn McKenna, Beth W. Gachuki, et al. "The role of IL-10 in B-cell chronic lymphocytic leukemia cell survival." Journal of Immunology 196, no. 1_Supplement (2016): 211.17. http://dx.doi.org/10.4049/jimmunol.196.supp.211.17.

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Abstract B-cell chronic lymphocytic leukemia (B-CLL) is characterized by the progressive accumulation of abnormal lymphocytes in the periphery. Typically the 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 B-CLL we use cells from the transgenic Eμ-Tcl1 mouse, which spontaneously develop B-CLL. Previously we showed that Eμ-Tcl1 CLL cells produce an anti-inflammatory cytokine, IL-10, constitutively. Here we studied the role of IL-10 in

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21

Enzler, Thomas, Weizhou Zhang, Arnon P. Kater, et al. "Constitutive Baff Signalling Plays a Key Role in CLL Development by Promoting Tumor Cell Survival." Blood 112, no. 11 (2008): 28. http://dx.doi.org/10.1182/blood.v112.11.28.28.

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Abstract The B cell-activating factor of the tumor necrosis factor family (BAFF) is a potent B-cell survival factor. We recently found that nurselike cells, which presumably reside in the leukemia-microenvironment, express BAFF, which promotes survival of leukemia cells of patients with chronic lymphocytic leukemia (CLL) cells through activation of the classical NF-kB pathway. To study the influence of BAFF on leukemogenesis, we crossed BAFF transgenic (Tg) mice with either Eμ-TCL-Tg mice, which develop a lymphoproliferative disease resembling human CLL at about 12 months of age, or Ea-MYC-Tg

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22

Gobessi, Stefania, Sara Bennardo, Pablo G. Longo, Brendan Doe, and Dimitar G. Efremov. "Development of a Transgenic Mouse Model to Study the Role of ZAP-70 in the Development and Progression of Chronic Lymphocytic Leukemia." Blood 118, no. 21 (2011): 2830. http://dx.doi.org/10.1182/blood.v118.21.2830.2830.

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Abstract Abstract 2830 The protein tyrosine kinase ZAP-70 is an important prognostic factor in chronic lymphocytic leukemia (CLL). Patients that are considered ZAP-70-positive typically express 30–100% of the levels of ZAP-70 in T-cells, whereas in the remaining patients ZAP-70 is either not expressed or is expressed at lower levels. ZAP-70-positive patients have more aggressive disease and shorter survival than patients with low or absent ZAP-70. In vitro experiments with human lymphoma cell lines and primary CLL B-cells have shown that ZAP-70 is involved in B cell receptor (BCR) signaling, i

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23

Lee, Avery C., Sai R. Pingali, Javier A. Pinilla-Ibarz, Chih-Hang A. Tang, and Chih-Chi A. Hu. "Abstract 142: Loss of AID exacerbates the malignant progression of CLL." Cancer Research 82, no. 12_Supplement (2022): 142. http://dx.doi.org/10.1158/1538-7445.am2022-142.

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Abstract Activation-induced cytidine deaminase (AID) is an enzyme that has been implicated as both a positive and a negative factor in the progression of B cell chronic lymphocytic leukemia (CLL), but the role that it plays in the development and progression of this disease is still unclear. Higher AID expression in patients has been correlated with a worse prognosis, but patients with mutated immunoglobulin (IgHV) genes, which requires AID activity, have a better prognosis. To elucidate the role of AID in leukemic progression, we generated an AID-deficient mouse model of CLL, AID-/-/Eμ-TCL1,

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24

Bondada, Subbarao, James P. Collard, Mary Kathryn McKenna, et al. "The role of the splenic microenvironment in Chronic Lymphocytic Leukemia." Journal of Immunology 204, no. 1_Supplement (2020): 163.6. http://dx.doi.org/10.4049/jimmunol.204.supp.163.6.

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Abstract Chronic Lymphocytic Leukemia (CLL), the most prevalent adult leukemia, is characterized by the clonal expansion of CD5+ CD19+ B cells within lymphoid organs and accumulation of quiescent cells in the blood. Eμ-Tcl1 transgenic mice expressing the Tcl1 oncogene in a B cell-specific manner develop CLL and adoptive transfer of CLL cells from these mice induces CLL growth in C57BL/6 mice. These models typically cause splenomegaly as the CLL burden increases, and CLL cells localize mainly in the spleen within the first 10 days post-injection. We hypothesized that the splenic microenvironmen

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25

Märklin, Melanie, Stefanie Bugl, Jonas S. Heitmann, et al. "Genetic Loss of NFAT2 Induces Profound Acceleration of CLL in the TCL1 Mouse Model." Blood 120, no. 21 (2012): 862. http://dx.doi.org/10.1182/blood.v120.21.862.862.

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Abstract Abstract 862 NFAT is a family of highly phosphorylated proteins residing in the cytoplasm of resting cells. Upon dephosphorylation by calcineurin, NFAT proteins translocate to the nucleus where they orchestrate developmental and activation programs in diverse cell types. NFAT is inactivated and relocated to the cytoplasm by a network of several kinases. Although identified originally as a major transcriptional regulator in T cells, it is now clear that NFAT transcription factors also possess important roles in other cells of the hematopoietic system including dendritic cells, mast cel

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26

McKenna, Mary Kathryn, Sunil K. Noothi, Sara Samir Alhakeem, et al. "Splenic microenvironment is important in the survival and growth of Chronic Lymphocytic Leukemia in mice." Journal of Immunology 198, no. 1_Supplement (2017): 130.20. http://dx.doi.org/10.4049/jimmunol.198.supp.130.20.

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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 the peripheral blood and secondary lymphoid organs. CLL cell survival is dependent on B cell receptor signaling and cross-talk within the leukemia microenvironment. CLL presents with enlargement of the spleen, and lymph nodes due to accumulation of long-lived lymphocytes with impaired apoptotic mechanisms. The Eμ-Tcl1 mice, with a B cell specific overexpression of the oncogene, T cell Leukemia 1 (Tcl1), serve as an ex

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27

Woyach, Jennifer A., Matthew R. Stefanovski, Virginia Goettl, et al. "Global Inhibition of Bruton's Tyrosine Kinase (BTK) Delays the Development and Expansion of Chronic Lymphocytic Leukemia (CLL) in the TCL1 Mouse Model of Disease." Blood 120, no. 21 (2012): 183. http://dx.doi.org/10.1182/blood.v120.21.183.183.

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Abstract Abstract 183 CLL is a common leukemia which demonstrates variable reactivity of the B cell receptor (BCR) to antigen ligation, but constitutive activation of this pathway. Bruton's Tyrosine Kinase (BTK) is a member of this pathway which shows transcriptional upregulation and constitutive activity in CLL. Ongoing trials of ibrutinib, an orally bioavailable inhibitor of BTK, have shown outstanding preliminary activity in CLL. However results with other known reversible and more selective irreversible BTK inhibitors have had variable results. As ibrutinib potentially has other targets in

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28

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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29

Minden, Marcus Dühren-von, Thomas Wossning, Hassan Jumaa та Hendrik Veelken. "The Role of the BCR Class Expressed by Eμ-TCL1tg Mice and Human CLL". Blood 120, № 21 (2012): 182. http://dx.doi.org/10.1182/blood.v120.21.182.182.

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Abstract Abstract 182 The B-cell antigen receptor (BCR) plays a critical role in the development and progression of B-cell lymphomas. In chronic lymphocytic leukemia (CLL), the existence of stereotyped heavy-chain complementarity determining regions (HCDR3) suggested that binding of external antigens might play a role in CLL pathogenesis. In contrast, we recently reported that BCRs derived from both human CLL patients and from Eμ-TCL1tg mice have the unique function to induce antigen-independent signaling. This capacity is mediated by the HCDR3 through binding to a BCR internal motif in adjace

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30

Motiwala, Tasneem, Nicola Zanesi, Jharna Datta, et al. "AP-1 elements and TCL1 protein regulate expression of the gene encoding protein tyrosine phosphatase PTPROt in leukemia." Blood 118, no. 23 (2011): 6132–40. http://dx.doi.org/10.1182/blood-2011-01-323147.

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Abstract We previously demonstrated that the gene encoding PTPROt, the truncated form of protein tyrosine phosphatase receptor type O expressed predominantly in hematopoietic cells, is a candidate tumor suppressor and is down-regulated in chronic lymphocytic leukemia (CLL). Here, we show that PTPROt expression is significantly reduced in CD19+ spleen B cells from Eμ-T cell leukemia 1 (TCL1) transgenic mice relative to the wild-type mice. Strikingly, as much as a 60% decrease in PTPROt expression occurs at 7 weeks independently of promoter methylation. To elucidate the potential mechanism for t

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31

Hertlein, Erin K., Timothy L. Chen, David M. Lucas, et al. "NFkB p50 (Nfkb1) Contributes to Disease in the Eu-TCL1 Mouse Model of Chronic Lymphocytic Leukemia." Blood 126, no. 23 (2015): 1248. http://dx.doi.org/10.1182/blood.v126.23.1248.1248.

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Abstract Chronic lymphocytic leukemia (CLL) is a disease of mature B-cells that are resistant to apoptosis and accumulate in the blood over time. Due to the slowly progressing nature of this disease, studies to determine the molecular events leading to defective apoptosis are challenging. Our group has previously reported that during disease progression in the Eμ-TCL1 CLL mouse model, genes become silenced in a progressive manner over the course of the disease. This silencing is due in part to a high degree of methylation at the promoters of key tumor suppressors. However, even though a high d

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32

Dong, Shuai, John C. Byrd, and Amy J. Johnson. "Genetic Inhibition of PI3K p110delta Antagonizes Survival Signals and Induces Immune Activation in Chronic Lymphocytic Leukemia (CLL)." Blood 126, no. 23 (2015): 1711. http://dx.doi.org/10.1182/blood.v126.23.1711.1711.

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Abstract Background: Chronic lymphocytic leukemia (CLL), the most common adult leukemia in the western world, is characterized by the accumulation of malignant mature B cells in the blood, lymph nodes, spleen and bone marrow. CLL cells display up-regulated B cell receptor (BCR) activation, which maintains B cell survival and proliferation through transmitting microenvironmental stimuli. Due to aberrant regulation of the BCR, CLL cells display constitutively activated survival and proliferation pathways, such as phosphoinositide-3 kinase (PI3K) p110δ pathway. In addition, immune tolerance, a cr

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33

Alhakeem, Sara, Mary McKenna, Beth Gachuki, et al. "Constitutive IL-10 production by normal and malignant B-1 cells is dependent on B cell receptor signaling (IRM10P.620)." Journal of Immunology 194, no. 1_Supplement (2015): 131.18. http://dx.doi.org/10.4049/jimmunol.194.supp.131.18.

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Abstract The most common human leukemia is B-cell chronic lymphocytic leukemia (B-CLL), which can have immunosuppressive effects. CLL cells share multiple phenotypic markers with B-1 B cells such as their surface expression of CD5. This study identifies some functional similarities between B-1 and CLL cells. B-1 B cells have been shown to produce a high level of interleukin-10 (IL-10) constitutively and upon toll-like receptor stimulation, a characteristic property of regulatory B cells. Eμ-Tcl1 mice, which express the Tcl1 oncogene in a B cell specific manner, spontaneously develop B-CLL. We

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34

Ontiveros, Evelena, David Dae-Young Kim, Jeffrey M. Calimlim, et al. "The PIM1 Oncogene Accelerates TCL1 Driven Lymphomagenesis in a Double-Transgenic Murine Model." Blood 114, no. 22 (2009): 2968. http://dx.doi.org/10.1182/blood.v114.22.2968.2968.

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Abstract Abstract 2968 Poster Board II-944 Previously, we identified and validated PIM1 as a differentially expressed gene in mantle cell lymphoma (MCL) patient samples. Further, we have shown PIM1 to be a significant prognostic biomarker in MCL. PIM1 is a serine/threonine kinase that is transcriptionally regulated by cytokines, mitogens, and numerous growth factors. PIM1 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. PIM1 is overexpressed in aggressive lymphomas

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35

Suljagic, Mirza, Pablo G. Longo, Luca Laurenti, and Dimitar G. Efremov. "The Syk Inhibitor R788 (FosD) Inhibits Tumor Growth in the TCL1 Transgenic Mouse Model of CLL by Blocking Antigen-Dependent BCR Signaling." Blood 114, no. 22 (2009): 887. http://dx.doi.org/10.1182/blood.v114.22.887.887.

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Abstract Abstract 887 CLL B-cells depend on various signals from the microenvironment for survival and proliferation. Among these, antigenic stimuli that are propagated through the B-cell receptor (BCR) are considered particularly important for the development and progression of CLL, suggesting that the BCR signaling pathway could be an important target for therapeutic intervention. We have previously characterized some of the critical components of the signaling pathway downstream of the BCR in CLL B cells and identified the protein tyrosine kinase Syk as a promising therapeutic target. In a

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36

Rößner, Philipp M., Bola S. Hanna, Thorsten Zenz, Stephan Stilgenbauer, Peter Lichter, and Martina Seiffert. "The role of CXCR3 in the microenvironment of chronic lymphocytic leukemia." Journal of Immunology 196, no. 1_Supplement (2016): 73.12. http://dx.doi.org/10.4049/jimmunol.196.supp.73.12.

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Abstract Chronic lymphocytic leukemia (CLL) is a B-cell malignancy that is stringently associated with a tumor-supportive microenvironment and defective anti-tumor immunity. T cells from CLL patients show features of exhaustion, including expression of PD-1, and are highly impaired in their activity. Our previous work showed that immune checkpoint blockade using anti-PD-L1 effectively prevents disease and restores T-cell activity in the Eμ-TCL1 mouse model of CLL. Development of disease in these mice was shown to be associated with a relative loss of naïve T cells and an enrichment of effector

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37

Schulze-Edinghausen, Lena, Claudia Dürr, Selcen Öztürk, et al. "Dissecting the Prognostic Significance and Functional Role of Progranulin in Chronic Lymphocytic Leukemia." Cancers 11, no. 6 (2019): 822. http://dx.doi.org/10.3390/cancers11060822.

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Chronic lymphocytic leukemia (CLL) is known for its strong dependency on the tumor microenvironment. We found progranulin (GRN), a protein that has been linked to inflammation and cancer, to be upregulated in the serum of CLL patients compared to healthy controls, and increased GRN levels to be associated with an increased hazard for disease progression and death. This raised the question of whether GRN is a functional driver of CLL. We observed that recombinant GRN did not directly affect viability, activation, or proliferation of primary CLL cells in vitro. However, GRN secretion was induced

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38

Chen, Shih-Shih, Rainer Claus, David M. Lucas, et al. "Silencing of the inhibitor of DNA binding protein 4 (ID4) contributes to the pathogenesis of mouse and human CLL." Blood 117, no. 3 (2011): 862–71. http://dx.doi.org/10.1182/blood-2010-05-284638.

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Abstract Inhibitor of DNA binding protein 4 (ID4) is a member of the dominant-negative basic helix-loop-helix transcription factor family that lacks DNA binding activity and has tumor suppressor function. ID4 promoter methylation has been reported in acute myeloid leukemia and chronic lymphocytic leukemia (CLL), although the expression, function, and clinical relevance of this gene have not been characterized in either disease. We demonstrate that the promoter of ID4 is consistently methylated to various degrees in CLL cells, and increased promoter methylation in a univariable analysis correla

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39

Gamal, Wael, Melanie Mediavilla-Varela, Angimar Uriepero-Palma, Javier Pinilla-Ibarz, and Eva Sahakian. "Optimization of In Vitro Th17 Polarization for Adoptive Cell Therapy in Chronic Lymphocytic Leukemia." International Journal of Molecular Sciences 25, no. 12 (2024): 6324. http://dx.doi.org/10.3390/ijms25126324.

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Although preclinical investigations have shown notable efficacy in solid tumor models utilizing in vitro-differentiated Th17 cells for adoptive cell therapy (ACT), the potential benefits of this strategy in enhancing ACT efficacy in hematological malignancies, such as chronic lymphocytic leukemia (CLL), remain unexplored. CLL is a B-cell malignancy with a clinical challenge of increased resistance to targeted therapies. T-cell therapies, including chimeric antigen receptor (CAR) T cells, have demonstrated limited success in CLL, which is attributed to CLL-mediated T-cell dysfunction and skewin

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40

Lapalombella, Rosa, Virginia Goettl, Katie Williams, et al. "Significant in Vivo Efficacy of the SINE KPT-330 in Mouse Models of CLL." Blood 120, no. 21 (2012): 2452. http://dx.doi.org/10.1182/blood.v120.21.2452.2452.

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Abstract Abstract 2452 CRM1 (chromosomal regional maintenance 1) or XPO1 (exportin 1) is the major protein that mediates nuclear export. XPO1 has been shown to be over-expressed in cancer cells leading to ineffective cytoplasmic localization of multiple tumor suppressor genes such us p53, FOX03a, and Iκ-β. Chronic Lymphocytic Leukemia (CLL) is characterized by disrupted apoptosis caused both by microenviromental stimuli and aberrant activation of survival pathways including PI3K/Akt, NF-kB, and p53. We previously showed that first generations Selective Inhibitor of Nuclear Export (SINE), KPT-1

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41

Maharaj, Kamira, John J. Powers, Alex Achille та ін. "The dual PI3Kδ/CK1ε inhibitor umbralisib exhibits unique immunomodulatory effects on CLL T cells". Blood Advances 4, № 13 (2020): 3072–84. http://dx.doi.org/10.1182/bloodadvances.2020001800.

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Abstract The in-clinic phosphatidylinositol 3-kinase (PI3K) inhibitors idelalisib (CAL-101) and duvelisib (IPI-145) have demonstrated high rates of response and progression-free survival in clinical trials of B-cell malignancies, such as chronic lymphocytic leukemia (CLL). However, a high incidence of adverse events has led to frequent discontinuations, limiting the clinical development of these inhibitors. By contrast, the dual PI3Kδ/casein kinase-1-ε (CK1ε) inhibitor umbralisib (TGR-1202) also shows high rates of response in clinical trials but has an improved safety profile with fewer sever

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42

Drengler, Erin M., Audrey L. Smith, Sydney A. Skupa, Elizabeth Schmitz, Eslam Mohamed, and Dalia El-Gamal. "BET Protein Inhibition Relieves MDSC-Mediated Immune Suppression in Chronic Lymphocytic Leukemia." Hemato 6, no. 2 (2025): 14. https://doi.org/10.3390/hemato6020014.

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Background: Myeloid-derived suppressor cells (MDSCs) contribute to immune suppression observed in chronic lymphocytic leukemia (CLL). MDSCs are immature myeloid cells that are hijacked during development and further reprogrammed by the tumor microenvironment (TME) to harbor immune-suppressive properties and inhibit T-cell functions. Bromodomain and extraterminal domain (BET) proteins, including BRD4, are epigenetic modulators that regulate genes implicated in CLL pathogenesis and TME interactions. Previously, we investigated how the novel BET inhibitor OPN-51107 (OPN5) prevents CLL disease exp

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43

Widhopf, George F., Bing Cui, Esther Avery, et al. "ROR1 Expression Accelerates Leukemia Development in RORxTCL1 Transgenic Mice,." Blood 118, no. 21 (2011): 3905. http://dx.doi.org/10.1182/blood.v118.21.3905.3905.

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Abstract Abstract 3905 ROR1 is a receptor tyrosine kinase-like orphan receptor and an oncofetal protein that is expressed on chronic lymphocytic leukemia (CLL) B cells, but not on normal B cells or most other adult tissues. The leukemia-associated expression of ROR1 suggests that it potentially could contribute to the development and/or progression of CLL. To investigate its functional significance in the development and/or progression of CLL, we generated B6 mice transgenic (Tg) for human ROR1 (hROR1) under the control of the murine Ig promoter/enhancer, which drives B-cell-restricted express

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44

Whipp, Ethan C., Krithik Tella, Aidan Macaskill, et al. "Temporally Controlled MYC Overexpression in Chronic Lymphocytic Leukemia Accelerates Progression and Promotes Large B Cell Lymphoma Transformation." Blood 144, Supplement 1 (2024): 2978. https://doi.org/10.1182/blood-2024-210328.

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Background: Richter's transformation (RT) is the progression of chronic lymphocytic leukemia (CLL) to a high-grade lymphoma, usually resembling diffuse large B-cell lymphoma, with a poor prognosis of 6-12 months. The molecular mechanisms behind CLL-to-RT are unclear but often involve MYC hyperactivation through alterations, such as t(8;14), del(MGA), MYC/n-MYC gain, and mutations or overexpression of MYC regulators (e.g., NOTCH1, PRMT5). Previous efforts to model MYC overexpression in CLL (Eμ- TCL1xMyc) led to concurrent development of CLL and lymphoma rather than clonal transformation, possib

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45

Hayakawa, Kyoko, Anthony M. Formica, Joni Brill-Dashoff, et al. "Early generated B1 B cells with restricted BCRs become chronic lymphocytic leukemia with continued c-Myc and low Bmf expression." Journal of Experimental Medicine 213, no. 13 (2016): 3007–24. http://dx.doi.org/10.1084/jem.20160712.

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In mice, generation of autoreactive CD5+ B cells occurs as a consequence of BCR signaling induced by (self)-ligand exposure from fetal/neonatal B-1 B cell development. A fraction of these cells self-renew and persist as a minor B1 B cell subset throughout life. Here, we show that transfer of early generated B1 B cells from Eμ-TCL1 transgenic mice resulted in chronic lymphocytic leukemia (CLL) with a biased repertoire, including stereotyped BCRs. Thus, B1 B cells bearing restricted BCRs can become CLL during aging. Increased anti-thymocyte/Thy-1 autoreactive (ATA) BCR cells in the B1 B cell sub

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46

Rattmann, Ina, David Zhu, Carlo M. Croce, et al. "The Expression of the GTPase-Deficient, Hematopoietic-Specific RhoH GTPase Is Implicated in Development of Chronic Lymphocytic Leukemia (CLL)." Blood 110, no. 11 (2007): 339. http://dx.doi.org/10.1182/blood.v110.11.339.339.

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Abstract RhoH is a hematopoietic-specific small GTPase which is constitutively active due to lack of intrinsic GTPase activity, suggesting that expression levels of RhoH regulate cellular function. Our lab has previously shown that RhoH in T-cells directly interacts with ZAP-70, a critical protein tyrosine kinase in TCR cell signaling and function (Gu et al., Nature Immunol., 2006). As in human B-CLL ZAP-70 expression has been correlated with an unmutated IgVH gene status and poor prognosis, we have investigated RhoH expression and function in B-CLL. PBMC samples from 29 B-CLL patients, all co

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47

Egle, Alexander, Josefina D. Pinon, Christoph Heyder, et al. "T Cell Dynamics during the Pretumor and Tumor Phase in the Murine Tcl1 Transgenic Chronic Lymphocytic Leukemia Model." Blood 112, no. 11 (2008): 3145. http://dx.doi.org/10.1182/blood.v112.11.3145.3145.

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Abstract Chronic lymphocytic leukaemia of B cells (B-CLL) is characterised by a clonal expansion of CD5-expressing B cells. However, the absolute number of T cells in patients with B-CLL is also increased, primarily due to an enlarged CD8+ population. Despite the enhanced number of T cells, they appear to be dysfunctional as they are largely devoid of anti-tumor activity and may even support the growth and maintenance of the malignant B-CLL clone. To further investigate the contribution this T cell dysfunction has on the establishment and progression of B-CLL, we monitored the changes in the T

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48

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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49

Papait, Andrea, Tiziana Vaisitti, Sara Serra та ін. "Targeting the Adenosinergic Axis in the Eμ-TCL1 Chronic Lymphocytic Leukemia Mouse Model Offers Novel Therapeutic Opportunities". Blood 132, Supplement 1 (2018): 240. http://dx.doi.org/10.1182/blood-2018-99-118057.

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Abstract Background. The tumor microenvironment is typically an immunosuppressive niche often characterized by low oxygen tension, representing an intrinsic limitation to the success of immunotherapeutic approaches. Several lines of evidence indicate hypoxia is a master regulator of the adenosinergic axis, up-regulating on one side expression of CD39 and CD73, the two enzymes that generate adenosine starting from ATP/ADP and on the other side the adenosine receptors, which are powerful inhibitors of immune responses. Our previous studies using primary samples indicate that CLL cells can produc

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50

Rivas, Jacqueline R., Sara S. Alhakeem, Joseph M. Eckenrode, et al. "Enhancing Anti-Tumor Immunity and Responses to Immune Checkpoint Blockade By Suppressing Interleukin-10 in Chronic Lymphocytic Leukemia." Blood 134, Supplement_1 (2019): 5486. http://dx.doi.org/10.1182/blood-2019-127178.

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B-cell Chronic Lymphocytic Leukemia (CLL) is the most common leukemia in the Western world, accounting for nearly one third of all leukemia cases. In CLL abnormal B-cells accumulate in the blood and lymphoid organs leading to serious immune dysfunction. This immune suppression is in part due to CLL-produced mediators that downregulate T-cell responses, such as the regulatory cytokine Interleukin-10 (IL-10). We previously found that eliminating T-cell IL-10 signaling enhanced their ability to control CLL growth in vivo. Therefore, we investigated the potential for IL-10 blockade to enhance the

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