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Journal articles on the topic 'B-cell malignancie'

Author: Grafiati

Published: 1 April 2023

Last updated: 31 July 2025

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1

Miao, Miao, Wu Depei, Aining Sun, Ying Wang, Lingzhi Yan, and Qian Wu. "The Efficacy and Safety of Recombinant Human Thrombopoietin in Patients with Hematological Malgnancies After Allogeneic Hematopoietic Stem Cell Transplantation." Blood 118, no. 21 (2011): 4565. http://dx.doi.org/10.1182/blood.v118.21.4565.4565.

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Abstract Abstract 4565 OBJECTIVE: To evaluate the efficacy and sefety of recombinant human thrombopoietin(rhTPO) prior to engraftment in adults with hematological malignancie who received allogeneic haematopoietil stem cell transplantation(Allo-HSCT). METHODS: This sutdy was a randomized, controlled clinical trial,38 patients were hematological malignancie, inclulding acute and chrinic myeloid leukemia, acute lymphoblastic leukemia, lymphoma.They received Allo-HSCT and were randomly divided into groups(group A 19 cases, group B 19 cases).The group A was no-rhTPO as control, the group B were re

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2

Lydyard, Peter M., Andrew P. Jewell, Christoph Jamin, and Pierre Y. Youinou. "CD5 B cells and B-cell malignancies." Current Opinion in Hematology 6, no. 1 (1999): 30. http://dx.doi.org/10.1097/00062752-199901000-00006.

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3

Zweidler-McKay, Patrick A., Yiping He, Lanwei Xu, et al. "Notch signaling is a potent inducer of growth arrest and apoptosis in a wide range of B-cell malignancies." Blood 106, no. 12 (2005): 3898–906. http://dx.doi.org/10.1182/blood-2005-01-0355.

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Although Notch receptor expression on malignant B cells is widespread, the effect of Notch signaling in these cells is poorly understood. To investigate Notch signaling in B-cell malignancy, we assayed the effect of Notch activation in multiple murine and human B-cell tumors, representing both immature and mature subtypes. Expression of constitutively active, truncated forms of the 4 mammalian Notch receptors (ICN1-4) inhibited growth and induced apoptosis in both murine and human B-cell lines but not T-cell lines. Similar results were obtained in human precursor B-cell acute lymphoblastic leu

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4

Brudno, Jennifer N., Robert P. T. Somerville, Victoria Shi, et al. "Allogeneic T Cells That Express an Anti-CD19 Chimeric Antigen Receptor Induce Remissions of B-Cell Malignancies That Progress After Allogeneic Hematopoietic Stem-Cell Transplantation Without Causing Graft-Versus-Host Disease." Journal of Clinical Oncology 34, no. 10 (2016): 1112–21. http://dx.doi.org/10.1200/jco.2015.64.5929.

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Purpose Progressive malignancy is the leading cause of death after allogeneic hematopoietic stem-cell transplantation (alloHSCT). After alloHSCT, B-cell malignancies often are treated with unmanipulated donor lymphocyte infusions (DLIs) from the transplant donor. DLIs frequently are not effective at eradicating malignancy and often cause graft-versus-host disease, a potentially lethal immune response against normal recipient tissues. Methods We conducted a clinical trial of allogeneic T cells genetically engineered to express a chimeric antigen receptor (CAR) targeting the B-cell antigen CD19.

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Ren, Anqi, Xiqin Tong, Na Xu, Tongcun Zhang, Fuling Zhou, and Haichuan Zhu. "CAR T-Cell Immunotherapy Treating T-ALL: Challenges and Opportunities." Vaccines 11, no. 1 (2023): 165. http://dx.doi.org/10.3390/vaccines11010165.

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T-cell acute lymphoblastic leukemia (T-ALL), a form of T-cell malignancy, is a typically aggressive hematological malignancy with high rates of disease relapse and a poor prognosis. Current guidelines do not recommend any specific treatments for these patients, and only allogeneic stem cell transplant, which is associated with potential risks and toxicities, is a curative therapy. Recent clinical trials showed that immunotherapies, including monoclonal antibodies, checkpoint inhibitors, and CAR T therapies, are successful in treating hematologic malignancies. CAR T cells, which specifically ta

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6

Hudecek, Michael, Thomas M. Schmitt, Sivasubramanian Baskar, et al. "The B-cell tumor–associated antigen ROR1 can be targeted with T cells modified to express a ROR1-specific chimeric antigen receptor." Blood 116, no. 22 (2010): 4532–41. http://dx.doi.org/10.1182/blood-2010-05-283309.

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Monoclonal antibodies and T cells modified to express chimeric antigen receptors specific for B-cell lineage surface molecules such as CD20 exert antitumor activity in B-cell malignancies, but deplete normal B cells. The receptor tyrosine kinase-like orphan receptor 1 (ROR1) was identified as a highly expressed gene in B-cell chronic lymphocytic leukemia (B-CLL), but not normal B cells, suggesting it may serve as a tumor-specific target for therapy. We analyzed ROR1-expression in normal nonhematopoietic and hematopoietic cells including B-cell precursors, and in hematopoietic malignancies. ROR

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7

Chattaraj, Asmi, Mohammad Ebad Ur Rehman, Israr Khan, et al. "Safety and efficacy of allogeneic CAR-T cells in B-cell malignancies: A systematic review and meta-analysis." Journal of Clinical Oncology 40, no. 16_suppl (2022): e19530-e19530. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e19530.

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e19530 Background: Immunotherapy with chimeric antigen receptor T (CAR-T) cells has proven effective in recent trials for patients with B cell malignancies, who relapsed after stem cell transplantation. Genetically modified allogeneic CAR T-cells used in advanced B cell malignancy engage with multiple target allo-antigens along with CD19 and/or CD20, leading to elimination of malignant B cells resulting in a potent graft versus malignancy effect with avoidance of tumor escape. Some concerns regarding their use exist like life-threatening graft-versus-host disease (GVHD) and rapid clearance by

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8

Tonino, Sanne H., Marinus H. J. Van Oers, Rene A. Van Lier, and Marie Jose Kersten. "CMV-Associated Expansion of CD8+CD45RA+CD27− T-Cells in Patients with B-Cell Malignancies." Blood 110, no. 11 (2007): 3592. http://dx.doi.org/10.1182/blood.v110.11.3592.3592.

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Abstract In patients with various malignancies of B-cell origin, changes in the T-cell compartment have been observed. In B-cell chronic lymphocytic leukemia (CLL), we have previously described an expansion of T-cells, largely due to an increase in T-cells exhibiting the CD45RA+CD27- effector phenotype. This was found only in cytomegalovirus (CMV) seropositive patients, suggesting that CMV-antigen drives this expansion. Indeed a considerable fraction of these T-cells were shown to be CMV-specific. At present it is unknown whether this alteration of the T-cell compartment is specific for CLL or

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9

Incrocci, Ryan, Molly McCormack, and Michelle Swanson-Mungerson. "Epstein–Barr virus LMP2A increases IL-10 production in mitogen-stimulated primary B-cells and B-cell lymphomas." Journal of General Virology 94, no. 5 (2013): 1127–33. http://dx.doi.org/10.1099/vir.0.049221-0.

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Epstein–Barr virus (EBV) latently infected B-cells are the precursors of EBV-associated malignancies. EBV-infection induces the production of pro-survival and anti-inflammatory cytokines that may be important in the transition between latency and malignancy. One EBV protein, LMP2A, can be detected in both latently infected resting B-cells and in EBV-associated malignancies. Therefore, we tested the ability of LMP2A to influence cytokine production using both LMP2A-Tg primary B-cells and LMP2A-expressing B-cell lines. Our data demonstrate that LMP2A does not globally alter B-cell-produced cytok

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10

Prakash, Ajay, and Alhossain A. Khalafallah. "Concurrent Hairy Cell Leukemia and Metastatic Merkel Cell Carcinoma." Case Reports in Oncological Medicine 2018 (November 14, 2018): 1–6. http://dx.doi.org/10.1155/2018/1736854.

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Hairy cell leukemia (HCL) and Merkel cell carcinoma (MCC) are two rare malignancies with distinct cells of origin. HCL is a lymphoid malignancy of mature B cells, and MCC derives from neuroendocrine cell origin. HCL has a favorable prognosis with most patients achieving long-term remission and potential cure. In contrast, MCC is an aggressive malignancy affecting the skin and can metastasize quickly with a dismal prognosis. Immunocompromised patients, such as those with AIDS, posttransplant, and the elderly, have higher incidences than the general population, suggesting a possible immune mecha

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11

Shishido, Stephanie N., Olivia Hart, Sujin Jeong, et al. "Liquid biopsy approach to monitor the efficacy and response to CAR-T cell therapy." Journal for ImmunoTherapy of Cancer 12, no. 2 (2024): e007329. http://dx.doi.org/10.1136/jitc-2023-007329.

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BackgroundChimeric antigen receptor (CAR)-T cells are approved for use in the treatment of hematological malignancies. Axicabtagene ciloleucel (YESCARTA) and brexucabtagene autoleucel (TECARTUS) genetically modified autologous T cells expressing an anti-CD19 scFv based on the FMC63 clone have shown impressive response rates for the treatment of CD19+B cell malignancies, but there remain challenges in monitoring long-term persistence as well as the functional characterization of low-level persisting CAR-T cells in patients. Furthermore, due to CD19-negative driven relapse, having the capability

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12

Maio, M., A. Pinto, A. Carbone, et al. "Differential expression of CD54/intercellular adhesion molecule-1 in myeloid leukemias and in lymphoproliferative disorders." Blood 76, no. 4 (1990): 783–90. http://dx.doi.org/10.1182/blood.v76.4.783.783.

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Abstract Indirect immunofluorescence staining with monoclonal antibody (MoAb) CL203.4 of malignant cells from 269 patients with hematologic malignancies showed a heterogeneous expression of CD54/intercellular adhesion molecule-1 (ICAM-1). This marker was expressed by malignant cells of 57 out of 118 patients with myeloid malignancies and 69 out of 135 with B-lymphoid malignancies. On the other hand, CD54 was not detected on malignant cells of 16 patients with T-lymphoid malignancies. In myeloid malignancies, CD54 is preferentially expressed by “stem cell-derived” malignancies, being detectable

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13

Maio, M., A. Pinto, A. Carbone, et al. "Differential expression of CD54/intercellular adhesion molecule-1 in myeloid leukemias and in lymphoproliferative disorders." Blood 76, no. 4 (1990): 783–90. http://dx.doi.org/10.1182/blood.v76.4.783.bloodjournal764783.

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Indirect immunofluorescence staining with monoclonal antibody (MoAb) CL203.4 of malignant cells from 269 patients with hematologic malignancies showed a heterogeneous expression of CD54/intercellular adhesion molecule-1 (ICAM-1). This marker was expressed by malignant cells of 57 out of 118 patients with myeloid malignancies and 69 out of 135 with B-lymphoid malignancies. On the other hand, CD54 was not detected on malignant cells of 16 patients with T-lymphoid malignancies. In myeloid malignancies, CD54 is preferentially expressed by “stem cell-derived” malignancies, being detectable on blast

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14

Swanson-Mungerson, Michelle, Ryan Incrocci, Molly McCormack, and Caroline Leof. "Effects of Epstein-Barr Virus Latent Membrane Protein 2A (LMP2A) on cytokine production in primary and transformed B cells (105.40)." Journal of Immunology 188, no. 1_Supplement (2012): 105.40. http://dx.doi.org/10.4049/jimmunol.188.supp.105.40.

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Abstract Epstein-Barr Virus (EBV) latently-infected B cells are precursors of EBV-associated malignancies. However, the transition from a latently-infected cell to a malignant tumor cell is poorly understood. Studies show that EBV modulates pro-survival and anti-inflammatory cytokine levels in EBV-transformed cell lines. However, gene expression in these cell lines may not reflect gene expression found in latent B cells and lymphomas. One EBV protein, LMP2A, is consistently detected in both latently-infected resting B cells, as well as in EBV-associated malignancies. Therefore, we hypothesized

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15

Kochenderfer, James N., Mark E. Dudley, Robert O. Carpenter, et al. "Donor-Derived Anti-CD19 Chimeric-Antigen-Receptor-Expressing T Cells Cause Regression Of Malignancy Persisting After Allogeneic Hematopoietic Stem Cell Transplantation." Blood 122, no. 21 (2013): 151. http://dx.doi.org/10.1182/blood.v122.21.151.151.

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Abstract Progressive malignancy is a leading cause of death in patients undergoing allogeneic hematopoietic stem cell transplantation (alloHSCT). To improve treatment of B-cell malignancies that persist despite alloHSCT, we conducted a clinical trial of allogeneic T cells genetically modified to express a chimeric antigen receptor (CAR) targeting the B-cell antigen CD19. Ten patients were treated on this trial. Four patients were recipients of human-leukocyte-antigen (HLA)-matched unrelated donor (URD) transplants and 6 patients were recipients of HLA-matched sibling transplants. T cells for g

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16

Dalla Pietà, Anna, Elisa Cappuzzello, Pierangela Palmerini, et al. "Innovative therapeutic strategy for B-cell malignancies that combines obinutuzumab and cytokine-induced killer cells." Journal for ImmunoTherapy of Cancer 9, no. 7 (2021): e002475. http://dx.doi.org/10.1136/jitc-2021-002475.

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BackgroundPatients affected by aggressive B-cell malignancies who are resistant to primary or salvage chemoimmunotherapy have an extremely poor prognosis and limited therapeutic options. Promising therapeutic success has been achieved with the infusion of CD19 chimeric antigen receptor-T cells, but several limits still restrain the administration to a limited proportion of patients. This unmet clinical need might be fulfilled by an adoptive immunotherapy approach that combines cytokine-induced killer (CIK) cells and monoclonal antibodies (mAb) to the CD20 antigen. Indeed, CIK cells are an effe

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Link, BK, and GJ Weiner. "Production and characterization of a bispecific IgG capable of inducing T-cell-mediated lysis of malignant B cells." Blood 81, no. 12 (1993): 3343–49. http://dx.doi.org/10.1182/blood.v81.12.3343.bloodjournal81123343.

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Bispecific monoclonal antibodies (bsabs) recognizing both CD3 and a tumor antigen can redirect T-cell-mediated cytotoxicity toward cells bearing that antigen. Such bsabs have been shown to be more effective than monospecific monoclonal antibodies (MoAbs) at preventing tumor growth in animal models of B-cell malignancy. The current studies describe the production and preliminary evaluation of a bsab designed to induce the lysis of malignant human B cells by human T cells. The bsab was obtained from a hybrid-hybridoma cell line produced by fusing OKT3-secreting hybridoma cells with hybridoma cel

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18

Li, Yangqiu, Lijian Yang, Shaohua Chen, Suxia Geng, Grzegorz Przybylski, and Christian A. Schmidt. "Changes in Thymic Recent Output Function in Patients with B-Cell Lymphocytic Malignancy." Blood 108, no. 11 (2006): 4464. http://dx.doi.org/10.1182/blood.v108.11.4464.4464.

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Abstract Since 1998 the use of signal joint T cell receptor excision circles (sjTRECs) to study changes in the frequency of recent thymic emigrants was reported, this study drew attention to the fact that the level of sjTRECs can be used to estimate the recent thymic output function. Therefore, sjTRECs was used as a new marker for analysis of thymic output function in different immunodeficiency diseases, immune reconstitution in patients after stem cell transplantation. Defects of cellular immunity, however, may also play a role in hematologic malignancies. Little is known about the feature of

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Cliff, Edward R. Scheffer, Penelope Lafeuille, Sheila Diamond, et al. "Secondary Hematologic Malignancies in Patients Following Chimeric Antigen Receptor T-Cell Therapy: Aggregated Clinical Trial Data from 1542 Patients." Blood 144, Supplement 1 (2024): 2077. https://doi.org/10.1182/blood-2024-203979.

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Overview Chimeric Antigen Receptor (CAR) T-cells are an effective treatment for a variety of hematologic malignancies, received by &gt;30,000 patients to date. Autologous T-cells are genetically modified ex-vivo using lenti- or retro-viral transduction to express a CAR receptor, which confers T-cells with HLA-independent tumor antigen recognition and thus tumor specificity. Recently, the FDA announced an investigation into 22 patients who developed T-cell malignancies following receipt of CD19- or BCMA-directed CAR T-cells and worked with manufacturers to add boxed warnings to approved CAR

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Leveille, Etienne, Eden Bramson, Mark Robinson, et al. "Abstract 2819: Metabolic determinants of ferroptosis in B-cell malignancies." Cancer Research 85, no. 8_Supplement_1 (2025): 2819. https://doi.org/10.1158/1538-7445.am2025-2819.

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Abstract Although the development of targeted approaches has been effective for the treatment of B-cell malignancies, outcomes remain poor in the relapsed and refractory settings. To expand the portfolio of B-cell-selective drugs, we developed an interactive computational tool (lymphoblasts.org) and identified ferroptosis, a form of cell death driven by iron-dependent membrane lipid peroxidation, as a previously unrecognized selective vulnerability in B-cell malignancies. Although ferroptosis has shown potential in therapy-resistant tumors, no potent ferroptosis inducers are available clinical

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21

Ashouri, Arghavan, Pathum Kossinna, Xuyao Li, et al. "Decoding the Epigenetic and Transcriptional Signatures of Pathogenic B-Cells in Patients at High Risk of Transformation to Lymphoma." Blood 144, Supplement 1 (2024): 2971. https://doi.org/10.1182/blood-2024-202826.

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Systemic Lupus Erythematosus (SLE) is a chronic, heterogenous autoimmune disorder characterized by diverse clinical manifestations and treatment responses due to various genetic, epigenetic, and immune-related factors (Kaul et al., 2016). SLE is characterized by the expansion of a rare B cell subset, double negative (DN), with the majority of these being DN2 cells (ZEB2hiITGAXhi, Jenks et al., 2018). These cells are known to be the main cause of SLE pathogenicity, and are precursors of pathogenic antibody secreting cells (Elsner & Shlomchik, 2020). SLE patients can experience several life

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Sud, Amit, Subhayan Chattopadhyay, Hauke Thomsen, et al. "Analysis of 153 115 patients with hematological malignancies refines the spectrum of familial risk." Blood 134, no. 12 (2019): 960–69. http://dx.doi.org/10.1182/blood.2019001362.

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Abstract Sud and colleagues interrogated the familial risk of hematological malignancy in association with over 150 000 patients. The majority of hematological malignancies showed increased familial relative risk, most prominently in association with B-cell malignancies.

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23

Link, BK, and GJ Weiner. "Production and characterization of a bispecific IgG capable of inducing T-cell-mediated lysis of malignant B cells." Blood 81, no. 12 (1993): 3343–49. http://dx.doi.org/10.1182/blood.v81.12.3343.3343.

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Abstract Bispecific monoclonal antibodies (bsabs) recognizing both CD3 and a tumor antigen can redirect T-cell-mediated cytotoxicity toward cells bearing that antigen. Such bsabs have been shown to be more effective than monospecific monoclonal antibodies (MoAbs) at preventing tumor growth in animal models of B-cell malignancy. The current studies describe the production and preliminary evaluation of a bsab designed to induce the lysis of malignant human B cells by human T cells. The bsab was obtained from a hybrid-hybridoma cell line produced by fusing OKT3-secreting hybridoma cells with hybr

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24

Kroeze, Emma, Laura Arias Padilla, Max Bakker, et al. "Pediatric Precursor B-Cell Lymphoblastic Malignancies: From Extramedullary to Medullary Involvement." Cancers 14, no. 16 (2022): 3895. http://dx.doi.org/10.3390/cancers14163895.

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B-cell lymphoblastic lymphoma (BCP-LBL) and B-cell acute lymphoblastic leukemia (BCP-ALL) are the malignant counterparts of immature B-cells. BCP-ALL is the most common hematological malignancy in childhood, while BCP-LBL accounts for only 1% of all hematological malignancies in children. Therefore, BCP-ALL has been well studied and treatment protocols have changed over the last decades, whereas treatment for BCP-LBL has stayed roughly the same. Clinical characteristics of 364 pediatric patients with precursor B-cell malignancies were studied, consisting of BCP-LBL (n = 210) and BCP-ALL (n = 1

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Abramowitz, Binyamin R., Nicholas Ridout, Hagar Attia, Zhonghua Li, Patrick J. Hammill, and Evan B. Grossman. "Periampullary Diffuse Large B-Cell Lymphoma Presenting as Acute Pancreatitis." ACG Case Reports Journal 11, no. 11 (2024): e01550. http://dx.doi.org/10.14309/crj.0000000000001550.

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ABSTRACT Periampullary malignancies are uncommon and encompass a wide variety of tumors. Early and accurate biopsy-proven diagnosis is important because different malignancy subtypes warrant different management and treatment plans. We present a unique and rare case of periampullary lymphoma, initially presenting as acute pancreatitis.

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Cooper, Kathrine A., Jonathan Lattell, Beverly Gonzalez, Stephanie Kliethermes, and Sucha Nand. "Prevalence of Multiple Primary Hematologic Malignancies Seen at a Tertiary Care Center." Blood 126, no. 23 (2015): 5017. http://dx.doi.org/10.1182/blood.v126.23.5017.5017.

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Abstract Background: There is a paucity of data regarding patients who develop multiple unrelated hematologic malignancies. This study aims to determine the prevalence of two or more hematologic malignancies in the same patient at Loyola University Medical Center (LUMC) over a period of 7 years and to explore associations with certain clinical risk factors. Methods: After obtaining IRB approval, the electronic medical record was queried for various hematologic malignancies according to ICD-9 codes from 2007-2014. Chemotherapy-associated and transformed malignancies were excluded. In addition,

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27

Bishop, Michael R. "Late complications and long-term care of adult CAR T-cell patients." Hematology 2024, no. 1 (2024): 109–15. https://doi.org/10.1182/hematology.2024000534.

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Abstract The success of chimeric antigen receptor (CAR) T-cell therapy in adult patients with hematologic malignancies has resulted in a large number of long-term survivors who may experience late complications distinct from those in the early CAR T-cell treatment period. These late complications, defined as occurring more than 90 days after CAR T-cell infusion, include cytopenias, infections, secondary malignancies, and delayed neurotoxicities. Late cytopenias may be from prolonged recovery after lymphodepleting (LD) chemotherapy or arise anew, raising concerns for recurrent primary disease o

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28

Jacobs, Lauren M., Peter H. Wiernik, Janice P. Dutcher, and Pablo Muxi. "Long-Term Response and Possible Cure of Patients With B-Cell Malignancies With Dose-Escalated Rituximab." Journal of Investigative Medicine High Impact Case Reports 5, no. 1 (2017): 232470961769130. http://dx.doi.org/10.1177/2324709617691307.

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Rituximab (R), a chimeric monoclonal antibody targeting CD20 antigen on B-cells, has become a standard of care in the treatment of B-cell malignancies, most often in conjunction with cytotoxic chemotherapy. Activity has been demonstrated in many subtypes of B-cell lymphoma, including diffuse large cell lymphoma, follicular lymphoma (FL), mantle cell lymphoma (MCL), chronic lymphocytic leukemia (CLL), lymphocyte-predominant Hodgkin lymphoma, and Waldenström macroglobulinemia (WM). Additionally, dose escalation of R as a single agent has demonstrated improved activity in previously treated/poor

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29

Green, Michael R., and Ash A. Alizadeh. "Common progenitor cells in mature B-cell malignancies." Current Opinion in Hematology 21, no. 4 (2014): 333–40. http://dx.doi.org/10.1097/moh.0000000000000049.

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30

Yazdani, Yaghoub, Mousa Mohammadnia-Afrouzi, Mehdi Yousefi, et al. "Myeloid-derived suppressor cells in B cell malignancies." Tumor Biology 36, no. 10 (2015): 7339–53. http://dx.doi.org/10.1007/s13277-015-4004-z.

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Sabbah, Shereen, Ya Jankey Jagne, Jianmin Zuo, et al. "T-cell immunity to Kaposi sarcoma–associated herpesvirus: recognition of primary effusion lymphoma by LANA-specific CD4+ T cells." Blood 119, no. 9 (2012): 2083–92. http://dx.doi.org/10.1182/blood-2011-07-366476.

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Abstract T-cell immunity is important for controlling Kaposi sarcoma–associated herpesvirus (KSHV) diseases such as the endothelial cell malignancy Kaposi sarcoma, or the B-cell malignancy, primary effusion lymphoma (PEL). However, little is known about KSHV-specific T-cell immunity in healthy donors and immune control of disease. Using PBMCs from healthy KSHV-infected donors, we found weak ex vivo responses to the KSHV latent antigens LANA, vFLIP, vCyclin, and Kaposin, with LANA most frequently recognized. CD4+ T-cell clones specific to LANA, a protein expressed in all KSHV-infected cells and

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Weng, Jinsheng, Flavio Egidio Baio, Kelsey E. Moriarty, et al. "Targeting B-cell malignancies through human B-cell receptor specific CD4+T cells." OncoImmunology 5, no. 11 (2016): e1232220. http://dx.doi.org/10.1080/2162402x.2016.1232220.

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Zhao, Zhigang, Lin Li, Meelad Dawlaty, et al. "Combined Loss of Tet1 and Tet2 Promotes B-Cell, but Not Myeloid Malignancies in Mice." Blood 126, no. 23 (2015): 3650. http://dx.doi.org/10.1182/blood.v126.23.3650.3650.

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Abstract Objective: Tet1/2/3 are methylcytosine dioxygenases regulating cytosine methylation in the genome. Tet1 and Tet2 are abundantly expressed in HSC/HPCs and implicated in hematological malignancies. Tet2 -deletion in mice causes myeloid malignancies, while Tet1 -null mice are overtly normal early in life. Here, we investigated the overlapping and non-redundant functions of Tet1/Tet2 in HSC maintenance and hematological malignancies using Tet1/2 double knockout (DKO) mice. Methods: 1) Kinetic analysis of the hematologicalparameters on WT, Tet1-/-, Tet2-/- and DKO mice; 2) Analysis of HSC,

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Ghimire, Krishna B., and Binay K. Shah. "Second Primary Malignancy in Diffuse Large B Cell Lymphoma (DLBCL)." Blood 124, no. 21 (2014): 2606. http://dx.doi.org/10.1182/blood.v124.21.2606.2606.

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Introduction: Patients with non-Hodgkin lymphoma are at significantly increased risk of second primary malignancies (SPM). There are few studies on SPM in diffuse large B-cell lymphoma. We aim to evaluate the risk of SPM after diagnosis of primary DLBCL using Surveillance, Epidemiology and End Results (SEER) database. Methods: We used SEER 13 database to select adult patients with primary DLBCL diagnosed between 1992- 2009. We used SEER*Stat’s Multiple Primary - Standardized Incidence Ratios (MP-SIR) to calculate SPM in DLBCL. We analyzed SPM by age (≥20, 20-59 and ≥60 years), sex and latency.

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Testa, Ugo, Patrizia Chiusolo, Elvira Pelosi, Germana Castelli, and Giuseppe Leone. "CAR-T CELL THERAPY FOR T-CELL MALIGNANCIES." Mediterranean Journal of Hematology and Infectious Diseases 16, no. 1 (2024): e2024031. http://dx.doi.org/10.4084/mjhid.2024.031.

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Chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of B-cell lymphoid neoplasia and, in some instances, improved disease outcomes. Thus, six FDA-approved commercial CAR-T cell products that target antigens preferentially expressed on malignant B-cells or plasma cells have been introduced in the therapy of B-cell lymphomas, B-ALLs and multiple myeloma. These therapeutic successes have triggered the application of CAR-T cell therapy to other hematologic tumors, including T-cell malignancies. However, the success of CAR-T cell therapies in T-cell neoplasms was

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Zhang, Jenny, Dereje D. Jima, Yuan Gao, et al. "Massively Parallel High Throughput Sequencing Identifies Novel Micrornas in Normal and Malignant B Cells." Blood 112, no. 11 (2008): 3350. http://dx.doi.org/10.1182/blood.v112.11.3350.3350.

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Abstract Background: MicroRNAs (miRNAs) are small non coding RNAs that have been shown to play a regulatory role in a number of different settings including development, hematopoiesis and lineage-selection. The expression patterns of miRNAs in various cellular processes and in various normal and malignant tissues are an area of active exploration. Bioinformatic analyses of the genome suggest that there might be thousands of miRNAs encoded in the genome. However, thus far only about 600 unique miRNAs have been identified in humans. The role of microRNAs in B cell malignancies is poorly understo

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Miletic, Ana V., Amy N. Anzelon-Mills, David M. Mills, et al. "Coordinate suppression of B cell lymphoma by PTEN and SHIP phosphatases." Journal of Experimental Medicine 207, no. 11 (2010): 2407–20. http://dx.doi.org/10.1084/jem.20091962.

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The inositol phosphatases phosphatase and tensin homologue (PTEN) and Src homology 2 domain–containing inositol phosphatase (SHIP) negatively regulate phosphatidylinositol-3-kinase (PI3K)–mediated growth, survival, and proliferation of hematopoietic cells. Although deletion of PTEN in mouse T cells results in lethal T cell lymphomas, we find that animals lacking PTEN or SHIP in B cells show no evidence of malignancy. However, concomitant deletion of PTEN and SHIP (bPTEN/SHIP−/−) results in spontaneous and lethal mature B cell neoplasms consistent with marginal zone lymphoma or, less frequently

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Chen, Zhengshan, and Markus Muschen. "Autoimmunity Checkpoints As Therapeutic Targets in B-Cell Malignancies." Blood 132, Supplement 1 (2018): 1587. http://dx.doi.org/10.1182/blood-2018-99-113674.

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Abstract Concept. Targeted therapy of cancer typically focuses on inhibitors (e.g. tyrosine kinase inhibitors) that suppress oncogenic signaling below a minimum threshold required for survival and proliferation of cancer cells. Acute lymphoblastic leukemia (ALL) and B cell lymphomas originate from various stages of development of B cells, which unlike other cell types are under intense selective pressure. The vast majority of newly generated B cells are autoreactive and die by negative selection at autoimmunity checkpoints (AIC). Owing to ubiquitous encounter of self-antigen, autoreactive B ce

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Zhang, Jenny, Dereje D. Jima, Cassandra Jacobs, et al. "Patterns of microRNA expression characterize stages of human B-cell differentiation." Blood 113, no. 19 (2009): 4586–94. http://dx.doi.org/10.1182/blood-2008-09-178186.

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Abstract Mature B-cell differentiation provides an important mechanism for the acquisition of adaptive immunity. Malignancies derived from mature B cells constitute the majority of leukemias and lymphomas. These malignancies often maintain the characteristics of the normal B cells that they are derived from, a feature that is frequently used in their diagnosis. The role of microRNAs in mature B cells is largely unknown. Through concomitant microRNA and mRNA profiling, we demonstrate a potential regulatory role for microRNAs at every stage of the mature B-cell differentiation process. In additi

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Michels, Kathryn R., Alyssa Sheih, Susana A. Hernandez, et al. "Preclinical proof of concept for VivoVec, a lentiviral-based platform for in vivo CAR T-cell engineering." Journal for ImmunoTherapy of Cancer 11, no. 3 (2023): e006292. http://dx.doi.org/10.1136/jitc-2022-006292.

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BackgroundChimeric antigen receptor (CAR) T-cell therapies have demonstrated transformational outcomes in the treatment of B-cell malignancies, but their widespread use is hindered by technical and logistical challenges associated with ex vivo cell manufacturing. To overcome these challenges, we developed VivoVec, a lentiviral vector-based platform for in vivo engineering of T cells. UB-VV100, a VivoVec clinical candidate for the treatment of B-cell malignancies, displays an anti-CD3 single-chain variable fragment (scFv) on the surface and delivers a genetic payload that encodes a second-gener

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Yavuz, Selim A., Dan-Paul Hartmann, Said Baidas, Peter E. Lipsky, and Metin Ozdemirli. "Demonstration of Biclonal Chronic Lymphocytic Leukemia with Mutated and Unmutated Clones and Concurrent but Clonally Unrelated Myeloma in the Same Patient by Single Cell Immunoglobulin Heavy and Light Chain Gene Analysis." Blood 104, no. 11 (2004): 4772. http://dx.doi.org/10.1182/blood.v104.11.4772.4772.

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Abstract Patients with chronic lymphocytic leukemia (CLL) may develop other B cell malignancies in their clinical course including aggressive diffuse large B-cell lymphomas and rarely myelomas. In a large proportion of cases, the secondary B cell malignancies reflected the emergence of immunophenotypically and genetically different clones. An immature type plasma cell myeloma developed in a 73-year-old female patient in whom CLL was diagnosed four years previously. The CLL expressed CD5, CD19, CD23, CD38 and surface kappa light chain, but were negative for ZAP-70. Trisomy 12 was detected by FI

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Linden, Michael, Nicole Kirchhof, Cathy Carlson, and Brian Van Ness. "Targeted overexpression of Bcl-XL in B-lymphoid cells results in lymphoproliferative disease and plasma cell malignancies." Blood 103, no. 7 (2004): 2779–86. http://dx.doi.org/10.1182/blood-2003-10-3399.

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Abstract Multiple myeloma is an incurable malignancy, and there is currently no mouse model that fully recapitulates the development and progression of the disease. We now describe a transgenic mouse that expresses a Bcl-XL transgene under the control of the 3′κ immunoglobulin light chain enhancer, which is most active in murine B cells in late developmental stages. These mice developed nonmalignant plasma cell foci in the bone marrow and soft tissues and hyaline tubular casts in the kidneys. Median survival of the 3′KE/Bcl-XL mice was similar to littermate controls. When the 3′KE/Bcl-XL mouse

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Kume, Kohei, Jaewoong Lee, Zhangliang Cheng, et al. "Optogenetic Control of Oncogenic Signaling in B-Cell Malignancies." Blood 142, Supplement 1 (2023): 4138. http://dx.doi.org/10.1182/blood-2023-190926.

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Background: B-cell receptor (BCR) signals are essential determinants of survival and proliferation throughout normal B-cell development. In B-cell malignancies, these signals are frequently generated by oncogenic mimics of the BCR signaling pathway. For instance, oncogenes in B-ALL, derived from B-cell precursors, typically mimic survival signals from a constitutively active pre-BCR, while tonic and chronic active BCR signaling were identified in mature B-cell lymphomas. Oncogenic BCR-signaling represents an important target of therapeutic intervention: for instance, small molecule inhibitors

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Kong, Ling-Yuan, Vaibhav Kapuria, Geoffrey Bartholomeusz, Moshe Talpaz, Waldemar Priebe, and Nicholas J. Donato. "Antitumor Activity and Mechanism of Action of a Novel Stat3 Inhibitor, WP1066, Against Human B-Cell Non-Hodgkin’s Lymphoma and Multiple Myeloma." Blood 106, no. 11 (2005): 1489. http://dx.doi.org/10.1182/blood.v106.11.1489.1489.

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Abstract B-cell non-Hodgkin’s lymphomas (B-NHL) have the highest incidence rates among all lymphomas, comprising more than 85% of malignant lymphomas worldwide. Multiple myeloma (MM) is a plasma cell malignancy that affects 14,000 patients per year. Although new therapies have recently been introduced to treat these malignancies, patient survival has not significantly improved, illustrating the need for additional agents that target and suppress this disease. B-cell malignancies over-express c-myc and frequently retain a constitutively activated Stat3, resulting in increased survival gene expr

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Chen, Weili, Quanzhi Li, Wendy A. Hudson, Ashish Kumar, Nicole Kirchhof, and John H. Kersey. "A murine Mll-AF4 knock-in model results in lymphoid and myeloid deregulation and hematologic malignancy." Blood 108, no. 2 (2006): 669–77. http://dx.doi.org/10.1182/blood-2005-08-3498.

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The 2 most frequent human MLL hematopoietic malignancies involve either AF4 or AF9 as fusion partners; each has distinct biology but the role of the fusion partner is not clear. We produced Mll-AF4 knock-in (KI) mice by homologous recombination in embryonic stem cells and compared them with Mll-AF9 KI mice. Young Mll-AF4 mice had lymphoid and myeloid deregulation manifest by increased lymphoid and myeloid cells in hematopoietic organs. In vitro, bone marrow cells from young mice formed unique mixed pro-B lymphoid (B220+CD19+CD43+sIgM–, PAX5+, TdT+, IgH rearranged)/myeloid (CD11b/Mac1+, c-fms+,

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Chintapatla, Rangaswamy, Leticia Varella, Peter Wiernik, Valerie Rusciano, and Janice P. Dutcher. "Association of Renal Cell Carcinoma and B-Cell Hematological Malignancy." Blood 120, no. 21 (2012): 5086. http://dx.doi.org/10.1182/blood.v120.21.5086.5086.

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Abstract Abstract 5086 Purpose of the study: We observed an increased frequency of hematologic malignancy (HM) in patients and family members of patients with renal cell cancer (RCC) and sought to characterize the association further in terms of frequency and characteristics of HM, and the importance of such an association. Methods: We performed a chart review of our data base of approximately 700 RCC patients seen by us from 2004 to the present in an effort to determine the frequency of HM in patients and in the families of patients diagnosed with RCC. Results: Of the 700 charts reviewed, bot

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Pylayeva-Gupta, Yuliya. "Abstract IA018: Determinants of B cell fate and function in cancer." Cancer Research 84, no. 22_Supplement (2024): IA018. http://dx.doi.org/10.1158/1538-7445.tumbody-ia018.

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Abstract Effector B cell responses in solid malignancies are associated with favorable response to immunotherapy. B cells can amplify anti-tumor immune responses via antibody production, antigen presentation, and pro-inflammatory cytokine release; yet B cells in cancer patients and tumor-bearing mice often fail to support these functions. We have evaluated the contribution of either systemic inflammatory cues or antigenic quality to B cell differentiation and function in cancer. First, we identify dysregulated transcriptional programs activated in pancreatic cancer-associated B cells that prom

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Elsawa, Sherine F., Anne J. Novak, Deanna M. Grote, et al. "B-lymphocyte stimulator (BLyS) stimulates immunoglobulin production and malignant B-cell growth in Waldenström macroglobulinemia." Blood 107, no. 7 (2006): 2882–88. http://dx.doi.org/10.1182/blood-2005-09-3552.

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AbstractWaldenström macroglobulinemia (WM) is a serious and frequently fatal B-cell malignancy associated with an elevated monoclonal IgM protein in the serum. Many of the mechanisms leading to this disease are not yet known. B-lymphocyte stimulator (BLyS) is a TNF family member that is critical for maintenance of normal B-cell development and homeostasis. BLyS is overexpressed in a variety of B-cell malignancies and has been shown to inhibit apoptosis in malignant B cells. It also regulates immunoglobulin secretion by normal B cells. To determine the relevance of BLyS in WM, we examined the

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Lichtman, Eben I., and Gianpietro Dotti. "Chimeric antigen receptor T-cells for B-cell malignancies." Translational Research 187 (September 2017): 59–82. http://dx.doi.org/10.1016/j.trsl.2017.06.011.

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Garg, Swati, Wei Ni, James D. Griffin, and Martin Sattler. "Chimeric Antigen Receptor T Cell Therapy in Acute Myeloid Leukemia: Trials and Tribulations." Hematology Reports 15, no. 4 (2023): 608–26. http://dx.doi.org/10.3390/hematolrep15040063.

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Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy that is often associated with relapse and drug resistance after standard chemotherapy or targeted therapy, particularly in older patients. Hematopoietic stem cell transplants are looked upon as the ultimate salvage option with curative intent. Adoptive cell therapy using chimeric antigen receptors (CAR) has shown promise in B cell malignancies and is now being investigated in AML. Initial clinical trials have been disappointing in AML, and we review current strategies to improve efficacy for CAR approaches. The extensive

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