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Journal articles on the topic 'Leukemia Lymphomas T cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Bollard, Catherine M., and A. John Barrett. "Cytotoxic T lymphocytes for leukemia and lymphoma." Hematology 2014, no. 1 (2014): 565–69. http://dx.doi.org/10.1182/asheducation-2014.1.565.

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Abstract This chapter focuses on the recent advances in adoptive T-cell immunotherapies, not only for patients after hematopoietic stem cell transplantation, but also in the autologous setting using T cells early in the disease process for the treatment of the highest-risk patients with leukemias and lymphomas. The particular emphasis is to highlight the role of T-cell therapies for hematologic malignancies using a non-gene-transfer approach to direct specificity, including the clinical use of T-cell therapies for EBV-associated lymphomas and strategies for targeting nonviral lymphoma- and leu

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2

Singh, Anju, Anne Flörcken, Antje van Lessen, Bernd Dörken, Antonio Pezzutto, and Jörg Westermann. "CD3-Negative CD4+ T-Cells: A Useful Diagnostic Tool with High Specificity in Angioimmunoblastic Lymphadenopathy (AILD)-Type T-Cell Lymphoma." Blood 112, no. 11 (2008): 5311. http://dx.doi.org/10.1182/blood.v112.11.5311.5311.

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Abstract Angioimmunoblastic lymphadenopathy (AILD)-type T-cell lymphoma is one of the common T cell lymphomas in Western countries. Many patients present with symptoms of a systemic disease and diagnosis can often be challenging. Particularly in cases in which histological confirmation cannot be easily achieved flowcytometry of peripheral blood can give important clues for the differential diagnosis of AILD. We have previously reported that CD4-negative CD3+ T-cells in peripheral blood are a characteristic immunophenotypic finding in AILD patients. Gene scan analysis for the TCR gamma chain an

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3

Shi, Yang, and Endi Wang. "Blastic Plasmacytoid Dendritic Cell Neoplasm: A Clinicopathologic Review." Archives of Pathology & Laboratory Medicine 138, no. 4 (2014): 564–69. http://dx.doi.org/10.5858/arpa.2013-0101-rs.

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Blastic plasmacytoid dendritic cell neoplasm is a rare entity grouped with the acute myeloid leukemia–related precursor neoplasms in the 2008 World Health Organization classification. It was previously postulated to originate from natural killer cells, T cells, or monocytes but is now believed to arise from the plasmacytoid dendritic cell. The pathogenesis of blastic plasmacytoid dendritic cell neoplasm is not well understood, although the neoplasm demonstrates frequent deletion of tumor suppressor genes, including RB1, CDKN1B, CDKN2A, and TP53. Blastic plasmacytoid dendritic cell neoplasm is

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4

Rosolen, A., M. Nakanishi, DG Poplack, et al. "Expression of interleukin-2 receptor beta subunit in hematopoietic malignancies." Blood 73, no. 7 (1989): 1968–72. http://dx.doi.org/10.1182/blood.v73.7.1968.1968.

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Abstract The expression of the interleukin-2 (IL-2) receptor was studied in neoplastic cells derived from acute leukemias, T-cell lymphoblastic lymphomas, peripheral T-cell lymphomas, chronic lymphocytic leukemias, well-differentiated lymphocytic lymphomas, and established cell lines by both flow cytometric analysis and sodium dodecyl sulfate/polyacrylamide gel electrophoresis (SDS-PAGE) after affinity crosslinking of radiolabeled IL-2. Cells from most acute leukemias (19 of 22), irrespective of their subtype (T, common or nonlymphoid leukemias), as well as T-cell lymphoblastic lymphomas and p

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5

Rosolen, A., M. Nakanishi, DG Poplack, et al. "Expression of interleukin-2 receptor beta subunit in hematopoietic malignancies." Blood 73, no. 7 (1989): 1968–72. http://dx.doi.org/10.1182/blood.v73.7.1968.bloodjournal7371968.

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The expression of the interleukin-2 (IL-2) receptor was studied in neoplastic cells derived from acute leukemias, T-cell lymphoblastic lymphomas, peripheral T-cell lymphomas, chronic lymphocytic leukemias, well-differentiated lymphocytic lymphomas, and established cell lines by both flow cytometric analysis and sodium dodecyl sulfate/polyacrylamide gel electrophoresis (SDS-PAGE) after affinity crosslinking of radiolabeled IL-2. Cells from most acute leukemias (19 of 22), irrespective of their subtype (T, common or nonlymphoid leukemias), as well as T-cell lymphoblastic lymphomas and peripheral

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6

Hsieh, Emily M., and Rayne H. Rouce. "Chimeric antigen receptor T cells for mature B-cell lymphoma and Burkitt lymphoma." Hematology 2020, no. 1 (2020): 487–93. http://dx.doi.org/10.1182/hematology.2020000133.

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Abstract Chimeric antigen receptor (CAR) T-cell therapy has changed the landscape of immunotherapy for B-cell malignancies, including mature B-cell lymphomas. Although two CD19 CAR T-cell products have been commercially approved to treat relapsed/refractory B-cell lymphomas, outcomes in these patients remain inferior to those of patients with B-cell leukemia, regardless of therapy. Recent clinical studies and preclinical reports suggest that certain characteristics, such as the suppressive lymphoma tumor microenvironment and inferior endogenous T-cell fitness, may contribute to discrepant resp

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7

Schwarzinger, Ilse, Markus Exner, Harald Esterbauer, et al. "Microvessel Endothelial Cells of Hematological Malignancies Harbor Disease Specific Genetic Aberrations." Blood 104, no. 11 (2004): 544. http://dx.doi.org/10.1182/blood.v104.11.544.544.

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Abstract The growth of most tumors depends on the formation of new blood vessels. In contrast to genetically unstable tumor cells, endothelial cells of tumor vessels are believed to be normal diploid cells that do not acquire mutations. We have recently observed that microvessel endothelial cells of patients with B-cell lymphomas carry lymphoma specific aberrations (NEJM351:250–9, 2004). The aim of this study was to determine whether hematological malignancies other than B-cell lymphomas also carry disease specific genetic aberrations. Using a combined immunohistochemical and fluorescence in s

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8

Jang, Min Soo, Dong Young Kang, Jong Bin Park, Sang Tae Kim, and Kee Suck Suh. "Cutaneous T-Cell Lymphoma in Asians." ISRN Dermatology 2012 (July 15, 2012): 1–8. http://dx.doi.org/10.5402/2012/575120.

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Cutaneous T-cell lymphoma describes a heterogeneous group of neoplasms of skin homing T cells that vary considerably in clinical presentation, histologic appearance, immunophenotype, and prognosis. This paper addresses the cutaneous T-cell lymphoma in Asians with respect to clinical-epidemiologic and histopathological features. Compared with Western countries, Asia usually has higher rates of cutaneous T-cell lymphomas such as extranodal NK/T-cell lymphoma, hydroa vacciniforme-like lymphoma, subcutaneous panniculitis T-cell lymphoma, and adult T-cell leukemia/lymphoma and lower rates of cutane

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9

Lança, Telma, Daniel V. Correia, Catarina F. Moita та ін. "The MHC class Ib protein ULBP1 is a nonredundant determinant of leukemia/lymphoma susceptibility to γδ T-cell cytotoxicity". Blood 115, № 12 (2010): 2407–11. http://dx.doi.org/10.1182/blood-2009-08-237123.

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Abstract On the path to successful immunotherapy of hematopoietic tumors, γδ T cells offer great promise because of their human leukocyte antigen (HLA)–unrestricted targeting of a wide variety of leukemias/lymphomas. However, the molecular mechanisms underlying lymphoma recognition by γδ T cells remain unclear. Here we show that the expression levels of UL16-binding protein 1 (ULBP1) determine lymphoma susceptibility to γδ T cell–mediated cytolysis. Consistent with this, blockade of NKG2D, the receptor for ULBP1 expressed on all Vγ9+ T cells, significantly inhibits lymphoma cell killing. Speci

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10

Moffitt, Andrea B., and Sandeep S. Dave. "Clinical Applications of the Genomic Landscape of Aggressive Non-Hodgkin Lymphoma." Journal of Clinical Oncology 35, no. 9 (2017): 955–62. http://dx.doi.org/10.1200/jco.2016.71.7603.

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In this review, we examine the genomic landscapes of lymphomas that arise from B, T, and natural killer cells. Lymphomas represent a striking spectrum of clinical behaviors. Although some lymphomas are curable with standard therapy, the majority of the affected patients succumb to their disease. Here, the genetic underpinnings of these heterogeneous entities are reviewed. We consider B-cell lymphomas, including Burkitt lymphoma, diffuse large B-cell lymphoma, Hodgkin lymphoma, and primary mediastinal B-cell lymphoma. We also examine T-cell lymphomas, including anaplastic large-cell lymphoma, a

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11

Taylor, Justin, Wenbin Xiao, and Omar Abdel-Wahab. "Diagnosis and classification of hematologic malignancies on the basis of genetics." Blood 130, no. 4 (2017): 410–23. http://dx.doi.org/10.1182/blood-2017-02-734541.

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Abstract Genomic analysis has greatly influenced the diagnosis and clinical management of patients affected by diverse forms of hematologic malignancies. Here, we review how genetic alterations define subclasses of patients with acute leukemias, myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPNs), non-Hodgkin lymphomas, and classical Hodgkin lymphoma. These include new subtypes of acute myeloid leukemia defined by mutations in RUNX1 or BCR-ABL1 translocations as well as a constellation of somatic structural DNA alterations in acute lymphoblastic leukemia. Among patients with M

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12

Tillman, Heather, Laura J. Janke, Amy Funk, Peter Vogel, and Jerold E. Rehg. "Morphologic and Immunohistochemical Characterization of Spontaneous Lymphoma/Leukemia in NSG Mice." Veterinary Pathology 57, no. 1 (2019): 160–71. http://dx.doi.org/10.1177/0300985819882631.

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The NOD.Cg- Prkdcscid Il2rgtm1Wjl/SzJ strain (NOD scid gamma, NSG) is a severely immunodeficient inbred laboratory mouse used for preclinical studies because it is amenable to engraftment with human cells. Combining scid and Il2rgnull mutations results in severe immunodeficiency by impairing the maturation, survival, and functionality of interleukin 2–dependent immune cells, including T, B, and natural killer lymphocytes. While NSG mice are reportedly resistant to developing spontaneous lymphomas/leukemias, there are reports of hematopoietic cancers developing. In this study, we characterized

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13

Algashaamy, Khaled, Yaohong Tan, Nicolas Mackrides, et al. "Splenic B-Cell Lymphomas with Diffuse Cyclin D1 Protein Expression and Increased Prolymphocytic Cells: A Previously Unrecognized Diagnostic Pitfall." Case Reports in Hematology 2018 (September 27, 2018): 1–9. http://dx.doi.org/10.1155/2018/5761953.

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Prolymphocytic transformation is a concept usually applied in the context of chronic lymphocytic leukemia/small lymphocytic lymphoma to describe the presence of a high percentage of prolymphocytes in peripheral blood (usually more than 55%). Prolymphocytic transformation has also been reported in mantle cell lymphoma (MCL) but only rarely in splenic marginal zone lymphoma (SMZL). We present two splenic B-cell lymphomas presenting in the leukemic phase and with increased prolymphocytes, both classified as SMZL with prolymphocytic transformation. One case clinically simulated B-prolymphocytic le

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14

Scarfò, Irene, Maria Ormhøj, Matthew J. Frigault, et al. "Anti-CD37 chimeric antigen receptor T cells are active against B- and T-cell lymphomas." Blood 132, no. 14 (2018): 1495–506. http://dx.doi.org/10.1182/blood-2018-04-842708.

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Abstract Chimeric antigen receptor (CAR) T cells have emerged as a novel form of treatment of patients with B-cell malignancies. In particular, anti-CD19 CAR T-cell therapy has effected impressive clinical responses in B-cell acute lymphoblastic leukemia and diffuse large B-cell lymphoma. However, not all patients respond, and relapse with antigen loss has been observed in all patient subsets. Here, we report on the design and optimization of a novel CAR directed to the surface antigen CD37, which is expressed in B-cell non-Hodgkin lymphomas, in chronic lymphocytic leukemia, and in some cases

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15

Carbone, A., A. Gloghini, V. Zagonel, et al. "The expression of CD26 and CD40 ligand is mutually exclusive in human T- cell non-Hodgkin's lymphomas/leukemias." Blood 86, no. 12 (1995): 4617–26. http://dx.doi.org/10.1182/blood.v86.12.4617.bloodjournal86124617.

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CD26 and CD40 ligand (CD40L) are surface molecules on human activated T lymphocytes that play a critical role in the regulation of lymphopoiesis. Both molecules are expressed on a restricted fraction of human T-cell non-Hodgkin's lymphomas (NHL)/leukemias; however, little is known about their functional and/or clinical significance in these disorders. In this study, the pattern of expression of CD40L was compared with that of the CD26 molecule. A series of 67 human T-cell NHL/leukemias and a panel of leukemia/lymphoma T-cell lines were evaluated by immunohistochemistry, flow cytometry, and RNA

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16

Shi, Yang, and Endi Wang. "Hepatosplenic T-Cell Lymphoma: A Clinicopathologic Review With an Emphasis on Diagnostic Differentiation From Other T-Cell/Natural Killer–Cell Neoplasms." Archives of Pathology & Laboratory Medicine 139, no. 9 (2015): 1173–80. http://dx.doi.org/10.5858/arpa.2014-0079-rs.

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Hepatosplenic T-cell lymphoma is a rare, aggressive T-cell lymphoma, characterized by hepatosplenic sinusoidal infiltration of monotonous, medium-sized, nonactivated cytotoxic T cells, usually of γ/δ T-cell receptor type. Hepatosplenic T-cell lymphoma occurs more frequently in immunocompromised patients, especially in those receiving long-term immunosuppressive therapy. Patients usually manifest hepatosplenomegaly without lymphadenopathy. The bone marrow is also involved in two-thirds of cases and is often accompanied by circulating lymphoma cells, which, along with anemia and thrombocytopenia

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17

Weng, Jinsheng, Seema Rawal, Fuliang Chu, et al. "TCL1: a shared tumor-associated antigen for immunotherapy against B-cell lymphomas." Blood 120, no. 8 (2012): 1613–23. http://dx.doi.org/10.1182/blood-2011-09-382838.

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Abstract Immunotherapy with therapeutic idiotype vaccines offers promise for treatment of B-cell malignancies. However, identification of novel immunogenic lymphoma-associated antigens that are universally expressed is necessary to overcome the barriers of patient-specific idiotype vaccines. Here, we determined whether T-cell leukemia/lymphoma 1 (TCL1) oncoprotein encoded by the TCL1 gene could be a target for immunotherapy of B-cell malignancies. We show that TCL1 mRNA and protein are selectively expressed in normal B cells but markedly hyperexpressed in multiple human B-cell lymphomas, inclu

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18

Rodig, Scott J., Jeremy S. Abramson, Geraldine S. Pinkus, Steven P. Treon, Margaret A. Shipp, and Jeffery L. Kutok. "Evaluation of CD52 Expression in Hematopoietic Neoplasms by Standard Immunohistochemistry: Implications for the Expanded Use of Alemtuzumab (CAMPATH-1H) in the Treatment of Hematological Malignancies." Blood 106, no. 11 (2005): 3346. http://dx.doi.org/10.1182/blood.v106.11.3346.3346.

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Abstract CD52 is a GPI-linked glycoprotein expressed by B cells, T cells, monocytes and macrophages. The humanized monoclonal antibody alemtuzumab (CAMPATH-1H) is specific for CD52 and is FDA-approved for the treatment of relapsed or refractory chronic lymphocytic leukemia (CLL). The utility of alemtuzumab in the treatment of other lymphoid and non-lymphoid malignancies has been recently explored; however, a comprehensive survey of CD52 expression among the various classes of hematopoietic neoplasms has not been completed. In addition, most methods of detecting CD52 rely on flow cytometric tec

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Gaudio, Eugenio, Riccardo Spizzo, Francesco Paduano та ін. "Tcl1 interacts with Atm and enhances NF-κB activation in hematologic malignancies". Blood 119, № 1 (2012): 180–87. http://dx.doi.org/10.1182/blood-2011-08-374561.

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Abstract The T-cell leukemia/lymphoma 1 (TCL1) oncogene is a target of chromosomal translocations and inversions at 14q31.2, and its rearrangement in T cells causes T-cell prolymphocytic leukemias. TCL1 dysregulation in B cells is responsible for the development of an aggressive form of chronic lymphocytic leukemia (CLL), the most common human leukemia. We have investigated the mechanisms underlying the oncogenic functions of Tcl1 protein using a mass spectrometry approach and have identified Atm (ataxia-telangiectasia mutated) as a candidate Tcl1-interacting protein. The Tcl1-Atm complex form

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20

Harrer, Dennis C., Gerold Schuler, Jan Dörrie, and Niels Schaft. "CSPG4-Specific CAR T Cells for High-Risk Childhood B Cell Precursor Leukemia." International Journal of Molecular Sciences 20, no. 11 (2019): 2764. http://dx.doi.org/10.3390/ijms20112764.

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The advent of CD19-specific chimeric antigen receptor (CAR) T cells has proven to be a powerful asset in the arsenal of cancer immunotherapy of acute lymphoblastic leukemia and certain B cell lymphomas. However, a sizable portion of patients treated with CD19-CAR T cells relapse with CD19-negative cancer cells, necessitating the quest for back-up antigens. Chondroitin sulfate proteoglycan 4 (CSPG4) expression has been reported on leukemic blasts bearing the ill-fated MLL 11q23 rearrangement. We aimed at exploring the use of CSPG4-specific CAR T cells against mixed-lineage leukemia (MLL)-rearra

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21

Gill, Saar, and Jennifer N. Brudno. "CAR T-Cell Therapy in Hematologic Malignancies: Clinical Role, Toxicity, and Unanswered Questions." American Society of Clinical Oncology Educational Book, no. 41 (June 2021): e246-e265. http://dx.doi.org/10.1200/edbk_320085.

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At the time of writing, five anti-CD19 CAR T-cell products are approved by the U.S. Food and Drug Administration for seven different indications in lymphoid malignancies, including B-cell non-Hodgkin lymphoma, pediatric B-cell acute lymphoblastic leukemia, and multiple myeloma. CAR T cells for chronic lymphocytic leukemia, acute myeloid leukemia, and less common malignancies such as T-cell lymphomas and Hodgkin lymphoma are being tested in early-phase clinical trials worldwide. The purpose of this overview is to describe the current landscape of CAR T cells in hematologic malignancies, outline

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Smith, Melody, Johannes Zakrzewski, Scott James, and Michel Sadelain. "Posttransplant chimeric antigen receptor therapy." Blood 131, no. 10 (2018): 1045–52. http://dx.doi.org/10.1182/blood-2017-08-752121.

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Abstract Therapeutic T-cell engineering is emerging as a powerful approach to treat refractory hematological malignancies. Its most successful embodiment to date is based on the use of second-generation chimeric antigen receptors (CARs) targeting CD19, a cell surface molecule found in most B-cell leukemias and lymphomas. Remarkable complete remissions have been obtained with autologous T cells expressing CD19 CARs in patients with relapsed, chemo-refractory B-cell acute lymphoblastic leukemia, chronic lymphocytic leukemia, and non-Hodgkin lymphoma. Allogeneic CAR T cells may also be harnessed

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Karschnia, Philipp, Jens Blobner, Nico Teske, et al. "CAR T-Cells for CNS Lymphoma: Driving into New Terrain?" Cancers 13, no. 10 (2021): 2503. http://dx.doi.org/10.3390/cancers13102503.

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Primary CNS lymphomas (PCNSL) represent a group of extranodal non-Hodgkin lymphomas and secondary CNS lymphomas refer to secondary involvement of the neuroaxis by systemic disease. CNS lymphomas are associated with limited prognosis even after aggressive multimodal therapy. Chimeric antigen receptor (CAR) T-cells have proven as a promising therapeutic avenue in hematological B-cell malignancies including diffuse large B-cell lymphoma, B-cell acute lymphoblastic leukemia, and mantle-cell lymphoma. CARs endow an autologous T-cell population with MHC-unrestricted effectivity against tumor target

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Morales, D., B. E. Beltran, C. Castañeda, A. Carrasco, P. Quiñones, and A. Yabar. "Treg phenotype in T-cell lymphomas." Journal of Clinical Oncology 25, no. 18_suppl (2007): 18513. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.18513.

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18513 Background: Foxp3 is a key regulatory gene required for the development and function of: regulatory CD4+CD25high T cells (Treg) specialized in maintaining the balance between immunity and tolerance and activated conventional CD4+CD25low T cells without suppressive activity. Previous studies had reported the origin of Adult T-cell Leukemia/Lymphoma cells (ATLL) in Foxp3 T cells and in other lymphomas types the FOXP3 expression was only detected in the reactive T-cell background. Our objetive was to determine the presence of Treg phenotype cells by the FOXP3 expression in T-cell lymphomas.

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Jacobson, Caron A., and Marcela V. Maus. "C(h)AR-ting a new course in incurable lymphomas: CAR T cells for mantle cell and follicular lymphomas." Blood Advances 4, no. 22 (2020): 5858–62. http://dx.doi.org/10.1182/bloodadvances.2020003391.

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Abstract Chimeric antigen receptor (CAR) T-cell therapy targeting CD19 has transformed the natural history of relapsed and refractory B-cell acute lymphoblastic leukemia and aggressive B-cell non-Hodgkin lymphoma. Based on these results, CD19 CAR T cells have since been tested in largely incurable lymphomas, including mantle cell lymphoma, follicular lymphoma, and marginal zone lymphoma, with promising early results that raise the question of whether this cellular immunotherapy could have curative potential and change the natural history of these diseases. This article reviews these results an

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Macon, WR, ME Williams, JP Greer, et al. "Natural killer-like T-cell lymphomas: aggressive lymphomas of T-large granular lymphocytes [see comments]." Blood 87, no. 4 (1996): 1474–83. http://dx.doi.org/10.1182/blood.v87.4.1474.bloodjournal8741474.

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Natural killer (NK)-like T cells are major histocompatibility complex- unrestricted cytotoxic T cells that are surface CD3-positive, express NK-cell antigens, and rearrange their T-cell receptor. Most neoplasms arising from this T-cell subpopulation have been a chronic lymphoproliferative disease referred to as T-large granular lymphocyte (LGL) leukemia. Only 10 NK-like T-cell lymphomas have been described in detail previously; this study presents the clinicopathologic features of six others and distinguishes these lymphomas from T-LGL leukemia. All patients presented with B-symptoms and often

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Parrula, C., B. Zimmerman, P. Nadella, et al. "Expression of Tumor Invasion Factors Determines Systemic Engraftment and Induction of Humoral Hypercalcemia in a Mouse Model of Adult T-cell Leukemia." Veterinary Pathology 46, no. 5 (2009): 1003–14. http://dx.doi.org/10.1354/vp.08-vp-0254-n-fl.

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Infection with human T-cell leukemia virus type 1 (HTLV-1) leads sometimes to the development of adult T-cell lymphoma/leukemia (ATL), which is invariably fatal and often associated with humoral hypercalcemia of malignancy. The transformation of infected CD4 T cells and the pathogenesis of leukemia have been studied with great limitation in tissue culture and patients. To better understand the pathogenesis and perform preclinical drug studies, animal models of ATL are urgently needed. In mice, inoculation of HTLV-1 cell lines mostly leads to development of localized lymphomas. To develop an AT

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Feuer, G., JA Zack, WJ Jr Harrington, et al. "Establishment of human T-cell leukemia virus type I T-cell lymphomas in severe combined immunodeficient mice." Blood 82, no. 3 (1993): 722–31. http://dx.doi.org/10.1182/blood.v82.3.722.722.

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Abstract Human T-cell leukemia virus type I (HTLV-I) is recognized as the etiologic agent of adult T-cell leukemia (ATL), a disease endemic in certain regions of southeastern Japan, Africa, and the Caribbean basin. Although HTLV-I can immortalize T lymphocytes in culture, factors leading to tumor progression after HTLV-I infection remain elusive. Previous attempts to propagate the ATL tumor cells in animals have been unsuccessful. Severe combined immunodeficient (SCID) mice have previously been used to support the survival of human lymphoid cell populations when inoculated with human periphera

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Feuer, G., JA Zack, WJ Jr Harrington, et al. "Establishment of human T-cell leukemia virus type I T-cell lymphomas in severe combined immunodeficient mice." Blood 82, no. 3 (1993): 722–31. http://dx.doi.org/10.1182/blood.v82.3.722.bloodjournal823722.

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Human T-cell leukemia virus type I (HTLV-I) is recognized as the etiologic agent of adult T-cell leukemia (ATL), a disease endemic in certain regions of southeastern Japan, Africa, and the Caribbean basin. Although HTLV-I can immortalize T lymphocytes in culture, factors leading to tumor progression after HTLV-I infection remain elusive. Previous attempts to propagate the ATL tumor cells in animals have been unsuccessful. Severe combined immunodeficient (SCID) mice have previously been used to support the survival of human lymphoid cell populations when inoculated with human peripheral blood l

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McGregor, Stephanie, Anant Shah, Gordana Raca та ін. "PLZF Staining Identifies Peripheral T-Cell Lymphomas Derived From Non-Conventional T-Cells With Limited α-Chain Diversity". Blood 122, № 21 (2013): 4300. http://dx.doi.org/10.1182/blood.v122.21.4300.4300.

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Abstract Peripheral T-cell lymphomas are uncommon and account for 10-15% of all non-Hodgkin lymphomas (NHL). The current classification and treatment strategy of peripheral T-cell lymphomas relies on integrating morphology with immunophenotype, genetics and clinical presentation. However, the most common category of peripheral T-cell lymphomas remains peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) reflecting the lack of specific parameters to better define these lymphomas in a biologically relevant way. As our understanding of the biology of peripheral T-cell development contin

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Banerjee, Prabal, Adam Tripp, Michael D. Lairmore, et al. "Adult T-cell leukemia/lymphoma development in HTLV-1–infected humanized SCID mice." Blood 115, no. 13 (2010): 2640–48. http://dx.doi.org/10.1182/blood-2009-10-246959.

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AbstractThe molecular and genetic factors induced by human T-lymphotropic virus type-1 (HTLV-1) that initiate adult T-cell leukemia/lymphoma (ATLL) remain unclear, in part from the lack of an animal model that accurately recapitulates leukemogenesis. HTLV-1–infected humanized nonobese diabetic severe combined immunodeficiency (HU-NOD/SCID) mice were generated by inoculation of NOD/SCID mice with CD34+ hematopoietic progenitor and stem cells (CD34+ HP/HSCs) infected ex vivo with HTLV-1. HTLV-1-HU-NOD/SCID mice exclusively developed CD4+ T-cell lymphomas with characteristics similar to ATLL and

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Grønbæk, Kirsten, Jesper Worm, Elisabeth Ralfkiaer, Vibeke Ahrenkiel, Peter Hokland, and Per Guldberg. "ATM mutations are associated with inactivation of theARF-TP53 tumor suppressor pathway in diffuse large B-cell lymphoma." Blood 100, no. 4 (2002): 1430–37. http://dx.doi.org/10.1182/blood-2002-02-0382.

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The ATM serine-threonine kinase plays a central role in the cellular response to DNA damage. Germ-line mutations in theATM gene cause ataxia-telangiectasia (A-T), a multisystem disorder associated with predisposition to lymphoma and acute leukemia. Moreover, somatic ATM mutations have been identified in T-cell prolymphocytic leukemia, mantle cell lymphoma, and B-cell chronic lymphocytic leukemia. In this study, the entire ATMcoding sequence was examined in genomic DNA from 120 lymphoid neoplasms. Novel mutations and mutations implicated in cancer and/or A-T were found in 9 of 45 diffuse large

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Campagnari, Francesco, Emilio Bombardieri, Filippo de Braud, Luca Baldini, and Anna Teresa Maiolo. "Terminal Deoxynucleotidyl Transferase, Tdt, as a Marker for Leukemia and Lymphoma Cells." International Journal of Biological Markers 2, no. 1 (1987): 31–42. http://dx.doi.org/10.1177/172460088700200105.

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Terminal deoxynucleotidyl transferase, TdT, was assayed in the mononucleate cells of blood and bone marrow from 121 patients with leukemias at the onset of disease and from 95 subjects with malignant lymphomas at diagnosis. This intracellular marker was also investigated by cytoimmunofluorescent tests in 17 other cases of initial leukemias and in 3 diagnosed lymphoblastic lymphomas. Generally, the TdT levels were significantly enhanced in the blasts of the following: acute undifferentiated leukemias; the more immature types of acute lymphoblastic leukemias i.e., the null, non-T non-B, common,

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Reschly, Erica J., Christina Spaulding, Tomas Vilimas, et al. "Notch1 promotes survival of E2A-deficient T cell lymphomas through pre–T cell receptor–dependent and –independent mechanisms." Blood 107, no. 10 (2006): 4115–21. http://dx.doi.org/10.1182/blood-2005-09-3551.

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Loss of E2A transcription factor activity or activation of the intracellular form of Notch1 (ICN) leads to the development of leukemia or lymphoma in humans or mice, respectively. Current models propose that ICN functions by suppressing E2A through a pre–T cell receptor (TCR)–dependent mechanism. Here we show that lymphomas arising in E2A–/– mice require the activation of Notch1 for their survival and have accumulated mutations in, or near, the Notch1 PEST domain, resulting in increased stability and signaling. In contrast, lymphomas arising in p53–/– mice show the activation of Notch1, but no

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35

Feller, AC, HH Wacker, G. Moldenhauer, HJ Radzun, and MR Parwaresch. "Monoclonal antibody Ki-B3 detects a formalin resistant antigen on normal and neoplastic B cells." Blood 70, no. 3 (1987): 629–36. http://dx.doi.org/10.1182/blood.v70.3.629.629.

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Abstract A new monoclonal antibody Ki-B3 produced by a fusion with leukemic cells of a centroblastic/centrocytic lymphoma (m.l. follicular) is introduced. This antibody predominantly recognizes B cells of follicular mantle and germinal center cells, as well as plasma cells in normal lymphoid tissue. Furthermore, 80% of all low- and high-grade B cell lymphomas are stained, whereas among T cell lymphomas, only four of 15 T lymphoblastic lymphomas were positive to Ki-B3. All peripheral T cell lymphomas showed a negative reaction. Additionally, Ki-B3 detects a small percentage of monocytes and som

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36

Feller, AC, HH Wacker, G. Moldenhauer, HJ Radzun, and MR Parwaresch. "Monoclonal antibody Ki-B3 detects a formalin resistant antigen on normal and neoplastic B cells." Blood 70, no. 3 (1987): 629–36. http://dx.doi.org/10.1182/blood.v70.3.629.bloodjournal703629.

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A new monoclonal antibody Ki-B3 produced by a fusion with leukemic cells of a centroblastic/centrocytic lymphoma (m.l. follicular) is introduced. This antibody predominantly recognizes B cells of follicular mantle and germinal center cells, as well as plasma cells in normal lymphoid tissue. Furthermore, 80% of all low- and high-grade B cell lymphomas are stained, whereas among T cell lymphomas, only four of 15 T lymphoblastic lymphomas were positive to Ki-B3. All peripheral T cell lymphomas showed a negative reaction. Additionally, Ki-B3 detects a small percentage of monocytes and some myelomo

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Däbritz, J. Henry M., Maja Milanovic, Zhen Zhao, et al. "Acquired Stem Cell Properties In Therapy-Induced Senescence Of Lymphomas and Acute Leukemias In Vitro and In Vivo." Blood 122, no. 21 (2013): 4193. http://dx.doi.org/10.1182/blood.v122.21.4193.4193.

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Abstract Introduction Premature senescence is a permanent proliferative arrest that occurs in response to oncogenic signaling or DNA-damaging chemotherapy. Although tumor cell senescence has been recognized as a prognostically relevant contribution to long-term outcome post-therapy in hematological tumor models, therapeutic utilization of senescence is still hampered by an incomplete understanding of biological properties and long-term fate of senescent tumor cells in patients. Interestingly, senescence-regulating factors have recently been shown to limit reprogramming of somatic cells to plur

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Beltrán-Gárate, Brady E., Pilar Quiñones, Domingo Morales, et al. "FOXP3 Expression in Diverse T-Cell Lymphomas." Blood 108, no. 11 (2006): 4760. http://dx.doi.org/10.1182/blood.v108.11.4760.4760.

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Abstract BACKGROUND: Foxp3 is a key regulatory gene required for the development and function of: regulatory CD4+CD25high T cells (Treg) specialized in maintaining the balance between immunity and tolerance and activated conventional CD4+CD25low T cells without suppressive activity. Until now it is not yet possible to study human FOXP3+ Treg irrespective of their CD25 expression. Previous studies had reported FOXP3+ T cells in Adult T-cell Leukemia/Lymphoma cells (ATLL) related to HTLV-1 and in other lymphomas types the FOXP3 expression was only detected in the reactive T-cell background. AIM:

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39

Berlier, Willy, Karine Aguera, Anne-Marie Chevrier, et al. "Asparagine Synthetase Expression and L-Asparaginase Sensitivity in Aggressive Lymphomas." Blood 124, no. 21 (2014): 5494. http://dx.doi.org/10.1182/blood.v124.21.5494.5494.

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Abstract L-asparaginase (L-ASPA) displays a strong clinical benefit in the treatment of acute lymphoblastic leukemia (ALL), where it is included in most of current chemotherapy regimen. L-ASPA depletes plasmatic asparagine (ASN), an amino acid essential for the proliferation of leukemic cells. Since these cells are deficient in asparagine synthetase (ASNS), they rely on external (plasmatic) source of ASN and can be starved to death by L-ASP treatment. Several studies evidenced the potential of ASN depletion to treat lymphomas. Indeed, many animal and human lymphoma cell lines have been shown t

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Longe, Harold, Douglas V. Faller, and Gerald V. Denis. "Telomere-Based Pre-Clinical Therapy in a Murine Model of Non-Hodgkin’s Lymphoma of the Diffuse Large B Cell (DLCL)Type." Blood 106, no. 11 (2005): 607. http://dx.doi.org/10.1182/blood.v106.11.607.607.

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Abstract The dual bromodomain Brd2 is closely related to the basal transcription factor TAFII250, which is essential for cyclin A transactivation and mammalian cell cycle progression. Constitutive expression of BRD2 (under Eμ control) in the lymphoid lineage of transgenic mice elevates basal transcription of cyclin A, destabilizes the cell cycle and leads to B cell leukemias and lymphomas that are monoclonal, morphologically uniform, transplantable and highly malignant. The surface immunophenotype of the lymphoma cells is: B220+, CD19+, sIgM+, CD5+, CD9+; B7-1 and B7-2 elevated, CD23low; CD11b

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41

Kohla, Samah, Feryal A. Ibrahim, Deena Mudawi, et al. "High-Grade Epstein-Barr Virus-Negative Biphenotypic Lymphoma with Expression of B- and T-Cell Markers and Leukemia Presentation: Case Report and Literature Review." Case Reports in Oncology 13, no. 3 (2020): 1215–26. http://dx.doi.org/10.1159/000510403.

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Lymphomas are presently categorized according to their origin from B or T lymphocytes. The co-expression of CD3 in B-cell lymphomas or CD20 in T-cell lymphomas has been rarely reported. Immature and less often mature lymphomas may incorporate the rearrangements of both B- and T-cell antigen receptor genes (dual genotype or bigenotype). Lymphoma cells with a sole genotype hardly concurrently express both B- and T-cell markers (biphenotypic lymphomas). We describe a 63-year-old female who was presented with obstructive jaundice and epigastric pain of 10 days. Initial CBC revealed 43x10<sup&gt

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Drakos, Elias, George Z. Rassidakis, Wei Guo, L. Jeffrey Medeiros, and Lalitha Nagarajan. "Differential Expression of the Homeobox Gene MIXL1 in Non Hodgkin (NHL) and Hodgkin Lymphomas (HL)." Blood 106, no. 11 (2005): 3014. http://dx.doi.org/10.1182/blood.v106.11.3014.3014.

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Abstract The gene MIXL1 (Mix1 homeobox-like) encodes a paired class homeobox transcription factor involved in early hematopoietic specification during embryogenesis. Previous studies have shown that MIXL1 gene is expressed in hematopoietic cells during adult life (Guo et al. Blood100;1;89–96, 2002). Furthermore 5′ MIXL1 sequences are a target of retroviral insertion in murine T-cell lymphoma (http:RTCGD.ncifcrf.gov), suggesting a selection advantage for aberrant expression of this gene. However, the status of MIXL1 expression in human lymphomas has not been examined. Using a highly specific an

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43

Chen, Jing, Meili Zhang, Wei Ju, and Thomas A. Waldmann. "Effective treatment of a murine model of adult T-cell leukemia using depsipeptide and its combination with unmodified daclizumab directed toward CD25." Blood 113, no. 6 (2009): 1287–93. http://dx.doi.org/10.1182/blood-2008-04-149658.

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Abstract Adult T-cell leukemia (ATL) is caused by human T-cell lymphotropic virus I (HTLV-1) and is an aggressive malignancy of CD4, CD25-expressing leukemia, and lymphoma cells. There is no accepted curative therapy for ATL. Depsipeptide, a histone deacetylase inhibitor, has demonstrated major antitumor effects in leukemias and lymphomas. In this study, we investigated the therapeutic efficacy of depsipeptide alone and in combination with daclizumab (humanized anti-Tac) in a murine model of human ATL. The Met-1 ATL model was established by intraperitoneal injection of ex vivo leukemic cells i

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Chevallier, Nathalie, Connie M. Corcoran, Christine Lennon, et al. "ETO protein of t(8;21) AML is a corepressor for Bcl-6 B-cell lymphoma oncoprotein." Blood 103, no. 4 (2004): 1454–63. http://dx.doi.org/10.1182/blood-2003-06-2081.

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Abstract The multiplicity of transcription factors involved in hematologic malignancies suggests a complicated scenario in which many different molecular mechanisms lead to malignant transformation. We hypothesized that some of these proteins might physically and functionally interact and thus mechanistically link different diseases. The ETO protein of t(8;21) acute myeloid leukemia (AML) is an excellent candidate as a common factor because it is normally expressed in human hematopoietic cells, it binds to histone deacetylases (HDACs), and it interacts with the PLZF protein of t(11;17) acute p

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45

Starkey, C. R., P. A. Lobelle-Rich, S. Granger, B. K. Brightman, H. Fan, and L. S. Levy. "Tumorigenic Potential of a Recombinant Retrovirus Containing Sequences from Moloney Murine Leukemia Virus and Feline Leukemia Virus." Journal of Virology 72, no. 2 (1998): 1078–84. http://dx.doi.org/10.1128/jvi.72.2.1078-1084.1998.

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ABSTRACT A recombinant retrovirus, termed MoFe2-MuLV, was constructed in which the U3 region of T-lymphomagenic Moloney murine leukemia virus (Mo-MuLV) was replaced by that of FeLV-945, a provirus of unique long terminal repeat (LTR) structure identified only in non-T-cell, non-B-cell lymphomas of the domestic cat. The LTR of FeLV-945 is unusual in that it contains only a single copy of the transcriptional enhancer followed 25 bp downstream by a 21-bp sequence in triplicate in tandem. Infectivity of MoFe2-MuLV was demonstrated in vitro in SC-1 cells and in vivo in neonatal NIH-Swiss mice. Tumo

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46

Allouche, M., A. Bourinbaiar, V. Georgoulias, et al. "T cell lineage involvement in lymphoid blast crisis of chronic myeloid leukemia." Blood 66, no. 5 (1985): 1155–61. http://dx.doi.org/10.1182/blood.v66.5.1155.1155.

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Abstract Cytochemical and immunologic analysis of cells obtained from two patients with chronic myeloid leukemia (CML) during blast crisis reveals markers suggestive of an immature lymphoid phenotype. Peripheral blood mononuclear cells from both patients generated spontaneous lymphoblastoid colonies in methylcellulose, a phenomenon observed in T cell acute lymphoblastic leukemias and T cell non- Hodgkin's lymphomas but not in any other type of leukemia. Colonies derived from one patient were composed predominantly of OKT3+ cells (89%), whereas those from the second patient displayed 42% OKT3+

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47

Allouche, M., A. Bourinbaiar, V. Georgoulias, et al. "T cell lineage involvement in lymphoid blast crisis of chronic myeloid leukemia." Blood 66, no. 5 (1985): 1155–61. http://dx.doi.org/10.1182/blood.v66.5.1155.bloodjournal6651155.

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Cytochemical and immunologic analysis of cells obtained from two patients with chronic myeloid leukemia (CML) during blast crisis reveals markers suggestive of an immature lymphoid phenotype. Peripheral blood mononuclear cells from both patients generated spontaneous lymphoblastoid colonies in methylcellulose, a phenomenon observed in T cell acute lymphoblastic leukemias and T cell non- Hodgkin's lymphomas but not in any other type of leukemia. Colonies derived from one patient were composed predominantly of OKT3+ cells (89%), whereas those from the second patient displayed 42% OKT3+ and OKT6+

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48

Takahashi, K., Y. Ohtsuki, H. Sonobe, et al. "S-100 beta positive T cell leukemia." Blood 71, no. 5 (1988): 1299–303. http://dx.doi.org/10.1182/blood.v71.5.1299.1299.

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Abstract We reported a peculiar case with T cell leukemia. The patient was a 34- year-old woman showing extensive splenomegaly and marked leukemic cell proliferation and running a rapid fatal clinical course. The leukemic cells were morphologically ordinary lymphocytes showing suppressor/cytotoxic(s/c) T cell phenotypes and containing S-100b protein. Southern blot analysis revealed rearrangement of the beta chain genes of the T cell receptor (TcR) of the leukemic cells. Because these phenotypic and morphologic features were identical with those of S-100 beta+T lymphocytes (S-100 beta +TL) in n

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49

Takahashi, K., Y. Ohtsuki, H. Sonobe, et al. "S-100 beta positive T cell leukemia." Blood 71, no. 5 (1988): 1299–303. http://dx.doi.org/10.1182/blood.v71.5.1299.bloodjournal7151299.

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We reported a peculiar case with T cell leukemia. The patient was a 34- year-old woman showing extensive splenomegaly and marked leukemic cell proliferation and running a rapid fatal clinical course. The leukemic cells were morphologically ordinary lymphocytes showing suppressor/cytotoxic(s/c) T cell phenotypes and containing S-100b protein. Southern blot analysis revealed rearrangement of the beta chain genes of the T cell receptor (TcR) of the leukemic cells. Because these phenotypic and morphologic features were identical with those of S-100 beta+T lymphocytes (S-100 beta +TL) in normal hum

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50

Markow, Michael, Abu-Sayeef Mirza, Lia Perez, et al. "Transformation of T-Cell Acute Lymphoblastic Lymphoma to Peripheral T-Cell Lymphoma: A Report of Two Cases." Case Reports in Hematology 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/9191582.

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Nonhepatosplenic/noncutaneous γδ peripheral T-cell lymphoma (NHNCγδ PTCL) represents a miscellaneous group of unrelated T-cell lymphomas of which only isolated cases have been reported. We describe two cases of transformation from T-lymphoblastic leukemia/lymphoma to NHNCγδ PTCL. Transformation into more aggressive disease is a rare event in T-cell lineage-derived hematologic malignancies compared to B-cell neoplasms. Nevertheless, both of our cases involved relapse as PTCL manifested with skin involvement and an overt shift from blastic morphology to large granular leukemia-like mature T cell

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