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Journal articles on the topic 'Lymphomas and leukemias'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Radich, Jerald P., Andrew D. Zelenetz, Wing C. Chan, et al. "NCCN Task Force Report: Molecular Markers in Leukemias and Lymphomas." Journal of the National Comprehensive Cancer Network 7, Suppl_4 (2009): S—1—S—34. http://dx.doi.org/10.6004/jnccn.2009.0077.

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The introduction of targeted therapies has revolutionized treatment and improved outcomes in patients with leukemias and lymphomas. However, many patients experience relapse caused by the persistence of residual malignant cells. Cytogenetic and molecular techniques are increasingly being used to assess and quantify minimal residual disease (MRD). The emergence of advanced technologies has led to the discovery of multiple novel molecular markers that can be used to detect MRD and predict outcome in patients with leukemias and lymphomas. Gene expression signatures that predict clinical outcomes

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2

Dunphy, Cherie H. "Gene Expression Profiling Data in Lymphoma and Leukemia: Review of the Literature and Extrapolation of Pertinent Clinical Applications." Archives of Pathology & Laboratory Medicine 130, no. 4 (2006): 483–520. http://dx.doi.org/10.5858/2006-130-483-gepdil.

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Abstract Context.—Gene expression (GE) analyses using microarrays have become an important part of biomedical and clinical research in hematolymphoid malignancies. However, the methods are time-consuming and costly for routine clinical practice. Objectives.—To review the literature regarding GE data that may provide important information regarding pathogenesis and that may be extrapolated for use in diagnosing and prognosticating lymphomas and leukemias; to present GE findings in Hodgkin and non-Hodgkin lymphomas, acute leukemias, and chronic myeloid leukemia in detail; and to summarize the pr

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3

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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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.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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5

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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6

Poon, Eileen Yi Ling, Evelyn Wong, Wei Lin Goh, et al. "Hematological malignancies in the adolescent and young adult (AYA) population in Singapore." Journal of Clinical Oncology 38, no. 15_suppl (2020): e13630-e13630. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e13630.

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e13630 Background: Hematological malignancies is thought to be one of the more common Adolescent and Young Adult (AYA) cancers and constitute leukemias and lymphomas. However, little is known about its incidence and prevalence in Asia. We also do not have any data on its behavior or its prognosticators. The outcomes of this group of patients is also unknown when compared to the pediatrics or geriatrics, but is expected to be not as ideal. There is no consensus on whether this group of patients should be treated as pediatrics or as the older adults. We have sought to evaluate the prevalence and

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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

Agrelo, Ruben, Fernando Setien, Jesus Espada, et al. "Inactivation of the Lamin A/C Gene by CpG Island Promoter Hypermethylation in Hematologic Malignancies, and Its Association With Poor Survival in Nodal Diffuse Large B-Cell Lymphoma." Journal of Clinical Oncology 23, no. 17 (2005): 3940–47. http://dx.doi.org/10.1200/jco.2005.11.650.

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Purpose Lamins support the nuclear envelope and provide anchorage sites for chromatin, but they are also involved in DNA synthesis, transcription, and apoptosis. Although the lack of expression of A-type lamins in lymphoma and leukemia has been reported, the mechanism was unknown. We investigated the possible role of CpG island hypermethylation in lamin A/C silencing and its prognostic relevance. Patients and Methods The promoter CpG island methylation status of the lamin A/C gene, encoding the A-type lamins, was analyzed by bisulfite genomic sequencing and methylation-specific polymerase chai

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9

Wang, Wei, Magdalena Czader, and Sa A. Wang. "Blood- and bone marrow–based mature T-cell and natural killer cell leukemias and lymphomas: a summary in the series of the 2023 SH/EAHP Workshop." American Journal of Clinical Pathology 164, no. 1 (2025): 7–25. https://doi.org/10.1093/ajcp/aqaf009.

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Abstract This session included 51 cases submitted to the workshop “Progress in T- and NK-cell Lymphomas and Leukemias” by the Society for Hematopathology and European Association for Haematopathology under “Blood/Bone Marrow–Based Mature T- and NK-Cell Leukemias/Lymphomas” or “T/NK-cell neoplasms with a Leukemic Presentation.” Entities encompassed T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia (LGLL), natural killer (NK)-LGLL/chronic lymphoproliferative disorder of NK cells, adult T-cell leukemia/lymphoma, aggressive NK-cell leukemia, and their mimics. Submitted cas

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10

Rodrigues, Paulo Henrique Silva, Cybelle Façanha Barreto Medeiros Linard, Francisco José Maia Pinto, Rafaela de Lima Gomes Soares, Germison Silva Lopes, and Henrique Girão Martins. "The role of chemotherapy toxicity scales in decision-making for acute leukemia and lymphoma: a scoping review." Concilium 23, no. 18 (2023): 59–78. http://dx.doi.org/10.53660/clm-1979-23n49.

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Acute leukemias and non-Hodgkin lymphomas together rank 4th among the most common neoplasms. With curative treatment options, even in adverse situations, however, the decision-making process is delicate and statistical models can help. To identify the chemotherapy toxicity scales and their role in decision-making for the treatment of patients with acute lymphomas and leukemias, we conducted a scoping review on the PUBMED, BIREME, COCHRANE, and CAPES journal data platforms. Thirty articles were selected using the PRISMA protocol approach. There is no ideal scale for assessing chemotherapy toxic

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11

Bardales, R. H., A. M. Al-Katib, A. Carrato, and B. Koziner. "Detection of intracytoplasmic immunoglobulin by flow cytometry in B-cell malignancies." Journal of Histochemistry & Cytochemistry 37, no. 1 (1989): 83–89. http://dx.doi.org/10.1177/37.1.2491755.

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The aim of this study was to compare the results of flow cytometric (FCM) determination of heavy and light chain cytoplasmic immunoglobulin (cIg) with those obtained by the peroxidase-antiperoxidase (PAP) method. Fifty-one patients, including five non-T-acute lymphoblastic leukemias, 16 B-chronic lymphocytic leukemias (CLL), 13 non-Hodgkin's lymphomas, seven hairy cell leukemias, four multiple myeloma/plasma cell leukemias, and six T-cell leukemia/lymphomas, as well as 12 normal controls, were studied. Saponin-permeabilized cell suspensions were indirectly stained with monoclonal antibodies an

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12

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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13

Yano, T., CA Sander, RE Andrade, et al. "Molecular analysis of the BCL-3 locus at chromosome 17q22 in B-cell neoplasms." Blood 82, no. 6 (1993): 1813–19. http://dx.doi.org/10.1182/blood.v82.6.1813.1813.

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Abstract To better understand the role of the BCL-3 locus at chromosome 17q22 in the pathogenesis and progression of leukemias and lymphomas, we examined its genomic configuration in 264 B-cell malignancies and its expression in a smaller subset. Cases studied included 39 chronic lymphocytic leukemias, 58 low-grade follicular lymphomas, 20 mantle cell lymphomas, 30 small noncleaved cell lymphomas, 25 acute lymphoblastic leukemias, 10 acquired immunodeficiency syndrome--related non-Hodgkin's lymphomas, and 44 diffuse mixed- or diffuse large-cell lymphomas. In addition, 38 aggressive lymphomas (

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14

Yano, T., CA Sander, RE Andrade, et al. "Molecular analysis of the BCL-3 locus at chromosome 17q22 in B-cell neoplasms." Blood 82, no. 6 (1993): 1813–19. http://dx.doi.org/10.1182/blood.v82.6.1813.bloodjournal8261813.

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To better understand the role of the BCL-3 locus at chromosome 17q22 in the pathogenesis and progression of leukemias and lymphomas, we examined its genomic configuration in 264 B-cell malignancies and its expression in a smaller subset. Cases studied included 39 chronic lymphocytic leukemias, 58 low-grade follicular lymphomas, 20 mantle cell lymphomas, 30 small noncleaved cell lymphomas, 25 acute lymphoblastic leukemias, 10 acquired immunodeficiency syndrome--related non-Hodgkin's lymphomas, and 44 diffuse mixed- or diffuse large-cell lymphomas. In addition, 38 aggressive lymphomas (transform

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15

Marie, J. P. "Leukemias and lymphomas." Leukemia Research 10, no. 2 (1986): 231. http://dx.doi.org/10.1016/0145-2126(86)90047-0.

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16

Malpas, J. S. "Leukemias and Lymphomas." Postgraduate Medical Journal 61, no. 721 (1985): 1022. http://dx.doi.org/10.1136/pgmj.61.721.1022-a.

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17

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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18

Tomacinschii, Victor, Maria Robu, Vasile Musteață, et al. "SECONDARY ACUTE PROMYELOCYTIC LEUKEMIA DEVELOPED AFTER TREATMENT OF NON-HODGKIN'S LYMPHOMA. CLINICAL CASE AND REVIEW OF LITERATURE." Arta Medica 76, no. 3 (2020): 115–18. https://doi.org/10.5281/zenodo.4070160.

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<strong>Background. </strong>Acute promyelocytic leukemia is an acute myeloid leukemia that accounts approximately 10% of acute myeloid leukemia cases. Acute promyelocytic leukemias usually appears as a de novo finding. The occurrence of secondary acute promyelocytic leukemias after chemotherapy is rare, and the development of secondary acute promyelocytic leukemias after an non-Hodgkin lymphoma is casuistic. The objective of the study is to describe a case of secondary acute promyelocytic leukemia developed  after non-Hodgkin lymphoma therapy <strong>Clinical case. </strong>Male B, 34 ye

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19

Chatterjee, M., M. Barcos, T. Han, XL Liu, Z. Bernstein, and KA Foon. "Shared idiotype expression by chronic lymphocytic leukemia and B-cell lymphoma." Blood 76, no. 9 (1990): 1825–29. http://dx.doi.org/10.1182/blood.v76.9.1825.1825.

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Abstract Antiidiotype (Id) antibodies identify unique determinants within the surface immunoglobulin (Ig) that are present on B-cell tumors. Anti-Ids have been used for diagnosis and therapy of B-cell lymphoma and leukemia. A panel of 29 anti-Id monoclonal antibodies (MoAbs) that recognize shared idiotypes (SIds) on B-cell lymphomas was tested for reactivity with both B-cell leukemias and lymphomas. Ten of 40 (25%) cases of chronic lymphocytic leukemia (CLL) reacted with at least one of the 29 anti-SId MoAbs. Three cases reacted with more than one anti- SId MoAb, but there was no repetitive pa

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20

Chatterjee, M., M. Barcos, T. Han, XL Liu, Z. Bernstein, and KA Foon. "Shared idiotype expression by chronic lymphocytic leukemia and B-cell lymphoma." Blood 76, no. 9 (1990): 1825–29. http://dx.doi.org/10.1182/blood.v76.9.1825.bloodjournal7691825.

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Antiidiotype (Id) antibodies identify unique determinants within the surface immunoglobulin (Ig) that are present on B-cell tumors. Anti-Ids have been used for diagnosis and therapy of B-cell lymphoma and leukemia. A panel of 29 anti-Id monoclonal antibodies (MoAbs) that recognize shared idiotypes (SIds) on B-cell lymphomas was tested for reactivity with both B-cell leukemias and lymphomas. Ten of 40 (25%) cases of chronic lymphocytic leukemia (CLL) reacted with at least one of the 29 anti-SId MoAbs. Three cases reacted with more than one anti- SId MoAb, but there was no repetitive pattern of

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21

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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22

Sørensen, Karina Dalsgaard, Leticia Quintanilla-Martinez, Sandra Kunder, Jörg Schmidt, and Finn Skou Pedersen. "Mutation of All Runx (AML1/Core) Sites in the Enhancer of T-Lymphomagenic SL3-3 Murine Leukemia Virus Unmasks a Significant Potential for Myeloid Leukemia Induction and Favors Enhancer Evolution toward Induction of Other Disease Patterns." Journal of Virology 78, no. 23 (2004): 13216–31. http://dx.doi.org/10.1128/jvi.78.23.13216-13231.2004.

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ABSTRACT SL3-3 murine leukemia virus is a potent inducer of T-lymphomas in mice. Using inbred NMRI mice, it was previously reported that a mutant of SL3-3 with all enhancer Runx (AML1/core) sites disrupted by 3-bp mutations (SL3-3dm) induces predominantly non-T-cell tumors with severely extended latency (S. Ethelberg, J. Lovmand, J. Schmidt, A. Luz, and F. S. Pedersen, J. Virol. 71:7273-7280, 1997). By use of three-color flow cytometry and molecular and histopathological analyses, we have now performed a detailed phenotypic characterization of SL3-3- and SL3-3dm-induced tumors in this mouse st

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23

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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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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Uckun, FM, K. Gajl-Peczalska, DE Myers, W. Jaszcz, S. Haissig, and JA Ledbetter. "Temporal association of CD40 antigen expression with discrete stages of human B-cell ontogeny and the efficacy of anti-CD40 immunotoxins against clonogenic B-lineage acute lymphoblastic leukemia as well as B- lineage non-Hodgkin's lymphoma cells." Blood 76, no. 12 (1990): 2449–56. http://dx.doi.org/10.1182/blood.v76.12.2449.bloodjournal76122449.

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Detailed immunophenotypic analyses of immunologically classified leukemias and lymphomas showed that CD40 displays an exquisite B- lineage specificity within the human lymphopoietic system. Notably, 82% of B-lineage chronic lymphocytic leukemias (CLLs), 82% of B-lineage hairy cell leukemias (HCLs), 86% of B-lineage non-Hodgkin's lymphomas (NHLs), and 29% of B-lineage acute lymphoblastic leukemias (ALLs) were CD40+. Quantitative analyses of the correlated expression of CD40 and other B-lineage differentiation antigens on fetal lymphoid precursor cells by multiparameter two-color/three-color flo

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26

Pallasch, Fabian Bernhard, Vera Freytag, Malte Kriegs, et al. "The Histogenetic Origin of Malignant Cells Predicts Their Susceptibility towards Synthetic Lethality Utilizing the TK.007 System." Cancers 16, no. 12 (2024): 2278. http://dx.doi.org/10.3390/cancers16122278.

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Background: Remarkable differences exist in the outcome of systemic cancer therapies. Lymphomas and leukemias generally respond well to systemic chemotherapies, while solid cancers often fail. We engineered different human cancer cells lines to uniformly express a modified herpes simplex virus thymidine kinase TK.007 as a suicide gene when ganciclovir (GCV) is applied, thus in theory achieving a similar response in all cell lines. Methods: Fifteen different cell lines were engineered to express the TK.007 gene. XTT-cell proliferation assays were performed and the IC50-values were calculated. F

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27

Sucharitha, Are. "An Overview of Cancer." Advances in Cancer Chemotherapy and Pharmacology 1, no. 1 (2023): 1–8. http://dx.doi.org/10.23880/accp-16000102.

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Cancer is defined as one of the large groups of diseases characterized by the development of abnormal cells that grow beyond their boundaries, which can invade adjoining tissues via circulation, and spread to other organs in the body. Cancer can be initiated anywhere in the body, where damaged cells grow and multiply where they shouldn't. These cells form tumors, also called neoplasm- an abnormal mass of cells. Tumors can be non-cancerous (benign) and cancerous (malignant). Cancers are grouped according to their origin of tissue or organ. Four major types of cancers- • Carcinomas – are maligna

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28

Turro, James, Pratiksha Singh, Manbeer Singh Sarao, Satish Tadepalli, and Pramil Cheriyath. "Adult Burkitt lymphoma- an Island between lymphomas and leukemias." Journal of Community Hospital Internal Medicine Perspectives 9, no. 1 (2019): 25–28. http://dx.doi.org/10.1080/20009666.2019.1574545.

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29

Uckun, FM, K. Gajl-Peczalska, DE Myers, W. Jaszcz, S. Haissig, and JA Ledbetter. "Temporal association of CD40 antigen expression with discrete stages of human B-cell ontogeny and the efficacy of anti-CD40 immunotoxins against clonogenic B-lineage acute lymphoblastic leukemia as well as B- lineage non-Hodgkin's lymphoma cells." Blood 76, no. 12 (1990): 2449–56. http://dx.doi.org/10.1182/blood.v76.12.2449.2449.

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Abstract Detailed immunophenotypic analyses of immunologically classified leukemias and lymphomas showed that CD40 displays an exquisite B- lineage specificity within the human lymphopoietic system. Notably, 82% of B-lineage chronic lymphocytic leukemias (CLLs), 82% of B-lineage hairy cell leukemias (HCLs), 86% of B-lineage non-Hodgkin's lymphomas (NHLs), and 29% of B-lineage acute lymphoblastic leukemias (ALLs) were CD40+. Quantitative analyses of the correlated expression of CD40 and other B-lineage differentiation antigens on fetal lymphoid precursor cells by multiparameter two-color/three-

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30

Ribeiro, Raul C., Robert Krance, Neyssa M. Marina, and William M. Crist. "LEUKEMIAS AND LYMPHOMAS IN CHILDREN." Primary Care: Clinics in Office Practice 19, no. 4 (1992): 853–69. http://dx.doi.org/10.1016/s0095-4543(21)00621-7.

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31

Kumar, Shaji. "Understanding Leukemias, Lymphomas and Myelomas." Mayo Clinic Proceedings 81, no. 11 (2006): 1515. http://dx.doi.org/10.4065/81.11.1515-a.

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32

James, Karen. "Immunophenotyping of Lymphomas and Leukemias." Laboratory Medicine 19, no. 4 (1988): 225–27. http://dx.doi.org/10.1093/labmed/19.4.225.

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Hokland, Peter. "Understanding Leukemias, Lymphomas and Myelomas." European Journal of Haematology 77, no. 2 (2006): 179. http://dx.doi.org/10.1111/j.1600-0609.2006.00683.x.

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Cook, James R. "Splenic B-Cell Lymphomas/Leukemias." Surgical Pathology Clinics 3, no. 4 (2010): 933–54. http://dx.doi.org/10.1016/j.path.2010.09.004.

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35

Antin, Joseph H., and David S. Rosenthal. "Acute Leukemias, Myelodysplasia, and Lymphomas." Clinics in Geriatric Medicine 1, no. 4 (1985): 795–826. http://dx.doi.org/10.1016/s0749-0690(18)30912-1.

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36

Janowski, Michel, and Jacques Boniver. "Radiation-induced lymphomas and leukemias." Leukemia Research 10, no. 7 (1986): 875–78. http://dx.doi.org/10.1016/0145-2126(86)90315-2.

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Hasserjian, Robert P., and Nancy Lee Harris. "NK-Cell Lymphomas and Leukemias." American Journal of Clinical Pathology 127, no. 6 (2007): 860–68. http://dx.doi.org/10.1309/2f39nx1al3l54wu8.

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38

Ward, Jerrold M. "Lymphomas and leukemias in mice." Experimental and Toxicologic Pathology 57, no. 5-6 (2006): 377–81. http://dx.doi.org/10.1016/j.etp.2006.01.007.

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39

Li, Aihong, Ulla-Britt Westman, Irina Golovleva, et al. "Wilms Tumor 1 Gene (WT1) Isoforms in Leukemia and Lymphoma." Blood 110, no. 11 (2007): 4265. http://dx.doi.org/10.1182/blood.v110.11.4265.4265.

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Abstract The Wilms tumor 1 gene (WT1) acts as a transcriptional activator or repressor and is important for normal development. Evidence has accumulated to show that WT1 is oncogenic in acute leukemia and in some solid tumors. WT1 has 4 major isoforms and each encoded polypeptide is thought to make a contribution to normal gene function, but no data are available on their expression in hematologic malignancies. We have analyzed the expression of WT1 and its four isoforms (A, B, C, and D) in 187 diagnostic samples from patients with leukemia or lymphoma. WT1 RNA expression was detected in 9/10

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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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Daiter, S., R. A. Larson, W. W. Weddington, and J. E. Ultmann. "Psychosocial symptomatology, personal growth, and development among young adult patients following the diagnosis of leukemia or lymphoma." Journal of Clinical Oncology 6, no. 4 (1988): 613–17. http://dx.doi.org/10.1200/jco.1988.6.4.613.

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Leukemias and lymphomas, especially Hodgkin's disease, are common cancers in young adults. Young adulthood is also a critical period for psychological and social development. The occurrence of cancer can interfere with the development of independence, self-image, and life goals of young adult patients. Young adult patients with leukemia or lymphoma, especially those with less favorable prognoses, experience areas of significant personal growth and maturation during their illness and treatment. Close family and social supports report as much psychosocial stress, and in many cases more stress, t

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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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Greer, John P. "Therapy of Peripheral T/NK Neoplasms." Hematology 2006, no. 1 (2006): 331–37. http://dx.doi.org/10.1182/asheducation-2006.1.331.

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AbstractThe mature T/natural killer (NK) lymphoma/leukemias represent 5–15% of all non-Hodgkin lymphoma. These diseases have a geographic variation, with more nodal disease in North America and Europe, including peripheral T cell lymphomas, unspecified, anaplastic large cell lymphoma, and angioimmunoblastic T cell lymphoma; and more extranodal disease in Asia due to Epstein-Barr virus–related nasal NK/T lymphoma and human T-cell leukemia virus (HTLV)-1–associated adult T cell leukemia/lymphoma. The prognosis in most peripheral T/NK neoplasms is poor, with 5-year survival less than 30%. Progres

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Weinberg, Olga K., Carlos E. Bueso-Ramos, and Rashmi Kanagal-Shamanna. "T and NK lymphoblastic leukemia/lymphoma: Report from the 2023 SH/EAHP Workshop." American Journal of Clinical Pathology 164, no. 1 (2025): 26–35. https://doi.org/10.1093/ajcp/aqaf015.

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Abstract Objectives The 2023 Society for Hematopathology/European Association for Hematopathology Workshop addressed advancements in the diagnosis and classification of T- and natural killer (NK)–cell lymphomas/leukemias. Methods Session 8 of the workshop collected a diverse set of 38 cases of immature T- and NK-cell lymphoma/leukemias, as well as acute leukemia of ambiguous lineage (ALAL) and other miscellaneous cases, including indolent T-lymphoblastic proliferations. Results Twenty patients with T-lymphoblastic leukemia/lymphoma (T-LBL/L) and 3 patients with early T-cell precursor acute lym

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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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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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Wren, Dörte, Brian A. Walker, Monika Brüggemann, et al. "Translocations and Clonality Detection in Lymphoproliferative Disorders By Capture-Based Next-Generation Sequencing. a Pilot Study By the Euroclonality-NGS Consortium." Blood 124, no. 21 (2014): 5169. http://dx.doi.org/10.1182/blood.v124.21.5169.5169.

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Abstract Background: Detection and characterization of clonal IG/TR rearrangements and translocations in lymphoproliferative neoplasms provides critical information in the diagnostic pathway in several clinical scenarios and is a valuable tool to address research questions around B and T cells. This includes ascertaining the clonal nature of lymphoid proliferations, characterization of translocations in lymphomas and leukemias, characterization of CDR3 regions for MRD target identification and stereotyping analysis, amongst others. Until now, collecting this information required a combination

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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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Guha, Amrita. "Imaging Recommendations for Diagnosis, Staging, and Management of Hematological Malignancies." Indian Journal of Medical and Paediatric Oncology 44, no. 03 (2023): 302–7. http://dx.doi.org/10.1055/s-0042-1760327.

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AbstractThe NIC defines hematological cancers as those that begin in blood forming tissues such as bone marrow or cells of the immune system and these broadly include three groups: leukemias, lymphomas, and myelomas. The role of imaging is also fundamentally different between the three main groups of hematological malignancies. While imaging is the main tool for staging as well as treatment response assessment in lymphoma, it represents one of several key criteria for the diagnosis and follow-up of myeloma; whereas in leukemia, imaging has a role to play in the detection and management of trea

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Tagawa, Hiroyuki, Yasuo Yamanaka, Atsushi Watanabe, Naoto Takahashi, and Ken-ichi Sawada. "Aberrant Overexpressions of MicroRNA-21 and MicroRNA-155 Activate AKT Signaling Via Downregulation of Tumor Suppressors in NK-Cell Lymphoma/Leukemia." Blood 114, no. 22 (2009): 1917. http://dx.doi.org/10.1182/blood.v114.22.1917.1917.

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Abstract Abstract 1917 Poster Board I-940 Background: Natural Killer (NK) cell lymphomas/leukemias are characterized groups of highly aggressive lymphoid malignancies, which are comprised of “extranodal NK/T cell lymphoma, nasal type” and “aggressive NK-cell leukemia”. Notably, these two subtypes show many similarities in their morphologic features, immmunophenotypes and genotypes, and are invariably associated with Epstein-Barr virus (EBV), which suggests they may share the same genetic alterations. The gene(s) responsible for natural killer (NK)-cell lymphoma/leukemia have not been identifie

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