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Relevant bibliographies by topics / Lymphomas - Genetic aspects

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Academic literature on the topic 'Lymphomas - Genetic aspects'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Lymphomas - Genetic aspects"

1

Ikeda, Tomoka, Yuka Gion, Yoshito Nishimura, Midori Filiz Nishimura, Tadashi Yoshino, and Yasuharu Sato. "Epstein–Barr Virus-Positive Mucocutaneous Ulcer: A Unique and Curious Disease Entity." International Journal of Molecular Sciences 22, no. 3 (January 21, 2021): 1053. http://dx.doi.org/10.3390/ijms22031053.

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Epstein–Barr virus (EBV)-positive mucocutaneous ulcer (EBVMCU) was first described as a lymphoproliferative disorder in 2010. EBVMCU is a unifocal mucosal or cutaneous ulcer that often occurs after local trauma in patients with immunosuppression; the patients generally have a good prognosis. It is histologically characterized by proliferating EBV-positive atypical B cells accompanied by ulcers. On the basis of conventional pathologic criteria, EBVMCU may be misdiagnosed as EBV-positive diffuse large B-cell lymphoma or other lymphomas. However, its prognosis differs from that of EBV-associated lymphomas, in that patients with EBVMCU frequently show spontaneous regression or complete remission without chemotherapy. Therefore, EBVMCU is now recognized as a low-grade malignancy or a pseudo-malignant lesion. Avoiding unnecessary chemotherapy by distinguishing EBVMCU from other EBV-associated lymphomas will reduce the burden and unnecessary harm on patients. On the basis of these facts, EBVMCU was first described as a new clinicopathological entity by the World Health Organization in 2017. In this review, we discuss the clinicopathological characteristics of previously reported EBVMCU cases, while focusing on up-to-date clinical, pathological, and genetic aspects.

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Lachar, Whitney A., Imran Shahab, and A. Joe Saad. "Accuracy and Cost-Effectiveness of Core Needle Biopsy in the Evaluation of Suspected Lymphoma: A Study of 101 Cases." Archives of Pathology & Laboratory Medicine 131, no. 7 (July 1, 2007): 1033–39. http://dx.doi.org/10.5858/2007-131-1033-aacocn.

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Abstract Context.—Lymphomas have traditionally been diagnosed on excisional biopsies of lymph nodes in order to evaluate tissue architecture and cytomorphology. Recent lymphoma classification schemes emphasize immunophenotypic, genetic, and molecular aspects in addition to morphology as diagnostic features. Core needle biopsies are increasingly being used to obtain tissue for diagnosis in patients with lymphadenopathy and a clinical suspicion of lymphoma. These procedures are rapid, minimally invasive, well tolerated, and may provide some architectural framework (unlike fine-needle aspirations), as well as material for ancillary studies. Objective.—To explore the accuracy, utility, and cost-effectiveness of this technique. Design.—Core needle biopsies of 101 consecutive patients from 2 large community hospitals who were suspected of having primary or recurrent lymphomas were retrospectively reviewed. All patients had hematoxylin-eosin–stained sections of needle cores. Specimens morphologically suspicious for lymphoma were subjected to ancillary studies, including immunohistochemistry, flow cytometry, and/or molecular studies. Core needle biopsy diagnoses were correlated with subsequent excisional biopsies, if performed. Results.—Core needle biopsies established a definitive pathologic diagnosis for the vast majority of cases. A diagnosis was considered sufficient to begin treatment for primary and recurrent lymphomas in most cases. Compared with an open biopsy, there is a cost savings of greater than 75%. Conclusion.—The accuracy of this technique, along with the cost savings and decreased morbidity, suggest that this method may be used safely and reliably as a first-line diagnostic technique.

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Christie, Amanda L., Samuel Y. Ng, Raphael Koch, Alexandra N. Christodoulou, Tiffany DeSouza, Mark A. Murakami, Moony Tseng, et al. "T-Cell Lymphoma Patient-Derived Xenografts and Newly Developed Cell Lines Recapitulate Aspects of Disease Biology and Represent Novel Tools for Preclinical Drug Development." Blood 128, no. 22 (December 2, 2016): 3015. http://dx.doi.org/10.1182/blood.v128.22.3015.3015.

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Abstract Lymphomas represent nearly 70 distinct diseases with unique clinical presentations, therapeutic responses and underlying biology. There is a pressing shortage of publically available cell line and in vivo models of nearly all of these diseases; T-cell lymphoma models are particularly under-represented compared to B-cell lymphomas, which has severely hampered efforts to understand and target their biology. The majority ofin vivo models of T-cell lymphomas are genetically-engineered mouse models, which often don't faithfully recapitulate human disease. To address this issue, we have established a repository of patient-derived xenografts (PDX) of lymphomas by engrafting human tumors into immunodeficient NOD/Scid/IL2rgnull mice with or without an MHC Class 1 deficiency (to prevent graft versus host disease). Blood and bone marrow specimens involved with tumor were injected by tail vein injection. Lymph node and extranodal biopsy specimens were implanted under the renal capsule as a 1x1x2mm tumor seed, which maintains the in situ microarchitecture. A description of T-cell lymphoma PDXs is included in the Table. PDXs have been extensively characterized by immunohistochemistry (IHC), flow cytometry, transcriptome sequencing and targeted DNA sequencing. These studies have demonstrated retention of key architectural, cellular, and molecular features of the primary tumors. Flow cytometric analysis of patient tumors and their respective xenografts revealed highly concordant patterns of surface marker expression. IHC of murine tissues confirmed retention of tumor immunophenotypes, architecture, and even tissue tropism in the PDXs. For example, blood from a patient with Sézary Syndrome manifested in the skin of recipient mice when injected into the lateral tail vein. A breast implant-associated ALK-negative anaplastic large cell lymphoma (ALCL) implanted under the renal capsule metastasized to the liver and spleen while uniformly retaining CD30 positivity. A peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) specimen implanted under the renal capsule engrafted in the spleen, with the notable admixture of nonmalignant T cells and scattered EBV-positive B cells in first passage. T-cell receptor gene rearrangement PCR performed on this PTCL-NOS demonstrated an identical rearrangement pattern in the primary tumor and the PDX. An angioimmunoblastic T-cell lymphoma (AITL) specimen engrafted in spleen, lymph node and bone marrow within 6 weeks and serially transplanted through three generations in an orthotopic manner while maintaining a CD3+CD4+PD1+CD30partial immunophenotype. The genetic characterization of the PDX models using a targeted DNA sequencing approach showed a mutational profile that clearly matched primary T-cell lymphoma samples and significantly expands the current repertoire of available pre-clinical models. For example, a PDX model of AITL showed mutations of TET2 and ARID1B; a model of an ALK-negative ALCL harbored mutations of STAT3 and STAT5. This massively extends the spectrum of clinically representative model systems that can be used to explore novel therapeutic strategies for T-cell lymphomas. Several early-passage PDXs have been used to generate T-cell lymphoma cells lines, including three cell lines from AITL PDX models. One of these AITL cell lines has proliferated through 30 passages and was validated by immunophenotype and molecular confirmation of bi-allelic TET2 mutations with loss of 6q, 7q, and 10q confirmed using Sanger and TruSeq Custom Amplicon Sequencings. To our knowledge, there have been no reports of an AITL cell line in the literature. Additional peripheral T-cell lymphoma cell lines are currently under development. These lymphomas, along with a spectrum of PDXs of other hematologic malignancies, are available to collaborators through the online portal PRoXe (Public Repository of Xenografts) at www.proxe.org. These models represent a unique opportunity to interrogate biology and perform preclinical studies with in vivo models. Table 1 Table 1. Disclosures Jacobson: Kite: Membership on an entity's Board of Directors or advisory committees. Armand:Pfizer: Research Funding; Sequenta Inc: Research Funding; Merck: Consultancy, Research Funding; Roche: Research Funding; Infinity Pharmaceuticals: Consultancy; Bristol-Myers Squibb: Consultancy, Research Funding. Shipp:Bristol-Myers Squibb: Consultancy, Research Funding; Cell Signaling: Honoraria; Merck, Gilead, Takeda: Other: Scientific Advisory Board; Bayer: Research Funding. Fisher:Pharmacyclics: Consultancy. Weinstock:Novartis: Consultancy, Research Funding.

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Konopleva, Maria V., Maxim S. Belenikin, Andrei V. Shanko, Alexey I. Bazhenov, Sergei A. Kiryanov, Tatyana A. Tupoleva, Maria V. Sokolova, Alexander V. Pronin, Tatyana A. Semenenko, and Anatoly P. Suslov. "Detection of S-HBsAg Mutations in Patients with Hematologic Malignancies." Diagnostics 11, no. 6 (May 27, 2021): 969. http://dx.doi.org/10.3390/diagnostics11060969.

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Multiple studies of hepatitis B virus (HBV) genetic variability and its relationship with the disease pathogenesis are currently ongoing, stemming from growing evidence of the clinical significance of HBV mutations. It is becoming increasingly evident that patients with hematologic malignancies may be particularly prone to a higher frequency of such mutations. The present report is the first extensive study of the prevalence of escape mutations in S-HBsAg, performed using isolates from 59 patients from hospital hematology departments with diagnoses of leukemia (n = 32), lymphoma (n = 20), multiple myeloma (n = 3), and non-tumor blood diseases (n = 4). The isolates were serologically examined for the presence of HBV markers and sequenced using either next-generation sequencing (NGS) or Sanger sequencing. Occult hepatitis B was found in 5.1% of cases. Genetic analysis of the region corresponding to S-HBsAg demonstrated an exceptionally high mutation frequency in patients with leukemias (93.4%) and lymphomas (85.0%), along with the prominent mutation heterogeneity. Additionally, more than 15 mutations in one sample were found in patients with leukemias (6.3% of cases) and lymphomas (5.0% of cases). Most of the mutations were clinically significant. The study analyzes the mutation profile of HBV in different oncohematological diseases and the frequency of individual mutations. The data strongly suggest that the NGS method, capable of detecting minor populations of HBV mutations, provides a diagnostic advantage, lays the foundation for the development of screening methods, and allows for the study of the virological and pathogenetic aspects of hepatitis B.

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Hildebrand, Joanne M., Zhenghua Luo, Michelle Manske, Steven Ziesmer, Tammy Price-troska, Wai Lin, Bruce Hostager, et al. "A BAFF-R Mutation Associated with Non-Hodgkin Lymphoma Exhibits Altered TRAF Binding and Reveals New Insights Into Proximal BAFF-R Signaling." Blood 116, no. 21 (November 19, 2010): 468. http://dx.doi.org/10.1182/blood.v116.21.468.468.

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Abstract Abstract 468 The requirement for BAFF and BAFF-R in normal human and murine B cells is well studied, but there is also significant evidence to suggest that BAFF plays an important role in malignant B cell proliferation and survival. Serum BAFF levels are elevated in patients with non-Hodgkin lymphoma (NHL) and high BAFF levels correlate with aggressive disease and a poor response to therapy. There is also increasing genetic evidence suggesting an association between the development of human disease and genetic variation in genes encoding BAFF and its receptors. Mutations in TNFRSF13B (TACI) were identified in patients with familial common variable immunodeficiency (CVID) and IgA deficiency and we have found that single nucleotide polymorphisms (SNP) in TNFSF13B (BAFF) are associated with elevated BAFF levels and risk for developing NHL. To build upon these findings we sequenced BAFF and its receptors; TNFSF13B, TNFRSF13B, TNFRSF17(BCMA), and TNFRSF13C (BAFF-R) in NHL patients to identify novel genetic variants that may be associated with NHL risk. Among 40 individual samples (20 controls and 20 follicular lymphoma (FL) cases) that were bi-directionally sequenced we identified a heterozygous cytosine to thymidine transition in 1 patient specimen at position 475 (C475T) of TNFRSF13C. The C475T transition encodes a missense substitution of tyrosine for histidine in codon 159 (H159Y) in the highly conserved cytoplasmic tail of BAFF-R, adjacent to the TRAF3 binding motif PVPAT. We next expanded our analysis of BAFF-R H159Y and analyzed NHL tumor biopsies for the presence of the mutation. 4/41 (10%) follicular lymphomas (FL), 2/42 (5%) diffuse large B cell lymphomas, 1/22 (5%) lymphoplasmacytic lymphomas (LPL), and 1/24 (4%) mucosal associate lymphoid tissue lymphomas carried the heterozygous mutation. The BAFF-R H159Y mutation was not detected in any of the normal control DNA from healthy donors (n=100). Given its close proximity to the TRAF3 binding site in the cytoplasmic domain of BAFF-R we first wanted to determine if the H159Y mutation altered BAFF induced signaling. We generated cell lines that express HA-tagged wildtype BAFF-R, BAFF-R with the H159Y mutation, or BAFF-R with an ablated TRAF3 binding site as a negative control. Analysis of cells expressing H159Y BAFF-R demonstrates that this mutation results in increased BAFF-R-mediated NFκB1 and NF-κB2 activation. The enhanced signal activated by BAFF-R H159Y is coupled with a several fold increase in TRAF3, TRAF2, and TRAF6 recruitment to BAFF-R and increased IgM production. We further demonstrate that recruitment of TRAF6 to BAFF-R is not unique to the mutant H159Y BAFF-R, but is also an important and necessary feature of BAFF-R signaling in normal B cells. Collectively, our data identify a novel lymphoma-associated mutation in BAFF-R and describe exciting new aspects of BAFF-R signaling that are important for understanding normal B cell homeostasis and function, as well as pathogenic BAFF-R contributions to human disease. Disclosures: No relevant conflicts of interest to declare.

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Braziel, Rita M., Margaret A. Shipp, Andrew L. Feldman, Virginia Espina, Mary Winters, Elaine S. Jaffe, Emanuel F. Petricoin, and Lance A. Liotta. "Molecular Diagnostics." Hematology 2003, no. 1 (January 1, 2003): 279–93. http://dx.doi.org/10.1182/asheducation-2003.1.279.

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Abstract It is increasingly evident that molecular diagnostics, that is, the use of diagnostic testing to understand the molecular mechanisms of an individual patient’s disease, will be pivotal in the delivery of safe and effective therapy for many diseases in the future. A huge body of new information on the genetic, genomic and proteomic profiles of different hematopoietic diseases is accumulating. This chapter focuses on new technologies and advancements in understanding the molecular basis of hematologic disorders, providing an overview of new information and its significance to patient care. In Section I, Dr. Braziel discusses the impact of new genetic information and research technologies on the actual practice of diagnostic molecular hematopathology. Recent and projected changes in methodologies and analytical strategies used by clinical molecular diagnostics laboratories for the evaluation of hematologic disorders will be discussed, and some of the challenges to clinical implementation of new molecular information and techniques will be highlighted. In Section II, Dr. Shipp provides an update on current scientific knowledge in the genomic profiling of malignant lymphomas, and describes some of the technical aspects of gene expression profiling. Analysis methods and the actual and potential clinical and therapeutic applications of information obtained from genomic profiling of malignant lymphomas are discussed. In Section III, Dr. Liotta presents an update on proteomic analysis, a new and very active area of research in hematopoietic malignancies. He describes new technologies for rapid identification of different important proteins and protein networks, and the potential therapeutic and prognostic value of the elucidation of these proteins and protein pathways in the clinical care of patients with malignant lymphomas.

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Turbatu, Andrei, Andrei Coliţă, Marilena Stoian, Ana-Maria Bordea, Mădălina Oprea, Cecilia Ghimici, Ionel Gelatu, et al. "How Epstein-Barr Virus “Manipulates” The Tumoral Microenvironment in Hodgkin Lymphoma?" Internal Medicine 16, no. 2 (April 1, 2019): 47–52. http://dx.doi.org/10.2478/inmed-2019-0059.

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AbstractThe Epstein-Barr virus (EBV) is a gamma-herpesvirus that colonizes the B-cell system of its human host, allowing it to persist asymptomatically in the majority of the world’s adult population. In most people primary infection goes unnoticed, whereas in a minority of individuals, primary infection results in infectious mononucleosis (IM), a benign condition that almost always resolves after several weeks or months. However, EBV is also causally linked with a number of malignancies, including B-cell lymphomas, such as classical Hodgkin lymphoma (cHL).A proportion of patients with cHL harbor EBV within their tumor cells. Emerging evidence suggests that while EBV is able to subvert cellular processes to promote the growth and survival of HRS cells or their progenitors, mutations in key cell signalization pathways are probably required to do this when EBV is absent. The challenge is to unravel exactly how EBV and its latent genes contribute to the pathogenesis of cHL particularly with respect to how the virus co-operates with cellular genetic and epigenetic changes to drive transformation. It is hoped that the development of better in vitro and in vivo models of disease will reveal more fundamental aspects of EBV’s role in Hodgkin lymphoma pathogenesis and pave the way for targeted therapies for patients with EBV-positive cHL.

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Macintyre, Elizabeth, Dennis Willerford, and Stephan W. Morris. "Non-Hodgkin's Lymphoma: Molecular Features of B Cell Lymphoma." Hematology 2000, no. 1 (January 1, 2000): 180–204. http://dx.doi.org/10.1182/asheducation.v2000.1.180.180.

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Abstract The rapid increase in the incidence of the B cell non-Hodgkin's lymphomas (NHL) and improved understanding of the mechanisms involved in their development renders timely a review of the theoretical and practical aspects of molecular abnormalities in B cell NHL. In Section I, Dr. Macintyre addresses the practical aspects of the use of molecular techniques for the diagnosis and therapeutic management of patients with B cell NHL. While detection of clonal Ig rearrangements is widely used to distinguish reactive from malignant lymphoproliferative disorders, molecular informativity is variable. The relative roles of cytogenetic, molecular and immunological techniques in the detection of genetic abnormalities and their protein products varies with the clinical situation. Consequently, the role of molecular analysis relative to morphological classification is evolving. Integrated diagnostic services are best equipped to cope with these changes. Recent evidence that large scale gene expression profiling allows improved prognostic stratification of diffuse large cell lymphoma suggests that the choice of diagnostic techniques will continue to change significantly and rapidly. In Section II, Dr. Willerford reviews current understanding of the mechanisms involved in immunoglobulin (Ig) gene rearrangement during B lymphoid development and the way in which these processes may contribute to Ig-locus chromosome translocations in lymphoma. Recent insights into the regulation of Ig gene diversification indicate that genetic plasticity in B lymphocytes is much greater than previously suspected. Physiological genomic instability, which may include isotype switching, recombination revision and somatic mutation, occurs in germinal centers in the context of immune responses and may explain longstanding clinical observations that link immunity and lymphoid neoplasia. Data from murine models and human disorders predisposing to NHL have been used to illustrate these issues. In Section III, Dr. Morris reviews the characteristics and consequences of deregulation of novel “proto-oncogenes” involved in B cell NHL, including PAX5 (chromosome 9p 13), BCL8 (15q11-q13), BCL9, MUC1, FcγRIIB and other 1q21-q22 genes and BCL10 (1p22). The AP12-MLT/MALT1 [t(11;18)(q21;q21)] fusion transcript is also described.

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Macintyre, Elizabeth, Dennis Willerford, and Stephan W. Morris. "Non-Hodgkin's Lymphoma: Molecular Features of B Cell Lymphoma." Hematology 2000, no. 1 (January 1, 2000): 180–204. http://dx.doi.org/10.1182/asheducation.v2000.1.180.20000180.

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The rapid increase in the incidence of the B cell non-Hodgkin's lymphomas (NHL) and improved understanding of the mechanisms involved in their development renders timely a review of the theoretical and practical aspects of molecular abnormalities in B cell NHL. In Section I, Dr. Macintyre addresses the practical aspects of the use of molecular techniques for the diagnosis and therapeutic management of patients with B cell NHL. While detection of clonal Ig rearrangements is widely used to distinguish reactive from malignant lymphoproliferative disorders, molecular informativity is variable. The relative roles of cytogenetic, molecular and immunological techniques in the detection of genetic abnormalities and their protein products varies with the clinical situation. Consequently, the role of molecular analysis relative to morphological classification is evolving. Integrated diagnostic services are best equipped to cope with these changes. Recent evidence that large scale gene expression profiling allows improved prognostic stratification of diffuse large cell lymphoma suggests that the choice of diagnostic techniques will continue to change significantly and rapidly. In Section II, Dr. Willerford reviews current understanding of the mechanisms involved in immunoglobulin (Ig) gene rearrangement during B lymphoid development and the way in which these processes may contribute to Ig-locus chromosome translocations in lymphoma. Recent insights into the regulation of Ig gene diversification indicate that genetic plasticity in B lymphocytes is much greater than previously suspected. Physiological genomic instability, which may include isotype switching, recombination revision and somatic mutation, occurs in germinal centers in the context of immune responses and may explain longstanding clinical observations that link immunity and lymphoid neoplasia. Data from murine models and human disorders predisposing to NHL have been used to illustrate these issues. In Section III, Dr. Morris reviews the characteristics and consequences of deregulation of novel “proto-oncogenes” involved in B cell NHL, including PAX5 (chromosome 9p 13), BCL8 (15q11-q13), BCL9, MUC1, FcγRIIB and other 1q21-q22 genes and BCL10 (1p22). The AP12-MLT/MALT1 [t(11;18)(q21;q21)] fusion transcript is also described.

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Cordoba, Raul, María Socorro Rodriguez-Pinilla, Narvaez Javier, Fina Climent, Joaquin Sanchez, Carlos Perez Seoane, Javier Lopez Jimenez, et al. "Peripheral T-Cell Lymphomas in Spain: Profiling Clinical, Phenotypic and Genetic Characteristics in Spanish Population." Blood 132, Supplement 1 (November 29, 2018): 2938. http://dx.doi.org/10.1182/blood-2018-99-116562.

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Abstract Purpose The objective of this study was to investigate clinicopathologic features and prognostic factors of patients diagnosed with PTCL in 13 sites across Spain. Patients and Methods A multicenter, retrospective study was carried out between September 2015-November 2017.Medical charts of patients diagnosed with PTCLs between January 2008 and December 2013 that have signed the approved informed consent form were reviewed. PTCLs were then classified according to the 2016 revision of the WHO classification of lymphoid neoplasms. Clinical characteristics,history, standard immunohistochemistry (IHC) data, International Prognostic Index (IPI) and Prognostic Index for T-cell lymphoma (TCL) (PIT) were also assessed. Medians (range), mean (standard deviation) and frequency as the number of patients (n) and percentages (%) with confidence intervals at 95% (CI95%) were calculated. Overall Survival (OS) and Progression Free Survival (PFS) were analyzed using the Kaplan Meier method. Results 175 (88.4%) patients were successfully analyzed, the male/female ratio was 1.7:1.0, and the median age was 67.2 years (range: 24.8 years -95.8 years). ECOG performance status >1 was reported for 31.9% patients. Ann Arbor stages were III and IV 27.4% and 45.7%, respectively, and LDH levels were elevated to 92 patients (52.6%). Those with B symptoms accounted for 39.4%, while soft tissue was the most frequent location (23,7%) among the 76 patient with extranodal disease; bone marrow infiltration was confirmed in 18.3% patients. Relevant clinical antecedents related to immunological aspects were also frequently reported, including previous neoplasia (18.9%), autoimmune disease (16%), immunosuppressive treatments (7.3%) and previous viral diseases (HIV, HBV or HCV, 5.7%, 4.6% and 7.4%, respectively). Most patients presented with angioimmunoblastic TCL (31.4%); similar proportions of patients were observed among nodal PTCL with TFH phenotype (13.1%, PTCL not otherwise specified (12.0%) and extranodal NK/TCL nasal type (11.4%). CD30 expression and staining pattern (ranged 1-4) allowed the stratification of patients according CD30 intensity (n= 121; weak: 35, moderate: 57, and intense: 29); Patients were also classified based on CD30 expression considering the median value of quantitative CD30 in our sample (15%) the cut-off point: n=132; Negative <15%: 64; Positive, ≥15%: 68). First-line treatment with a CHOP/CHOP-like regimen was the most common finding (69.7%). Best response was observed after a median of 4 months since the start of first-line treatment (range 0.0 months - 65.2 months). Overall response rate after first-line treatment was 66.9%, with 61/151 patients reaching complete response (CR). Median PFS (n=157) and OS (n=175) of this series were 7.87 months (CI95%: 4.98 months-10.75months) and 15.77 months (CI95%: 10.23 months -21.30 months), respectively. Overall, IPI and PIT scores influenced the PFS and OS (p<0.001). A higher number of adverse factors was associated with a shorter survival. Reaching a CR was associated with a better PFS (CR: 62.6m; CI95%: 20.2 months -105.1 months) than the rest of patients (3.97m: CI95%: 3.08 months -4.85m; p<0.001). Response was also associated with OS; patients with CR showed an average OS of 67.01 months (CI95%: 58.2 months -75.9 months) that were significantly longer than that of patients with No-CR (median: 7.34 months; CI95%: 5.85 months -8.83 months; p<0.001). Conclusion This is the largest series of T cell Lymphoma reported in Spain and has allowed the description of distribution of PTCL subtypes, analyzed through central hematopathologists reanalysis and reclassification of samples from 175 PTCL patients, according to the WHO 2016 classification of lymphoid neoplasms. Our data confirm the poor prognosis of these patients, as well as the impact of prognostic indexes and the response to first line treatment on their outcome. Disclosures Rodriguez-Pinilla: Takeda: Honoraria. Piris:Takeda: Honoraria; Janssen: Honoraria; Gilead: Honoraria; Kura: Honoraria. Ruiz-Zorrilla:Takeda: Employment. Montoto:Takeda: Employment.

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Dissertations / Theses on the topic "Lymphomas - Genetic aspects"

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馮家禮 and Ka-lai Fung. "Patterns of gene promoter methylation in malignant lymphoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B3122734X.

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Guo, Tianhuan, and 郭天欢. "Identification of tumor suppressor genes in the commonly deleted region of chromosome 6q in NK-cell malignancies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43785761.

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Ma, Huan, and 马欢. "Molecular analysis of ocular adnexal lymphomas in the search for potential biomarkers." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46921655.

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Hu, Xiaotong, and 胡曉彤. "Novel IGH translocations in gastric non-Hodgkin's B-cell lymphoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38688098.

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Lo, Yee-nga, and 盧懿雅. "Effect of t(11;14)(p13;q32) translocation on the expression of PDHX, the telomeric gene on chromosome 11p13, in mature B-cell malignancies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46632505.

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Wong, Hoi-ning Karen, and 黃凱寧. "Role of PRDM1{221}-isoform (with a disrupted PR domain) as a negative regulator of the tumor suppressor PRDM1α in NK-cell neoplasms." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48334303.

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NK-cell malignancies (NKLL) consist of two separate entities: Extranodal NK-cell lymphoma, nasal type (ENKL) and aggressive NK-cell leukemia (ANKL). ENKL is the second most common group of extranodal lymphomas in Hong Kong. Deletions in the 6q21 region in ENKL have been consistently reported in the literature and differential expression data indicated that the transcription factor PRDM1 (PR domain containing 1, with ZNF domain) located at 6q21-q22.1 is a candidate TSG in NK-cell neoplasms. PRDM1 exists as 2 isoforms generated from the same gene by alternative transcription promoter. PRDM1- differs from PRDM1-βin that it lacks the amino-terminal 101 amino acids with a disrupted PR domain. As the PRDM1- is functionally impaired, with a loss of repressive function on multiple target genes while maintaining normal DNA-binding activity, we hypothesize that the  -isoform, which is overexpressed in NKLLs, may act as a negative regulator of the tumor suppressive α-isoform in NKLLs. In this study, we investigated the possible role of PRDM1- as a negative regulator of tumor suppressor PRDM1-α in NK-cell lymphoma by using a gene silencing technique. Short hairpin-RNA (sh-RNA) construct with sequence targeting to PRDM1- purchasing from biotechnology company was used to knockdown of the gene expression. Series of functional assays were then performed to evaluate the effect of the PRDM1-  knockdown in two NK cell line, YT and NKYS, which xpress endogenous PRDM1-. Comparison was made between the 1) shRNA targeting to nt65-nt94 of PRDM1- sequence, sh-PRDM1 -pGFP-V-RS (shV2), and 2) scrambled-pGFPV-RS (scrambled shRNA), negative control with a non-effective shRNA cassette in pGFP-VRS plasmid. Western blot analysis was performed to examine the efficiency of shRNA in knockdown the expression of PRDM1-  in 293T cells (normal human embryonic kidney cells). The protein expression level for ectopic PRMD1- was reduced in cells expressing shV2 when compared with the negative control. NKYS cell line expressed with shV2 showed a significant reduction in the number of colonies. Percentage of dead cells was found higher in these cells. The proliferation rate of shV2 expressing cells started to retarded significantly on the third day of measurement in the MTS proliferation assay. The cell also underwent G1 cell cycle arrest and had lower proliferation rate, as indicated by cell cycle analysis. For YT cell line expressed with shV2, significant reduction in both colony number and size in methylcellulose colony formation assay was observed. Base on the results obtained from the two NK-cell lines, we suggest that the shV2 inhibit the tumor cell growth. The knockdown of the PRDM1-  lead to an increase level of PRDM1- α. PRDM1- α is a tumor suppressor gene with suppressive function by preventing damaged cells from proliferation or inhibiting the clonogenecity of the tumor cells. An imbalance expression of PRDM1- and PRDM1-αplay an important role in tumor growth and formation, and PRDM1 could possibly be the new tumor suppressor gene in NK-cells lymphoma.
published_or_final_version
Pathology
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Master of Medical Sciences

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Au, Wing-yan, and 區永仁. "Pathogenesis and progression of malignant B cell neoplasms." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45007676.

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Yim, Lok-hay Rita, and 嚴樂晞. "DNA methylation of tumour suppressive microRNA in mantle cell lymphoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/210192.

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陳遠雯 and Yun-wen Wendy Chen. "Molecular genetics of gastric non-Hodgkin's B-cell lymphomas." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B3124404X.

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Kercher, Lisa A. "Search for the retroviral origin of a novel murine spontaneous lymphoma." Virtual Press, 1994. http://liblink.bsu.edu/uhtbin/catkey/902487.

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It is known that many types of leukemias and lymphomas are of viral origin. A new strain of immunologically deficient mice, the BALB/c x C57B1/6 beige nude mice, has been observed to develop spontaneous lymphomas of unknown origin at a high frequency. It is possible the tumors originate from a retroviral infection, which we attempted to show by detection of viral reverse transcriptase (RT) activity. We measured the (RT) activity in the supernatants of cocultures from the spleen and lymph node tissues of the beige nude animals by two methods, tritiated thymidine triphosphate incorporation in a standard RT assay, and the commercially available RT-DetectTM (DuPont) method. Of all supernatants tested, none showed a significant amount of RT activity compared with a cell line that was known to be actively producing the retrovirus MuLV. Upon electron microscopic analysis of the tumor-like cells grown in coculture, no viral particles were observed. Flow cytometric analysis of the tumor-like cells showed two general phenotypes; one predominately of a helper T cell type, and the other of a less differentiated immature thymocyte type.
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Books on the topic "Lymphomas - Genetic aspects"

1

Leukemia Research Fund. International Workshop. Epidemiology of leukemia and lymphoma: Report of the Leukemia Research Fund International Workshop, Oxford, UK, September 1984. Edited by Greaves M. F. 1941- and Chan L. C. Oxford [Oxfordshire]: Pergamon Press, 1985.

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Secker-Walker, Lorna M. Chromosomes and genes in acute lymphoblastic leukemia. New York: Springer, 1997.

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United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: The human genome project and disease prediction. Bethesda, Md: National Institutes of Health, National Cancer Institute, 1995.

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United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Evaluating the National Cancer Program : Huntsman Cancer Institute, Salt Lake City, Utah : November 19, 1999. [Bethesda, MD (31 Center Drive, Room 4A48, Bethesda, MD 20892-2473): National Cancer Institute, 1999.

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United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting. [Bethesda, MD]: The Institute, 1992.

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United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting: Cancer and the cultures of America. [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1994.

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United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Transcript of proceedings, July 29-30, 2002 : hosted by the Yakama Nation, Eagle Seelatsee Auditorium, Yakama Nation Agency Building, Toppenish, WA. [Bethesda, Md: National Cancer Institute, 2002.

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United States. President's Cancer Panel. Meeting. President's Cancer Panel meeting: Transcript of proceedings, November 15, 1993. [Bethesda, Md.]: National Institutes of Health, National Cancer Institute, 1993.

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United States. President's Cancer Panel. Meeting. President's Cancer Panel Meeting: Transcript of proceedings, May 27-28, 2003 : Lisbon Marriott Hotel, Lisbon, Portugal. [Bethesda, Md.] (31 Center Dr., Room 3A-18 MSC 2440, Bethesda 20892-2440): [National Cancer Institute, 2003.

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Meeting, United States President's Cancer Panel. President's Cancer Panel meeting: Evaluating the national cancer program, an ongoing process. Bethesda, Md: National Institutes of Health, National Cancer Institute, 1993.

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Book chapters on the topic "Lymphomas - Genetic aspects"

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Fonatsch, C., G. Gradl, and J. Rademacher. "Genetics of Hodgkin’s Lymphoma." In New Aspects in the Diagnosis and Treatment of Hodgkin’s Disease, 35–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83781-4_4.

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