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Relevant bibliographies by topics / B-cell malignancie

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Academic literature on the topic 'B-cell malignancie'

Author: Grafiati

Published: 1 April 2023

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Journal articles on the topic "B-cell malignancie"

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Miao, Miao, Wu Depei, Aining Sun, Ying Wang, Lingzhi Yan, and Qian Wu. "The Efficacy and Safety of Recombinant Human Thrombopoietin in Patients with Hematological Malgnancies After Allogeneic Hematopoietic Stem Cell Transplantation." Blood 118, no. 21 (November 18, 2011): 4565. http://dx.doi.org/10.1182/blood.v118.21.4565.4565.

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Abstract Abstract 4565 OBJECTIVE: To evaluate the efficacy and sefety of recombinant human thrombopoietin(rhTPO) prior to engraftment in adults with hematological malignancie who received allogeneic haematopoietil stem cell transplantation(Allo-HSCT). METHODS: This sutdy was a randomized, controlled clinical trial,38 patients were hematological malignancie, inclulding acute and chrinic myeloid leukemia, acute lymphoblastic leukemia, lymphoma.They received Allo-HSCT and were randomly divided into groups(group A 19 cases, group B 19 cases).The group A was no-rhTPO as control, the group B were received rhTPO 15000U/d from +1 day, and continued until the untransfused platelet count was >70×109/L for two consecutived days. Patients received platelete transfusion when they developed severe thrombocytopenia<20×109/L. Efficacy and sefety of rhTPO on the outcome of Allo-HSCT were evaluated. RESULTS: In both group A and B, platelet decrease after Allo-HSCT had no sognificant difference. The platelet engraftment duration of group A and B was 15.68±1.36(range 11–31) days and 13.47±0.72(range 9–21) days, respectively. The amount of platelet transfusion of group A and B was 4±0.55(range 20–130) units and 2.89±0.36(range 0–50) units, respectively. The effects of rhTPO on neutrophil engraftment, hepatic function, renal function, alloergic reations and acute GVHD were not found. CONCLUSION: The platelet engraftment duration of group B was shorter than that of group A(t=27.2, p<0.001), the amount of need platelet transfusion was significently less than those in the group A.There was a statistically significant difference in platelet engraftment and platelet transfusion needed(t=2.523, p<0.05). Administration of rhTPO prior to platelet engraftment after Allo-HSCT seem to be efficacy and safe. Disclosures: No relevant conflicts of interest to declare.

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

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Zweidler-McKay, Patrick A., Yiping He, Lanwei Xu, Carlos G. Rodriguez, Fredrick G. Karnell, Andrea C. Carpenter, Jon C. Aster, David Allman, and Warren S. Pear. "Notch signaling is a potent inducer of growth arrest and apoptosis in a wide range of B-cell malignancies." Blood 106, no. 12 (December 1, 2005): 3898–906. http://dx.doi.org/10.1182/blood-2005-01-0355.

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Although Notch receptor expression on malignant B cells is widespread, the effect of Notch signaling in these cells is poorly understood. To investigate Notch signaling in B-cell malignancy, we assayed the effect of Notch activation in multiple murine and human B-cell tumors, representing both immature and mature subtypes. Expression of constitutively active, truncated forms of the 4 mammalian Notch receptors (ICN1-4) inhibited growth and induced apoptosis in both murine and human B-cell lines but not T-cell lines. Similar results were obtained in human precursor B-cell acute lymphoblastic leukemia lines when Notch activation was achieved by coculture with fibroblasts expressing the Notch ligands Jagged1 or Jagged2. All 4 truncated Notch receptors, as well as the Jagged ligands, induced Hes1 transcription. Retroviral expression of Hairy/Enhancer of Split-1 (Hes1) recapitulated the Notch effects, suggesting that Hes1 is an important mediator of Notch-induced growth arrest and apoptosis in B cells. Among the B-cell malignancies that were susceptible to Notch-mediated growth inhibition/apoptosis were mature B-cell and therapy-resistant B-cell malignancies, including Hodgkin, myeloma, and mixed-lineage leukemia (MLL)–translocated cell lines. These results suggest that therapies capable of activating Notch/Hes1 signaling may have therapeutic potential in a wide range of human B-cell malignancies.

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Brudno, Jennifer N., Robert P. T. Somerville, Victoria Shi, Jeremy J. Rose, David C. Halverson, Daniel H. Fowler, Juan C. Gea-Banacloche, et al. "Allogeneic T Cells That Express an Anti-CD19 Chimeric Antigen Receptor Induce Remissions of B-Cell Malignancies That Progress After Allogeneic Hematopoietic Stem-Cell Transplantation Without Causing Graft-Versus-Host Disease." Journal of Clinical Oncology 34, no. 10 (April 1, 2016): 1112–21. http://dx.doi.org/10.1200/jco.2015.64.5929.

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Purpose Progressive malignancy is the leading cause of death after allogeneic hematopoietic stem-cell transplantation (alloHSCT). After alloHSCT, B-cell malignancies often are treated with unmanipulated donor lymphocyte infusions (DLIs) from the transplant donor. DLIs frequently are not effective at eradicating malignancy and often cause graft-versus-host disease, a potentially lethal immune response against normal recipient tissues. Methods We conducted a clinical trial of allogeneic T cells genetically engineered to express a chimeric antigen receptor (CAR) targeting the B-cell antigen CD19. Patients with B-cell malignancies that had progressed after alloHSCT received a single infusion of CAR T cells. No chemotherapy or other therapies were administered. The T cells were obtained from each recipient’s alloHSCT donor. Results Eight of 20 treated patients obtained remission, which included six complete remissions (CRs) and two partial remissions. The response rate was highest for acute lymphoblastic leukemia, with four of five patients obtaining minimal residual disease–negative CR. Responses also occurred in chronic lymphocytic leukemia and lymphoma. The longest ongoing CR was more than 30 months in a patient with chronic lymphocytic leukemia. New-onset acute graft-versus-host disease after CAR T-cell infusion developed in none of the patients. Toxicities included fever, tachycardia, and hypotension. Peak blood CAR T-cell levels were higher in patients who obtained remissions than in those who did not. Programmed cell death protein-1 expression was significantly elevated on CAR T cells after infusion. Presence of blood B cells before CAR T-cell infusion was associated with higher postinfusion CAR T-cell levels. Conclusion Allogeneic anti-CD19 CAR T cells can effectively treat B-cell malignancies that progress after alloHSCT. The findings point toward a future when antigen-specific T-cell therapies will play a central role in alloHSCT.

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Ren, Anqi, Xiqin Tong, Na Xu, Tongcun Zhang, Fuling Zhou, and Haichuan Zhu. "CAR T-Cell Immunotherapy Treating T-ALL: Challenges and Opportunities." Vaccines 11, no. 1 (January 12, 2023): 165. http://dx.doi.org/10.3390/vaccines11010165.

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T-cell acute lymphoblastic leukemia (T-ALL), a form of T-cell malignancy, is a typically aggressive hematological malignancy with high rates of disease relapse and a poor prognosis. Current guidelines do not recommend any specific treatments for these patients, and only allogeneic stem cell transplant, which is associated with potential risks and toxicities, is a curative therapy. Recent clinical trials showed that immunotherapies, including monoclonal antibodies, checkpoint inhibitors, and CAR T therapies, are successful in treating hematologic malignancies. CAR T cells, which specifically target the B-cell surface antigen CD19, have demonstrated remarkable efficacy in the treatment of B-cell acute leukemia, and some progress has been made in the treatment of other hematologic malignancies. However, the development of CAR T-cell immunotherapy targeting T-cell malignancies appears more challenging due to the potential risks of fratricide, T-cell aplasia, immunosuppression, and product contamination. In this review, we discuss the current status of and challenges related to CAR T-cell immunotherapy for T-ALL and review potential strategies to overcome these limitations.

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Hudecek, Michael, Thomas M. Schmitt, Sivasubramanian Baskar, Maria Teresa Lupo-Stanghellini, Tetsuya Nishida, Tori N. Yamamoto, Marie Bleakley, et al. "The B-cell tumor–associated antigen ROR1 can be targeted with T cells modified to express a ROR1-specific chimeric antigen receptor." Blood 116, no. 22 (November 25, 2010): 4532–41. http://dx.doi.org/10.1182/blood-2010-05-283309.

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Monoclonal antibodies and T cells modified to express chimeric antigen receptors specific for B-cell lineage surface molecules such as CD20 exert antitumor activity in B-cell malignancies, but deplete normal B cells. The receptor tyrosine kinase-like orphan receptor 1 (ROR1) was identified as a highly expressed gene in B-cell chronic lymphocytic leukemia (B-CLL), but not normal B cells, suggesting it may serve as a tumor-specific target for therapy. We analyzed ROR1-expression in normal nonhematopoietic and hematopoietic cells including B-cell precursors, and in hematopoietic malignancies. ROR1 has characteristics of an oncofetal gene and is expressed in undifferentiated embryonic stem cells, B-CLL and mantle cell lymphoma, but not in major adult tissues apart from low levels in adipose tissue and at an early stage of B-cell development. We constructed a ROR1-specific chimeric antigen receptor that when expressed in T cells from healthy donors or CLL patients conferred specific recognition of primary B-CLL and mantle cell lymphoma, including rare drug effluxing chemotherapy resistant tumor cells that have been implicated in maintaining the malignancy, but not mature normal B cells. T-cell therapies targeting ROR1 may be effective in B-CLL and other ROR1-positive tumors. However, the expression of ROR1 on some normal tissues suggests the potential for toxi-city to subsets of normal cells.

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Chattaraj, Asmi, Mohammad Ebad Ur Rehman, Israr Khan, Diana Franco, Atif Ibrahim, Razwana Khanam, Nayha Tahir, et al. "Safety and efficacy of allogeneic CAR-T cells in B-cell malignancies: A systematic review and meta-analysis." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): e19530-e19530. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e19530.

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e19530 Background: Immunotherapy with chimeric antigen receptor T (CAR-T) cells has proven effective in recent trials for patients with B cell malignancies, who relapsed after stem cell transplantation. Genetically modified allogeneic CAR T-cells used in advanced B cell malignancy engage with multiple target allo-antigens along with CD19 and/or CD20, leading to elimination of malignant B cells resulting in a potent graft versus malignancy effect with avoidance of tumor escape. Some concerns regarding their use exist like life-threatening graft-versus-host disease (GVHD) and rapid clearance by the host immune system. This study summarises the efficacy and safety of allogeneic CAR-T therapy in B cell malignancies. Methods: A systematic literature search was conducted on PubMed, Embase, Cochrane and Clinicaltrials.gov from inception to Jan 26, 2022, using MeSH terms and keywords for B cell malignancies and CAR-T therapy. We also screened the data presented in various conferences and handpicked references from previous systematic reviews. Outcomes of interest were complete remission (CR), 1-year overall survival (OS), GVHD, cytokine release syndrome (CRS), and immune effector cell associated neurotoxicity (ICANS). Proportional outcomes were pooled using a random effects model (Freeman-Tukey double arcsine transformation) in OpenMetaAnalyst software. Results: The initial search retrieved 1247 articles. After excluding reviews, duplicates and non-relevant articles, we included data from 9 clinical trials (n = 146 patients). The most common malignancy was acute lymphoblastic leukemia (125 patients, 86%). The median age of patients ranged from 19 to 49 years. All patients received CD19 targeting therapy and the cell dose administered ranged from 0.4×10^6 to 5×10^8 cells/kg. CR was reported in 93 of 146 patients, with a pooled rate of 63% (95% CI 47.4 - 78.6%; I2 78.5%). The pooled 1-year OS was 57.3% (95% CI 30.8 - 82%; I2 79.2%). The pooled proportion of GVHD was 9.4% (95% CI 3.1- 15.6%; I2 47.6%). The pooled CRS and ICANS rates were 59.3% (95% CI 30.5 - 88.1%; I2 95.2%) and 15.4% (95% CI 4.6 - 26.3%; I2 72.7%), respectively. Conclusions: Allogeneic CAR-T therapy has demonstrated acceptable efficacy and safety in B cell malignancies, with CR being reported in about 60% of patients and GVHD in < 10% of patients. Although allogeneic CAR-T cells are showing promise, several trials are ongoing and we need longer follow up.[Table: see text]

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Tonino, Sanne H., Marinus H. J. Van Oers, Rene A. Van Lier, and Marie Jose Kersten. "CMV-Associated Expansion of CD8+CD45RA+CD27− T-Cells in Patients with B-Cell Malignancies." Blood 110, no. 11 (November 16, 2007): 3592. http://dx.doi.org/10.1182/blood.v110.11.3592.3592.

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Abstract In patients with various malignancies of B-cell origin, changes in the T-cell compartment have been observed. In B-cell chronic lymphocytic leukemia (CLL), we have previously described an expansion of T-cells, largely due to an increase in T-cells exhibiting the CD45RA+CD27- effector phenotype. This was found only in cytomegalovirus (CMV) seropositive patients, suggesting that CMV-antigen drives this expansion. Indeed a considerable fraction of these T-cells were shown to be CMV-specific. At present it is unknown whether this alteration of the T-cell compartment is specific for CLL or rather any B-cell malignancy could induce similar changes. We performed an immunophenotypic analysis of the T-cell compartment in the peripheral blood of 56 patients with a B-cell malignancy (CLL, n=16; indolent lymphoma, n=20; aggressive lymphoma, n=10; multiple myeloma, n=10) and 12 healthy controls. Subjects of the different disease categories and controls were age-matched. We assessed the total CD3 compartment, naïve (CD27+CD45RA+), memory (CD27+CD45RA−) and memory effector (CD27−CD45RA+) CD8+ T cells. Latent CMV infection was assessed both by CMV-IgG titers (ELISA) and CMV viral load (PCR). The absolute number of T-cells was significantly increased (2.5 – 3 fold) in CLL, but not in the other B-cell malignancies. However, in all disease categories the CD4/CD8 ratio was decreased when compared to healthy controls. This was due to a slight decrease in CD4+ T-cells and an increase in CD8+ T-cells. Irrespective of the nature of the malignancy, the expansion of CD8+ T-cells resulted from a significant increase in CD45RA+CD27− effector T-cells. In agreement with our previous observation, CD8+ T-cell changes were only found in CMV-seropositive patients. Based on our earlier studies we expect these T-cells to be CMV-specific. No correlation between CMV-specific antibody titers and effector T-cell numbers was found. We conclude that the, possibly CMV-specific, effector T-cell compartment is expanded in all B-cell maligancies, although these changes seem to be more pronounced in CLL. The expansion of the total T cell compartment is restricted to CLL. The skewing of the T-cell compartment in CMV-seropositive patients could be the result of increased pressure of latent CMV-infection on the cellular immune system due to failure of other aspects of host defence, brought about by the malignancy.

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Incrocci, Ryan, Molly McCormack, and Michelle Swanson-Mungerson. "Epstein–Barr virus LMP2A increases IL-10 production in mitogen-stimulated primary B-cells and B-cell lymphomas." Journal of General Virology 94, no. 5 (May 1, 2013): 1127–33. http://dx.doi.org/10.1099/vir.0.049221-0.

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Epstein–Barr virus (EBV) latently infected B-cells are the precursors of EBV-associated malignancies. EBV-infection induces the production of pro-survival and anti-inflammatory cytokines that may be important in the transition between latency and malignancy. One EBV protein, LMP2A, can be detected in both latently infected resting B-cells and in EBV-associated malignancies. Therefore, we tested the ability of LMP2A to influence cytokine production using both LMP2A-Tg primary B-cells and LMP2A-expressing B-cell lines. Our data demonstrate that LMP2A does not globally alter B-cell-produced cytokine levels, but specifically targets IL-10. Additional studies using ELISA and real-time-RT-PCR confirm that LMP2A utilizes PI3-kinase to increase IL-10 levels. Finally, the data demonstrate that LMP2A-expressing B-cell lines are more dependent on IL-10 for survival in comparison to LMP2A-negative B-cell lines. These data identify a novel function of LMP2A in the alteration of a cytokine that is important for both tumour survival and anti-tumour responses.

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

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Hairy cell leukemia (HCL) and Merkel cell carcinoma (MCC) are two rare malignancies with distinct cells of origin. HCL is a lymphoid malignancy of mature B cells, and MCC derives from neuroendocrine cell origin. HCL has a favorable prognosis with most patients achieving long-term remission and potential cure. In contrast, MCC is an aggressive malignancy affecting the skin and can metastasize quickly with a dismal prognosis. Immunocompromised patients, such as those with AIDS, posttransplant, and the elderly, have higher incidences than the general population, suggesting a possible immune mechanism. We report a case where a patient presented with HCL and metastatic MCC synchronously. This is the first reported case of these two rare malignancies occurring concurrently at initial presentation and may represent a role of immunosuppression in the pathogenesis of MCC.

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Dissertations / Theses on the topic "B-cell malignancie"

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Runarsson, Gudmundur. "Biosynthesis of leukotriene B₄ in hematological malignancies /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-386-8/.

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Green, Michael R. "Molecular Profiling of B-Cell Malignancies." Thesis, Griffith University, 2009. http://hdl.handle.net/10072/366546.

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Non-Hodgkin’s lymphoma (NHL) is a group of B-cell malignancies that is the 5th most common cancer in males and the 4th most common cancer in females. Three of the four most common histological subtypes of NHL are Diffuse Large B-cell Lymphoma (DLBCL), Follicular Lymphoma (FL) and B-cell Chronic Lymphocytic Leukemia (B-CLL), which together make up over 60% of NHL cases. These diseases vary in both aetiology and aggressiveness, with patient prognosis predicted using indices that rely on biological surrogates in order to predict disease behavior. This results in a large degree of heterogeneity within prognostic groups, with some high-risk patients demonstrating long survival and low-risk patients undergoing rapid transformation and succumbing to an early death. The use of molecular profiling allows interrogation of genetic and transcriptional features of tumor samples that are directly indicative of cellular mechanisms of disease pathogenesis. This is therefore an attractive option for more accurately predicting patient prognosis and thereby allowing design of risk-adapted therapeutic regimes in order to increase survival rates. In this work whole-genome gene expression and single nucleotide polymorphism (SNP) microarrays have been employed in order to interrogate the transcriptome and genome of NHL tumor samples. In order to allow informed analysis of genomic data-sets within the context of gene networks, novel bioinformatic methods were required. This work therefore included the development of novel methods for informed analysis of genome-wide SNP microarray data, visualization of the subsequent gene-set enrichment analysis (GSEA) results, as well as bioinformatic methods for mapping loss-of-heterozygosity without the need for patient-matched control samples. Following development, the utility of these genome-wide approaches for the elucidation of pathogenic mechanisms with the use of small sample sizes was investigated by the interrogation of a novel immunodeficiency disorder. This resulted in our characterization of the first described case of immunodeficiency linked with a chromosomal duplication of the IL25 locus at 14q11.2 and an aberrant Th2-switching mechanism. It also provided proof that whole-genome analyses could be used to determine pathogenic mechanisms of disease.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Mosti, Laura [Verfasser], and Anton [Akademischer Betreuer] Cathomen. "Generation of safe CAR T cells to target B cell malignancies." Freiburg : Universität, 2021. http://d-nb.info/1232174378/34.

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Kokhaei, Parviz. "Preclinical therapeutic vaccination strategies in malignancies with focus on B-cell chronic lymphocytic leukemia /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-595-X/.

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Martínez-Martín, Sandra. "Targeting MYC in B-cell haematologic malignancies." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670653.

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La importància de la funció de MYC en el càncer (i l’origen del nom de la oncoproteïna) es va descobrir a finals dels 70, amb la identificació de la seqüència del retrovirus aviar causant de la leucèmia mielocítica. Durant més de 40 anys d’investigació, s’ha subratllat la rellevància d’aquesta proteïna en la divisió cel·lular normal i la seva implicació en la transformació tumoral. De fet, una de les primeres connexions entre la sobreexpressió de proto-oncògens (com MYC), reordenaments gènics i el càncer es va fer en el limfoma de Burkitt, la leucèmia mieloide crònica i els plasmacitomes de ratolí. Tenint en compte el paper de MYC en els càncers, sembla òbvia la necessitat de desenvolupar estratègies terapèutiques contra aquesta proteïna. No obstant, dirigir teràpies contra MYC era i segueix sent, un repte, donades les seves propietats úniques: no disposa d’estructura tridimensional, localització nuclear i absència d’un domini enzimàtic. Malgrat aixó, molts estudis han demostrat l’impacte terapèutic potencial de la inhibició de MYC, ja sigui directa o indirectament. En aquesta tesi, descrivim el potencial de la inhibició directa de MYC en el limfoma de Burkitt (BL) i el mieloma múltiple (MM), fent ús de dues estratègies diferents: petites molècules peptidomimètiques i disruptors del complex MYC / MAX / ADN (la mini-proteïna Omomyc i una variant derivada, anomenada variant 26 o V26): - La validació del potencial terapèutic dels peptidomimètics es va fer en col·laboració amb una startup biotecnològica. Tot i la prometedora eficàcia demostrada in vitro, un cop administrats in vivo, els compostos van provocar toxicitat severa local acompanyada de canvis en el comportament dels animals, fet que ens va portar a suspendre aquesta línia d’investigació. - Pel que fa a la validació de la mini-proteïna Omomyc com a estratègia farmacològica per tractar el BL i el MM, aquí vam mostrar la seva eficàcia in vitro i resultats preliminars en un model de peix zebra, on el pretractament amb Omomyc evita la colonització de la medul·la òssia. D’aquesta manera, s’evidencia per primera vegada l’ús potencial d’aquest “candidat a fàrmac” per al tractament de tumors líquids. Els nostres resultats in vivo en ratolins mostren que, tot i que l’administració d’Omomyc com a monoteràpia té una eficàcia limitada (probablement a causa d’un lliurament insuficient de pèptid a les cèl·lules de BL i MM), la seva combinació amb un inhibidor del proteasoma (teràpia estàndard del MM) resulta en efectes sinèrgics tant in vitro com in vivo en models de MM. A més, hem demostrat que l’administració intravenosa de Omomyc encapsulada en liposomes és segura i que aquesta formulació liposomal allarga la vida mitjana d’Omomyc en el sèrum, encara que no aconseguim augmentar l’entrada a les cèl·lules diana. - Per últim, hem caracteritzat la V26, un derivat de Omomyc, dissenyada per millorar la localització nuclear i la capacitat d’escapar dels endosomes. Aquí mostrem que la V26 pot homodimerizar i heterodimerizar amb MAX, a més d’unir-se a l’ADN en qualsevol de les dues formes dimèriques. Tal i com esperàvem, la V26 va mostrar ser més nuclear i va induir mort cellular in vitro. No obstant, també va resultar ser menys soluble que Omomyc, de manera que caldria fer millores en la seva formulació per poder ser utilitzada in vivo. En conjunt, els resultats suggereixen que la mini-proteïna Omomyc, o altres derivats com la V26, poden servir com a base pel disseny de nous fàrmacs anti-MYC pel tractament del BL i del MM. Així mateix, la combinació d’aquests amb les teràpies estàndard podrien constituir una estratègia prometedora, mentre que l’encapsulació en liposomes podria ajudar a resoldre aquells possibles problemes de biodisponibilitat derivats del seu ús in vivo.
La importancia de la función de MYC en el cáncer (y el origen del nombre de la oncoproteína) se descubrió a finales de los años 70, con la identificación de la secuencia del retrovirus aviar causante de la leucemia mielocítica. Durante más de 40 años de investigación, se ha subrayado la relevancia de esta proteína en la división celular normal y su implicación en la transformación tumoral. De hecho, una de las primeras conexiones entre la sobreexpresión de proto-oncogenes (como MYC), reordenamientos génicos y el cáncer se hizo en el linfoma de Burkitt, la leucemia mieloide crónica y los plasmacitomas en ratón. Teniendo en cuenta el papel que desempeña MYC en los cánceres, parece obvia la necesidad de desarrollar estrategias terapéuticas contra esta proteína. Sin embargo, dirigir terapias contra MYC era y sigue siendo, un reto, dadas las propiedades únicas que lo caracterizan: su carencia de estructura tridimensional, localización nuclear y ausencia de un "bolsillo" enzimático. A pesar de estas particularidades, muchos estudios han demostrado el impacto terapéutico potencial que tendría la inhibición de MYC, ya sea directa o indirecta. En esta tesis, describimos el potencial de la inhibición directa de MYC en el linfoma de Burkitt (BL) y el mieloma múltiple (MM), usando dos estrategias distintas: pequeñas moléculas peptidomiméticas y disruptores del complejo MYC/MAX/ADN (la mini-proteína Omomyc y una variante derivada, llamada variante 26 o V26): - La validación del potencial terapéutico de los peptidomiméticos se hizo en colaboración con una "startup" biotecnológica. A pesar de la prometedora eficacia demostrada in vitro, los compuestos provocaron toxicidad severa local in vivo, además de cambios en el comportamiento de los animales, que nos llevaron a discontinuar la investigación. - Respecto a la validación de la mini-proteína Omomyc como estrategia farmacológica para tratar el BL y el MM, aquí mostramos su eficacia in vitro y resultados preliminares en un modelo de pez cebra, donde el pretratamiento con Omomyc previene la colonización de la médula ósea. De esta forma, se evidencia por primera vez el uso potencial de este "candidato a fármaco" para el tratamiento de tumores líquidos. Nuestros resultados in vivo en ratones muestran que, aunque la administración de Omomyc como monoterapia tiene una eficacia limitada (probablemente debido a la insuficiente llegada de péptido a las células de BL y MM), su combinación con un inhibidor del proteasoma (terapia estándar del mieloma) resulta en efectos sinérgicos tanto in vitro como in vivo en modelos de mieloma. Además, hemos mostrado que la administración intravenosa de Omomyc encapsulada en liposomas es segura y que dicha formulación liposomal prolonga la vida media de Omomyc en el suero, aunque no conseguimos aumentar la entrada en las células diana. - Por último, hemos caracterizado la V26, un derivado de la mini-proteína Omomyc, diseñada con el objetivo de mejorar la localización nuclear y el escape de los endosomas. Aquí mostramos que, como Omomyc, la V26 puede homodimerizar y heterodimerizar con MAX, además de unirse al ADN en cualquiera de las dos formas diméricas. Como esperábamos, la V26 se mostró más nuclear e indujo muerte celular in vitro. Sin embargo, también resultó ser menos soluble que Omomyc, de forma que sería necesario hacer mejoras en su formulación para poder usarla in vivo. En conjunto, nuestros resultados sugieren que la mini-proteína Omomyc, u otros derivados, como la V26, pueden servir como base para el diseño de nuevos fármacos anti-MYC para el tratamiento del BL y MM. Además, la combinación de éstos con las terapias estándar podrían constituir una estrategia prometedora, mientras que la encapsulación en liposomas podría ayudar a resolver aquellos posibles problemas de biodisponibilidad derivados de su uso in vivo.
The importance of MYC function in cancer (and the origin of the oncoprotein's name) was discovered in the late '70s when the sequence of the avian retrovirus that causes myelocytic leukaemia was identified. Since then, over 40 years of unceasing research have highlighted the significance of this protein in regular cell division, and importantly, its involvement in malignant transformation. Indeed, some of the earliest connections between the higher expression of proto-oncogenes (such as MYC), genetic rearrangements and their relation to cancer development were made in Burkitt lymphoma, chronic myeloid leukaemia and mouse plasmacytomas. Given the role of MYC in cancer, the need for the design of therapeutic strategies against it seems obvious. However, targeting MYC was - and somehow, still is - challenging due to its unique properties: lack of defined three-dimensional, structure nuclear localisation and absence of enzymatic pocket. Despite these difficulties, many studies have shown the potential therapeutic impact of direct or indirect MYC inhibition. In this thesis, we outline the potential of direct MYC inhibition in Burkitt lymphoma (BL) and multiple myeloma (MM) making use of 3 different strategies: small molecule peptidomimetics and disruptors of the MYC/MAX/DNA complex (Omomyc mini-protein and the derivative variant 26 or V26): - In the first case, the validation of the peptidomimetics therapeutic potential was done in collaboration with a start-up biotech company. Despite evidencing some promising efficacy in vitro, the compounds displayed severe local toxicity in vivo, accompanied by changes in animal behaviour that prompted us to discontinue the investigation. - Regarding the validation of Omomyc mini-protein as a pharmacological approach in the treatment of BL and MM, we demonstrated in vitro efficacy and showed preliminary results in the prevention of bone marrow homing upon Omomyc pre-treatment in a zebrafish model, indicating, for the first time, the potential use of this drug candidate to treat liquid tumours. Our in vivo data in mice show that, even if the administration of Omomyc as monotherapy has limited efficacy (probably due to insufficient delivery of peptide to BL and MM target cells), the combination with a proteasome inhibitor (the standard of care for myeloma) both in vitro and in vivo displays synergic effects in myeloma models. In addition, we were able to show that intravenous administration of the Omomyc mini-protein encapsulated in liposomes was safe and the liposomal formulation prolonged the serum half-life of the mini-protein, although it did not promote increased penetrance in MM target cells. - Lastly, we characterised V26, a rationally designed derivative of the Omomyc mini-protein, meant to display improved nuclear localisation and endosomal escape. Here we evidenced that, like Omomyc, V26 can homodimerise and heterodimerise with MAX, as well as bind DNA in both dimeric forms. As expected, V26 displayed better nuclear localisation and induced cell death in vitro. However, it also turned out to be less soluble than Omomyc, indicating that it would require further formulation efforts to be used in vivo. Altogether, our results suggest that Omomyc mini-protein itself or other Omomyc-derivatives, like V26, can serve as the backbone for the design of new anti-MYC agents to treat BL and MM. In this context, combination therapy with the standard of care seems to be a promising strategy, while encapsulation in liposomes might help to address potential bioavailability issues that might arise from its use in vivo.

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6

McCann, Katy. "Immunogenetic analysis of aggressive B-cell malignancies." Thesis, University of Southampton, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494386.

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7

Gupta, Sneha Veeraraghavan. "Targeting Protein Metabolism in B-cell Malignancies." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1343169973.

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8

Jiménez, Bernal Isabel. "Tumor immune microenvironment in B-cell lymphoid malignancies." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/671173.

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El microambient immune tumoral juga un paper fonamental en les etapes inicials de la formació dels tumors i en la progressió d’aquests. Teràpies dirigides a aquest microambient ofereixen noves opcions terapèutiques i també serveixen per a millorar les teràpies actuals enfront de molts càncers, incloent els que afecten les cèl·lules B. No obstant això, són necessàries més recerques per a entendre en major profunditat els mecanismes d’evasió del sistema immune que afavoreixen la progressió dels tumors i dissenyar immunoteràpies més precises. Els nostres principals objectius són aportar noves evidències sobre mecanismes immunes associats a la progressió tumoral i les bases pre-clíniques per al desenvolupament de noves estratègies terapèutiques amb potencial immunomodulador. Per a això, ens centrem en la leucèmia limfàtica crònica (LLC) i en el limfoma cerebral primari (LCP). Els mecanismes de progressió en LLC des d’estadis inicials no són coneguts íntegrament. Encara que l’adquisició d’alteracions moleculars és escassa suggerint que la LLC no progressa exclusivament per mecanismes d’evolució clonal, encara no s’ha dut a terme una anàlisi exhaustiva del microambient immune que demostri que la progressió sí que pugui deure’s a canvis immunes. Per això, hem realitzat un estudi longitudinal abastant tant els escenaris genètics com immunològics en pacients de LLC sense tractar que han progressat clínicament i en pacients asimptomàtics durant un llarg període de temps. Els nostres resultats mostren que els pacients que progressen experimenten un increment de cèl·lules T CD8+ efectores de memòria i terminalment exhaustes T-betmid/-*EomeshiPDhi a la progressió. Aquest increment no s’observa en els pacients de LLC que no han progressat. A més, les cèl·lules T a la progressió adquireixen un perfil transcripcional diferent. Això va acompanyat d’un augment en les propietats immunosupressores de les cèl·lules leucèmiques a la progressió. Vam demostrar que les cèl·lules de LLC en el moment de la progressió tenen major capacitat d’induir exhaustió tant en cèl·lules T CD8+ de LLC com aquelles procedents d’individus sans, i que ho fan mitjançant un mecanisme dependent de factors solubles que inclou IL-10. Els escassos canvis genètics que trobem després de seqüenciar el exoma dels nostres pacients ens permeten concloure que les variacions immunes que hem identificat són fonamentals per a la progressió de la LLC. El desenllaç dels pacients diagnosticats amb LCP és normalment desfavorable a causa de l’escassetat d’opcions terapèutiques efectives. Les cèl·lules malignes de LCP presenten amb freqüència una desregulació de la via del receptor de la cèl·lula B (de l’anglès, BCR), però la seva inhibició mitjançant ibrutinib mostra respostes molt breus en pacients. No obstant això, la via del BCR també pot bloquejar-se mitjançant la inhibició de la exportina nuclear XPO1 amb selinexor. Selinexor travessa la barrera hemato-encefàlica i ha mostrat activitat en un pacient diagnosticat amb limfoma difús de cèl·lules grans B amb recaiguda en el sistema nerviós central. Per consegüent, decidim avaluar els efectes de selinexor en monoteràpia i combinat amb ibrutinib en models preclínics murinos de LCP. La nostra anàlisi mostra que selinexor bloqueja el creixement tumoral i prolonga la supervivència en un model de ratolí bioluminiscent i la combinació amb ibrutinib prolonga encara més la supervivència. Vam demostrar que els limfomes cerebrals en ratolí estan infiltrats amb macròfags pro-tumorals M2 que expressen PD-1 i SIRPα. A més, el tractament amb selinexor i ibrutinib afavoreix la resposta immune anti-tumoral induint un canvi en la polarització dels macròfags cap a un perfil pro-inflamatori i reduint l’expressió de PD-1 i SIRPα en els macròfags M2 associats al tumor.
El microambiente inmune tumoral juega un papel fundamental en las etapas tempranas de la formación de los tumores y en la progresión de éstos. Terapias dirigidas a este microambiente ofrecen nuevas opciones terapéuticas y también sirven para mejorar las terapias actuales frente a muchos cánceres, incluyendo los que afectan a las células B. Sin embargo, son necesarias más investigaciones para entender en mayor profundidad los mecanismos de evasión del sistema inmune que favorecen la progresión de los tumores y diseñar inmunoterapias más precisas. Nuestros principales objetivos son aportar nuevas evidencias sobre mecanismos inmunes asociados a la progresión tumoral y las bases pre-clínicas para el desarrollo de nuevas estrategias terapéuticas con potencial inmuno-modulador. Para ello, nos centramos en la leucemia linfática crónica (LLC) y en el linfoma cerebral primario (LCP). Los mecanismos de progresión en LLC desde estadios tempranos no son conocidos en su totalidad. Aunque la adquisición de alteraciones moleculares es escasa sugiriendo que la LLC no progresa exclusivamente por mecanismos de evolución clonal, todavía no se ha llevado a cabo un análisis exhaustivo del microambiente inmune que demuestre que la progresión sí pueda deberse a cambios inmunes. Por ello, hemos realizado un estudio longitudinal abarcando tanto los escenarios genéticos como inmunológicos en pacientes de LLC sin tratar que han progresado clínicamente y en pacientes asintomáticos durante un largo periodo de tiempo. Nuestros resultados muestran que los pacientes que progresan experimentan un incremento de células T CD8+ efectoras de memoria y terminalmente exhaustas T-betmid/-EomeshiPDhi a la progresión. Este incremento no se observa en los pacientes de LLC que no han progresado. Además, las células T a la progresión adquieren un perfil transcripcional diferente. Esto va acompañado de un aumento en las propiedades inmunosupresoras de las células leucémicas a la progresión. Demostramos que las células de LLC en el momento de la progresión tienen mayor capacidad de inducir exhaustión tanto en células T CD8+ de LLC como aquellas procedentes de individuos sanos, y que lo hacen mediante un mecanismo dependiente de factores solubles que incluye IL-10. Los escasos cambios genéticos que encontramos tras secuenciar el exoma de nuestros pacientes nos permiten concluir que las variaciones inmunes que hemos identificado son fundamentales para la progresión de la LLC. El desenlace de los pacientes diagnosticados con LCP es normalmente desfavorable debido a la escasez de opciones terapéuticas efectivas. Las células malignas de LCP presentan con frecuencia una desregulación de la vía del receptor de la célula B (del inglés, BCR), pero su inhibición mediante ibrutinib muestra respuestas muy breves en pacientes. Sin embargo, la vía del BCR también puede bloquearse mediante la inhibición de la exportina nuclear XPO1 con selinexor. Selinexor atraviesa la barrera hemato-encefálica y ha mostrado actividad en un paciente diagnosticado con linfoma difuso de células grandes B con recaída en el sistema nervioso central. Por consiguiente, decidimos evaluar los efectos de selinexor en monoterapia y combinado con ibrutinib en modelos pre-clínicos murinos de LCP. Nuestro análisis muestra que selinexor bloquea el crecimiento tumoral y prolonga la supervivencia en un modelo de ratón bioluminiscente y la combinación con ibrutinib prolonga aún más la supervivencia. Demostramos que los linfomas cerebrales en ratón están infiltrados con macrófagos pro-tumorales M2 que expresan PD-1 y SIRPα. Además, el tratamiento con selinexor e ibrutinib favorece la respuesta inmune anti-tumoral induciendo un cambio en la polarización de los macrófagos hacia un perfil pro-inflamatorio y reduciendo la expresión de PD-1 y SIRPα en los macrófagos M2 asociados al tumor.
The tumor immune microenvironment (TIME) plays a critical role in the early formation of tumors and their progression. Targeting the TIME has offered new therapeutic approaches and improved current ones in several cancers, including B-cell malignancies. Nonetheless, further investigation is needed in order to more deeply understand immune evasion mechanisms that lead to tumor progression and to design therapies that modulate the immune system more precisely. Here, our main objectives are to provide new insights into immune mechanisms that favor tumor progression and a pre-clinical rationale for the design of new therapeutic strategies with immunomodulatory potential. To accomplish these goals our study will focus on chronic lymphocytic leukemia (CLL) and primary central nervous system lymphoma (PCNSL). Mechanisms driving the progression of CLL from its early stages are not fully understood. This hampers detecting progression in advance and developing therapies that could intervene in the early stages. Although the limited acquisition of molecular changes suggests that CLL progression is not mainly driven by clonal evolution, a deeper analysis of the immune microenvironment that demonstrates immune variations over time that contribute to progression has not been performed. Hence, we longitudinally studied the immune and genetic landscapes of untreated progressing and non-progressing patients. Our results show that progressed CLL patients experience an increase in effector memory and terminally exhausted T-betmid/-EomeshiPDhi CD8+ T cells over time, not observed in non-progressing patients. In addition, T cells at progression acquire a distinct transcriptional profile. This is accompanied by enhanced immunosuppressive properties in leukemic cells at progression. We prove that progressed CLL cells are intrinsically more capable of inducing CD8+ T-cell exhaustion in T cells affected by CLL and healthy T cells by a mechanism dependent on soluble factors including IL-10. In addition, the reduced genetic changes we found by whole-exome sequencing in our cohort indicate these immune variations are fundamental for progression in CLL. Patients diagnosed with PCNSL often face dismal outcomes due to the limited availability of therapeutic options. PCNSL cells frequently have deregulated B-cell receptor (BCR) signaling, but its inhibition using ibrutinib only offers a brief effective response in PCNSL patients. Nonetheless, the BCR pathway can also be blocked by inhibiting the nuclear exportin XPO1 using selinexor. Selinexor is able to cross the blood–brain barrier and has shown positive clinical activity in a patient with refractory diffuse large B-cell lymphoma in the CNS. Accordingly, we evaluated the effects of selinexor alone and also combined it with ibrutinib in pre-clinical mouse models of PCNSL. Our analysis shows that selinexor blocks tumor growth and prolongs survival in a bioluminescent mouse model and its combination with ibrutinib further increases survival. We demonstrate that CNS lymphomas in mice are infiltrated by tumor-promoting M2-like macrophages expressing PD-1 and SIRPα. Moreover, the treatment with selinexor and ibrutinib favors an anti-tumoral immune response by shifting macrophage polarization toward an inflammatory phenotype and diminishing the expression of PD-1 and SIRPα in M2 tumor-associated macrophages.

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Caeser, Rebecca. "Elucidating oncogenic mechanisms in human B cell malignancies." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/285011.

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This study consists of two pieces of work investigating haematological malignancies; Acute Lymphoblastic Leukaemia (ALL) and Diffuse Large B Cell Lymphoma (DLBCL). Firstly, Pre-B ALL represents the most common paediatric malignancy and despite increasingly improved outcomes for patients, ~ 20% of all patients diagnosed with ALL relapse. Activating mutations in the RAS pathway are common (~50%) and result in hyperactivation of the MAPK pathway. I identified Erk negative feedback control via DUSP6 to be crucial for NRASG12D-mediated pre-B cell transformation and investigated its potential as a therapeutic target. I showed that a small molecule inhibitor of DUSP6 (BCI) selectively induced cell death in patient-derived pre-B ALL cells; with a higher sensitivity observed in relapse pre-B ALL. I also discovered that a high level of Erk activity is required for proliferation of normal pre-B cells, but dispensable in leukemic pre-B ALL cells. In addition, I found that human B cell malignancies can be grouped into three categories that fundamentally differ in their ability to control Erk signalling strength. Secondly, DLBCL is the most common haematological malignancy and although potentially curable with chemotherapy, 40% of patients still succumb from their disease. Recent exome sequencing studies have identified hundreds of genetic alterations but, for most, their contribution to disease, or their importance as therapeutic targets, remains uncertain. I optimised a novel approach to screen the functional importance of these mutations. This was achieved by reconstituting non-malignant, primary, human germinal centre B cells (GC B cells) with combinations of wildtype and mutant genes to recapitulate the genetic events of DLBCL. When injected into immunodeficient mice, these oncogene-transduced GC B cells gave rise to tumours that closely resemble human DLBCL, reinforcing the biological relevance of this system. To screen potential tumour suppressor mutations in this system in a high throughput fashion, I developed a lymphoma-focused CRISPR library of 692 genes recurrently altered in B cell lymphomas. These experiments identified GNA13 as an unexpectedly potent tumour suppressor in human GC B cells and provided new understanding to its mechanism of action. These findings provide novel understanding of the complexity of oncogenic mechanisms in human B cell malignancies.

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10

Forster, Jade. "Evaluating the genomic landscape of B cell malignancis." Thesis, University of Southampton, 2016. https://eprints.soton.ac.uk/408724/.

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Splenic marginal zone lymphoma (SMZL) and chronic lymphocytic leukaemia (CLL) are B cell malignancies, predominately affecting the elderly. The disease course of both SMZL and CLL is highly variable, with some patients dying rapidly within a month whilst other remain stable and live a normal lifespan. Biomarkers are used to help to distinguish those patients who may progress. Genomic abnormalities such as copy number alterations and mutation of genes may have prognostic value in CLL and SMZL. Several technologies were used to assess the genomic landscape in B cell malignancies; low resolution technology such as multiplex ligation-dependant probe amplification (MLPA) and Sanger sequencing as well as higher resolution methods such as SNP 6.0 arrays and next generation sequencing technologies; whole exome sequencing, TruSeq and Nextera XT. MLPA was used to assess both the copy number alterations (CNA) and mutational abnormalities in the well-defined CLL4 clinical trial cohort. Though the technology is restrictive in terms of probe location and sensitivity, there was statistical concordance with Sanger sequencing and fluorescence in situ hybridisation (FISH). Novel CNA, independently associated with survival were uncovered; 1) a very indolent disease course in patients carrying a biallelic 13q deletion with IGHV mutated genes and 2) a very poor prognosis in patients with a 9p deletion. Exome sequencing of CLL (n=6) and SMZL (n=7) patients uncovered novel variants via a bioinformatical pipeline; this pipeline was validated using more traditional sequencing methods. The candidate genes; U2AF1, BIRC3, POT1 and MYD88 are implicated in CLL and were screened in a larger cohorts of patients. Analysis of the 11q loci in relation to ATM and BIRC3 gene mutations, identified alterations of ATM that impact most significantly on survival. Nextera technology was optimised to screen ibrutinib treated CLL patients for BTK and PLCG2 mutations. DNAH9 and SPEN were also sequenced in a small cohort of patients. A breakpoint deletion was identified in the DNAH9 gene, suggesting this gene may be relevant in CLL. Further studies are needed to examine these newly defined high and low risk groups, and other genetic abnormalities in another well-defined CLL cohort, to ascertain their pathogenic and biological significance.

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Books on the topic "B-cell malignancie"

1

Shokri, Fazel. Expression, production and regulation of rheumatoid factor associated cross-reactive idiotypes in systemic autoimmune diseases and B-cell malignancies. Birmingham: University of Birmingham, 1990.

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Perez-Chacon, Gema, Christelle Vincent-Fabert, and Juan M. Zapata, eds. Mouse Models of B Cell Malignancies. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-896-2.

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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Bone and soft tissue malignancies. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199689842.003.0025.

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Haematological malignancies examines the epidemiology, genetics, clinical presentation and classification of these diseases, and presents current treatment approaches for each. First are the acute leukaemias, and the management of acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML). Chronic myeloid leukaemia, its genetics and sensitivity to tyrosine kinase inhibitors, is described. Myelodysplastic syndromes and their management, are followed by chronic lymphoid leukaemias, a large heterogeneous group of diseases, and their treatment. Hodgkin lymphoma, its pathology and presentation, staging and role of PET scanning, is described along with current treatment with chemotherapy and limited radiotherapy. Non-Hodgkin lymphoma is another heterogeneous group of diseases, divided into low-grade and high-grade pathology, and varying in their genetics, presentation, and management. Rituximab is a key component of chemotherapy regimens against B-cell lymphoma. Myeloma and other plasma cell dyscrasias are described, and treatment options reviewed. Myeloma remains incurable, but with appropriate management consistent with prolonged good quality life. Treatment includes chemotherapy, bisphosphonate therapy, analgesics and radiotherapy, Throughout this chapter is emphasised the importance of clinical trials in driving the rapid improvements in treatment of these diseases.

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Paggetti, Jérôme, Martina Seiffert, and Etienne Moussay, eds. New Insights into the Complexity of Tumor Immunology in B-cell Malignancies: Disease Biology and Signaling. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-241-7.

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Paggetti, Jérôme, Etienne Moussay, and Martina Seiffert, eds. New Insights into the Complexity of Tumor Immunology in B-cell Malignancies: Tumor Immunology and Immunotherapy. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-206-6.

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Paggetti, Jérôme, Martina Seiffert, and Etienne Moussay, eds. New Insights into the Complexity of Tumor Immunology in B-cell Malignancies: Prognostic and Predictive Biomarkers and Therapy. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-207-3.

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Purdue, Mark P., Jonathan N. Hofmann, Elizabeth E. Brown, and Celine M. Vachon. Multiple Myeloma. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0041.

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Multiple myeloma (MM) is the most common malignancy arising from plasma cells, fully differentiated B lymphocytes that produce the immunoglobulin (Ig) heavy- and light-chain molecules comprising antibodies. MM is characterized by an overproduction of clonal plasma cells in the bone marrow and, in most cases, monoclonal secretion of IgG, IgA, or light-chain Ig. Symptoms of end organ damage (hypercalcemia [C], renal failure [R], anemia [A], or bone lesions [B]), herein referred to as CRAB features, were traditionally a necessary criterion for diagnosing MM; however, improvements in treatment and diagnostic techniques have led to updated diagnostic criteria, enabling intervention among patients before the onset of organ damage. Multiple myeloma is an important cause of lymphoid malignancy (LM) mortality in Western populations. In the United States in 2015, MM was estimated to account for approximately one in every five newly diagnosed LMs, and one in every three LM-related deaths.

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Hjalgrim, Henrik, Ellen T. Chang, and Sally L. Glaser. Hodgkin Lymphoma. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0039.

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Hodgkin lymphoma (HL) is a malignant neoplasm of the lymphatic system. The malignant cell clone derives from germinal center B lymphocytes in ~98% of cases, the rest being of T-lymphocyte origin. Each year, HL is diagnosed in roughly 66,000 individuals worldwide. HL is curable with modern therapy in the vast majority of patients, with five-year survival rates exceeding 90% for early-stage disease. However, so far this excellent prognosis has been achieved at the expense of a high incidence of severe long-term treatment complications such as secondary malignancies, and endocrine and cardiovascular diseases. In affluent Western countries, HL occurrence follows a distinctive and unusual bimodal age distribution, with one incidence peak among adolescents and younger adults and another in older adults. In socioeconomically less affluent populations, in contrast, the adolescent and younger-adult incidence peak is less pronounced, whereas incidence of HL in young boys may be higher than in affluent populations.

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Book chapters on the topic "B-cell malignancie"

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Dunlap, Jennifer B., Guang Fan, Nicky Leeborg, and Rita M. Braziel. "B-Cell Malignancies." In Molecular Pathology in Clinical Practice, 579–602. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19674-9_42.

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Barta, Stefan K., Kieron Dunleavy, and Nicolas Mounier. "Diffuse Large B-Cell Lymphoma." In HIV-associated Hematological Malignancies, 39–65. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26857-6_3.

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Pritsch, Otto, and Guillaume Dighiero. "Autoimmunity and B-Cell Malignancies." In Autoimmune Reactions, 19–30. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-4612-1610-0_3.

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Mikhaeel, N. George, and Lena Specht. "Diffuse Large B-Cell Lymphoma." In Radiation Therapy in Hematologic Malignancies, 29–43. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42615-0_2.

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Guba, Susan C., and Bart Barlogie. "Stem Cell Transplants for Hematopoietic Malignancies." In Molecular Biology of B-Cell and T-Cell Development, 505–21. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4757-2778-4_25.

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Tao, Jianguo, and Chih-Chi Andrew Hu. "B Cell Growth, Differentiation and Malignancies." In Hematologic Cancers: From Molecular Pathobiology to Targeted Therapeutics, 1–20. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5028-9_1.

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Juszczyński, Przemysław, and Krzysztof Warzocha. "Molecular Pathogenesis of Aggressive B-cell Lymphomas." In Molecular Aspects of Hematologic Malignancies, 55–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-29467-9_3.

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Ng, Andrea K. "Primary Mediastinal (Thymic) Large B-Cell Lymphoma." In Radiation Therapy in Hematologic Malignancies, 73–83. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42615-0_5.

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Kimberley, Fiona C., Jan Paul Medema, and Michael Hahne. "APRIL in B-cell Malignancies and Autoimmunity." In Results and Problems in Cell Differentiation, 161–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/400_2008_19.

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Strefford, Jonathan C., Jude Fitzgibbon, Matthew J. J. Rose-Zerilli, and Csaba Bödör. "The genetics of mature B-cell malignancies." In The Genetic Basis of Haematological Cancers, 265–311. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118527948.ch6.

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Conference papers on the topic "B-cell malignancie"

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Kuttikrishnan, Shilpa, Kirti S. Prabhu, Tamam Elimat, Ashraf Khalil, Nicholas H. Oberlies, Feras Q. Alali, and Shahab Uddin. "Anticancer Activity of Neosetophomone B, An Aquatic Fungal Secondary Metabolite, Against Hematological Malignancie S." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0106.

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Cancer is one of the most life threatening diseases, causing nearly 13% death in the worldwide. Leukemia, cancer of the hematopoetic cells is the main cause of cancer death in adults and children. Therapeutic agents used in treatment of cancer are known to have narrow therapeutic window and tendency to develop resistance against some cancer cell lines thus, proposing a need to discover some novel agents to treat cancer. In the present study we investigated the anticancer activity of Neosetophomone B(NSP-B), an aquatic fungal metabolite isolated from Neosetophoma sp against leukemic cells (K562 and U937). MTT results demonstrated a dose dependent inhibition of cell proliferation in K562 and U937 cell lines. Annexin staining using flow cytometry indicated that NSP-B treatment cause a dose dependent apoptosis in leukemic cells.Western blot analysis showed that NSP-B mediated apoptosis involves sequential activation of caspase 9, 3 and poly (ADP-ribose) polymerase (PARP) cleavage. Furthermore NSP-B treatment of leukemic cells resulted in upregulation of pro-apoptotic proteins (Bax) with downregulation of anti-apoptotic proteins ( Bcl-2 ).Thus, present study focuses on exploring the mechanism of anticancer activity of NSP-B on leukemic cells, raising the possibility of its use as a novel therapeutic agent for hematological malignancies. Results: We sought to determine whether NSP-B suppresses the growth of leukemic cell lines. We tested a panel of leukemic cell lines with different doses of NSP-B. Cell viability decreased in a concentration-dependent manner in K562 and U937 cell lines. NSP-B induced apoptosis in K562 and U937 cell lines via downregulation of anti-apoptotic proteins and enhancement of pro-apoptotic proteins. NSP-B induced the activation of caspase cascade signaling pathway. Altogether our results suggest that the NSP-B plays an important role in apoptosis in leukemic cell lines .Conclusions: Our data provides insight on anticancer activities of NSP-B in leukemic cell lines (K562 and U937). NSP-B inhibit cell viability via inducing apoptosis. The NSP-B mediated apoptosis occurs via downregulation of anti-apoptotic proteins and enhancement of pro-apototic proteins, thereby activating the caspase-cascade signaling. Further studies are required to elicit role of NSP-B in regulating molecular pathway involved in the progression of cancer. Taken together, above results suggest that NSP-B may have a future therapeutic role in leukemia and possibly other hematological malignancies.

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Weng, Jinsheng, Owhofasa Agbedia, Jingjing Cao, Xiaoyun Cheng, Shao Qing Kuang, Fuliang Chu, Sridevi Patchv, et al. "296 Targeting B-cell malignancies with anti-ROR1 CAR T-cell therapy." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0296.

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Heymann, J., F. Vogiatzi, T. Rösner, L. Lenk, G. Cario, M. Schrappe, T. Valerius, M. Peipp, C. Kellner, and DM Schewe. "Venetoclax enhances the efficacy of therapeutic antibodies in B-cell malignancies." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687156.

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Cosgun, Kadriye Nehir, Anna Hecht, Xin Yang, Maurizio Mangolini, Ali Aghajanirefah, Gang Xiao, Teresa Sadras, et al. "Abstract 4515: Lgr5 mediates positive B-cell selection and is critical for initiation and survival of B-cell malignancies." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4515.

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Morton, Laura T., Anne K. Wouters, Dennis F. Remst, Renate S. Hagedoorn, Marleen M. Van Loenen, Renate de Boer, J. H. F. Falkenberg, and Mirjam H. M. Heemskerk. "Abstract A038: Effective rerouting of NK cell cytotoxicity against B-cell malignancies upon TCR gene transfer." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a038.

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Pasqualucci, Laura. "Abstract IA39: The genetic basis of diffuse large B cell lymphoma." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-ia39.

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Kraljacic-Culkjovic, Biljana, Tharu Fernando, Rebecca Goldstein, Charles Mctavish, Jayeshkumar Patel, Shaoning Yang, Fabrizio Tabbo, et al. "Abstract B12: EIF4E deregulation drives simultaneous expression of B-cell lymphoma oncogenes." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-b12.

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Wang, Peiyin, Maria Hristopoulos, Robyn Clark, Yvonne Chen, Diego Ellerman, Mary Mathieu, Christoph Spiess, et al. "Abstract 3628: T cell-dependent bispecific antibody anti-CD79b/CD3 as a potential therapy for B-cell malignancies." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3628.

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Melnick, Ari M. "Abstract IA47: Epigenetic programming and therapy in germinal center derived B-cell lymphomas." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-ia47.

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Adams, Clare M., Ramkrishna Mitra, Jerald Z. Gong, Annette S. Kim, John K. Choi, and Christine M. Eischen. "Abstract 02: BCL-W significantly contributes to B-cell lymphoma survival and development." In Abstracts: Second AACR Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; May 6-9, 2017; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3265.hemmal17-02.

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Reports on the topic "B-cell malignancie"

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Fitzgerald, David. Anti-CDR3 Therapy for B-Cell Malignancies. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada590597.

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Fitzgerald, David. Anti-CDR3 Therapy for B-Cell Malignancies. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada619137.

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Xie, Ping. Regulation of Mitochondria Function by TRAF3 in B Lymphocytes and B Cell Malignancies. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada610687.

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Wang, Jinjin, H. Zhou, and T. Niu. Risk of Bleeding Associated With Ibrutinib in Patients With B-Cell Malignancies A Systematic Review and Meta-analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0076.

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Zhao, Kangjia, Jiwen Sun, Nanping Shen, Mengxue He, Haishan Ruan, Geng Lin, Jiali Ma, and Yanhua Xu. Treatment-Related Adverse Events of Chimeric Antigen receptor T-Cell (CAR-T) Cell Therapy in B-cell hematological malignancies in the Pediatric and Young Adult Population: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0034.

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