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Статті в журналах з теми "B-cell malignancie"
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.
Повний текст джерелаLydyard, 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.
Повний текст джерелаZweidler-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.
Повний текст джерелаBrudno, 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.
Повний текст джерелаRen, 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.
Повний текст джерелаHudecek, 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.
Повний текст джерелаChattaraj, 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.
Повний текст джерелаTonino, 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.
Повний текст джерелаIncrocci, 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.
Повний текст джерелаPrakash, 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.
Повний текст джерелаДисертації з теми "B-cell malignancie"
Runarsson, Gudmundur. "Biosynthesis of leukotriene B₄ in hematological malignancies /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-386-8/.
Повний текст джерелаGreen, Michael R. "Molecular Profiling of B-Cell Malignancies." Thesis, Griffith University, 2009. http://hdl.handle.net/10072/366546.
Повний текст джерелаThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
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.
Повний текст джерелаKokhaei, 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/.
Повний текст джерелаMartínez-Martín, Sandra. "Targeting MYC in B-cell haematologic malignancies." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670653.
Повний текст джерелаLa 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.
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.
Повний текст джерелаGupta, Sneha Veeraraghavan. "Targeting Protein Metabolism in B-cell Malignancies." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1343169973.
Повний текст джерелаJiménez, Bernal Isabel. "Tumor immune microenvironment in B-cell lymphoid malignancies." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/671173.
Повний текст джерелаEl 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.
Caeser, Rebecca. "Elucidating oncogenic mechanisms in human B cell malignancies." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/285011.
Повний текст джерелаForster, Jade. "Evaluating the genomic landscape of B cell malignancis." Thesis, University of Southampton, 2016. https://eprints.soton.ac.uk/408724/.
Повний текст джерелаКниги з теми "B-cell malignancie"
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.
Знайти повний текст джерелаPerez-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.
Повний текст джерелаCassidy, 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.
Повний текст джерелаPaggetti, 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.
Повний текст джерелаPaggetti, 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.
Повний текст джерелаPaggetti, 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.
Повний текст джерелаPurdue, 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.
Повний текст джерелаHjalgrim, Henrik, Ellen T. Chang, and Sally L. Glaser. Hodgkin Lymphoma. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0039.
Повний текст джерелаЧастини книг з теми "B-cell malignancie"
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.
Повний текст джерелаBarta, 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.
Повний текст джерелаPritsch, 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.
Повний текст джерелаMikhaeel, 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.
Повний текст джерелаGuba, 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.
Повний текст джерелаTao, 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.
Повний текст джерелаJuszczyński, 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.
Повний текст джерелаNg, 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.
Повний текст джерелаKimberley, 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.
Повний текст джерелаStrefford, 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.
Повний текст джерелаТези доповідей конференцій з теми "B-cell malignancie"
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.
Повний текст джерелаWeng, 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.
Повний текст джерелаHeymann, 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.
Повний текст джерелаCosgun, 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.
Повний текст джерелаMorton, 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.
Повний текст джерелаPasqualucci, 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.
Повний текст джерелаKraljacic-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.
Повний текст джерелаWang, 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.
Повний текст джерелаMelnick, 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.
Повний текст джерелаAdams, 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.
Повний текст джерелаЗвіти організацій з теми "B-cell malignancie"
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.
Повний текст джерелаFitzgerald, David. Anti-CDR3 Therapy for B-Cell Malignancies. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada619137.
Повний текст джерелаXie, 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.
Повний текст джерелаWang, 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.
Повний текст джерелаZhao, 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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