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Статті в журналах з теми "Chronic myeloid leukemia gene therapy"
Ghosn, Youssef, Mohammed Hussein Kamareddine, Antonios Tawk, Carlos Elia, Ahmad El Mahmoud, Khodor Terro, Nadia El Harake, Bachar El-Baba, Joseph Makdessi, and Said Farhat. "Inorganic Nanoparticles as Drug Delivery Systems and Their Potential Role in the Treatment of Chronic Myelogenous Leukaemia." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381985324. http://dx.doi.org/10.1177/1533033819853241.
Повний текст джерелаJamieson, Catriona H. "Chronic Myeloid Leukemia Stem Cells." Hematology 2008, no. 1 (January 1, 2008): 436–42. http://dx.doi.org/10.1182/asheducation-2008.1.436.
Повний текст джерелаDeininger, Michael W. "Diagnosing and Managing Advanced Chronic Myeloid Leukemia." American Society of Clinical Oncology Educational Book, no. 35 (May 2015): e381-e388. http://dx.doi.org/10.14694/edbook_am.2015.35.e381.
Повний текст джерелаTrela, Ewelina, Sylwester Glowacki, and Janusz Błasiak. "Therapy of Chronic Myeloid Leukemia: Twilight of the Imatinib Era?" ISRN Oncology 2014 (January 30, 2014): 1–9. http://dx.doi.org/10.1155/2014/596483.
Повний текст джерелаWarfvinge, Rebecca, Mikael Sommarin, Parashar Dhapola, Ulrich Pfisterer, Linda Geironson Ulfsson, Fatemeh Safi, Ram Krishna Thakur, Johan Richter, and Göran Karlsson. "Characterization of Leukemic Stem Cells Heterogeneity in Chronic Myeloid Leukemia." Blood 134, Supplement_1 (November 13, 2019): 4140. http://dx.doi.org/10.1182/blood-2019-130956.
Повний текст джерелаHusnain, Muhammad, Trent Wang, Maikel Valdes, James Hoffman, and Lazaros Lekakis. "Multiple Myeloma in a Patient with ANKRD26-Related Thrombocytopenia Successfully Treated with Combination Therapy and Autologous Stem Cell Transplant." Case Reports in Hematology 2019 (June 2, 2019): 1–3. http://dx.doi.org/10.1155/2019/9357572.
Повний текст джерелаGao, Liquan, Ilaria Bellantuono, Annika Elsässer, Stephen B. Marley, Myrtle Y. Gordon, John M. Goldman, and Hans J. Stauss. "Selective elimination of leukemic CD34+ progenitor cells by cytotoxic T lymphocytes specific for WT1." Blood 95, no. 7 (April 1, 2000): 2198–203. http://dx.doi.org/10.1182/blood.v95.7.2198.
Повний текст джерелаGao, Liquan, Ilaria Bellantuono, Annika Elsässer, Stephen B. Marley, Myrtle Y. Gordon, John M. Goldman, and Hans J. Stauss. "Selective elimination of leukemic CD34+ progenitor cells by cytotoxic T lymphocytes specific for WT1." Blood 95, no. 7 (April 1, 2000): 2198–203. http://dx.doi.org/10.1182/blood.v95.7.2198.007k38_2198_2203.
Повний текст джерелаXin, Jiajia, Dandan Yin, Wei Fu, Hui-Jie Zhang, Yaozhen Chen, Yazhou Wang, Mingkai Li, and Xingbin Hu. "A Novel Compound Inhibits Chronic Myeloid Leukemia Via Upregulating Apoptosis." Blood 126, no. 23 (December 3, 2015): 5559. http://dx.doi.org/10.1182/blood.v126.23.5559.5559.
Повний текст джерелаDeshmukh, Komal Galani, and Katalin Kelemen. "Lessons Learned from Donor Cell-Derived Myeloid Neoplasms: Report of Three Cases and Review of the Literature." Life 12, no. 4 (April 8, 2022): 559. http://dx.doi.org/10.3390/life12040559.
Повний текст джерелаДисертації з теми "Chronic myeloid leukemia gene therapy"
Miller-Reynolds, Angela Rose-Marie. "Suicide gene therapy in murine models of chronic myeloid leukaemia." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412871.
Повний текст джерелаYazdanparast, Haniyeh [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "Myeloid cells and therapy resistance in Chronic Lymphocytic Leukemia / Haniyeh Yazdanparast ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177385988/34.
Повний текст джерелаRoos, Cecilia. "Studies of leukotriene C4 synthase expression and regulation in chronic myeloid leukaemia /." Karlstad : Faculty of Technology and Science, Biomedical Science, Karlstads universitet, 2008. http://www.diva-portal.org/kau/abstract.xsql?dbid=1598.
Повний текст джерелаOlsson-Strömberg, Ulla. "Clinical and experimental studies in chronic myeloid leukemia : studies of treatment outcome, in vitro cellular drug resistance and gene expression /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7841.
Повний текст джерелаMascarenhas, Cintia do Couto 1982. "Avaliação de mutações pontuais no gene ABL por metodo de cromatografia liquida desnaturante de alta performance (D-HPLC) em pacientes com leucemia mieloide cronica tratados com inibidores de tirosina quinase." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308623.
Повний текст джерелаDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: O desenvolvimento da Leucemia Mielóide Crônica (LMC) tem como característica a formação do cromossomo Philadelphia que envolve a quebra do gene BCR gerando um rearranjo molecular denominado BCR-ABL, cujo produto final é uma proteína de fusão citoplasmática que determina a patogenia da doença. Esta proteína é uma tirosina quinase (TK) que possui capacidade de auto-ativação e para a inativação desta proteína, foram desenvolvidos os inibidores da tirosina quinase (ITK), que tem a capacidade de se ligar no mesmo sítio de ligação da molécula de ATP. Esta ligação impede a transferência dos grupos fosfatos aos substratos subseqüentes, bloqueando a cascata de transdução de sinais e prevenindo a ativação das vias mitogênica dependente da quinase Bcr-Abl e anti-apoptóticas levando à morte do fenótipo BCR-ABL.Um dos principais mecanismos de resistência ao tratamento com ITK são as mutações pontuais, sendo a T315I foco de estudos mais detalhados por tornar a proteína mutante altamente insensível a todas as drogas inibidoras da proteína TK disponíveis atualmente Foi utilizado neste trabalho a técnica de D-HPLC para fazer screening de mutações nos pacientes com LMC com resposta sub ótima ou falha de tratamento de acordo com os critérios da Leukemia Net. Para o screening do éxon 6 foram selecionados 93 pacientes com LMC: 5 eram intolerantes, 67 resistentes e 21 com resposta subótima. Como controle negativo foi usado o sangue periférico doadores de sangue do Hemocentro da UNICAMP. Para o screening de mutações de todo o gene BCR-ABL foram estudados 37 pacientes com LMC e como controle negativo, usamos a linhagem celular HL60 que não possui a translocação BCR-ABL. No screening do éxon 6, 23 amostras (25%) mostraram um perfil de eluição no D-HPLC anormal em relação ao controle, o que sugeriu a presença de mutação. A sobrevida global (OS) para todo grupo foi de 80% em uma mediana de tempo de observação de 30 meses. OS para pacientes sem mutações foi de 87% e para os pacientes com mutações foi de 56% em uma mediana de tempo de observação 37 e 10 meses, respectivamente (p <0,0001, RR = 68). No screening de todo o gene BCR-ABL 17 (46%) tiveram perfil cromatográfico diferente do controle Como estávamos estabelecendo a padronização do método, procedemos com o seqüenciamento de todas as amostras e os resultados obtidos foram comparados com a seqüência depositada no banco de dados GenBank (U07563). Das 17 amostras com alteração do perfil cromatográfico, observamos a presença de mutação em 13 amostras. Acreditamos que isso se deva a sensibilidade do método de D-HPLC que é capaz de identificar tanto polimorfismos quanto mutações com maior eficiência que o seqüenciamento. Em resumo, o D-HPLC demonstrou ser um método sensível e prático para o acompanhamento do aparecimento de mutações no domínio da quinase na rotina clínica. Mutações nessa região estudada são clinicamente relevantes e podem conferir um pior prognóstico. A detecção precoce pode ser uma ferramenta importante para otimizar a terapêutica na LMC.
Abstract: The development of chronic myeloid leukemia (CML) is the formation of the characteristic Philadelphia chromosome involving breach of the BCR gene generating a molecular rearrangement called BCR-ABL, whose final product is a cytoplasmic fusion protein that determines the pathogenesis of the disease. This is a protein tyrosine kinase (TK) that has self-ativaçãoe to inactivate this protein have developed the inhibitors of tyrosine kinase (ITK), which has ability to connect on the same site of binding of molecule of ATP. This connection prevents the transfer of phosphate groups to substrates subsequent, blocking the cascade of signal transduction and preventing the activation of mitogenic pathways dependent kinase BCR-ABL and anti leading to apoptotic death phenotype of BCR-ABL.One major mechanisms of resistance to treatment with ITK are mutations off, and the T315I focus of more detailed studies by making mutant protein highly insensitive to all drugs Inhibit TK protein currently available was used in this work to D-HPLC technique to screening for mutations in patients with CML with sub-optimal response or failure of treatment according to the criteria Leukemia Net For the screening of exon 6 were selected 93 CML patients: 5 were intolerant, 67 resistant and 21 with answer sub-optimal. The negative control we used the peripheral blood donors Blood from the blood of UNICAMP. For the screening of mutations throughout the BCR-ABL gene were studied 37 patients with CML and control negative, we used the HL60 cell line that does not have the translocation BCR-ABL. In the screening of exon 6, 23 samples (25%) showed a profile of the D-HPLC elution abnormal in the control, which suggested the presence of mutation. The overall survival (OS) for whole group was 80% in a median time of observation of 30 months. OS for patients with mutations was 87% and for patients with mutations was 56% in the median observation time of 37 and 10 months respectively (p <0.0001, RR = 68). In screening the entire gene BCR-ABL 17 (46%) had chromatographic profile different from the control we were setting the standardization of methods, procedures with the sequencing of all samples and the results were compared with the sequence deposited in the GenBank database (U07563). Of the 17 samples with change the chromatographic profile, we observed the presence of mutation in 13 samples. We believe that this is due to sensitivity of the method of D-HPLC is able to identify the mutations both polymorphisms with greater efficiency to the sequencing. In summary, the D-HPLC has proved a sensitive and practical method for monitoring the appearance of mutations in the kinase domain in the clinical routine. Mutations studied in this region are clinically relevant and may confer worse prognosis. Early detection can be a tool important to optimize therapy in CML.
Mestrado
Ciencias Basicas
Mestre em Clinica Medica
Istook, Diana Lee. "Differential gene expression between patients with acute lymphocytic leukemia and patients with acute myeloid leukemia : the use of analysis of variance models in microarray data analysis /." Oklahoma City : [s.n.], 2004.
Знайти повний текст джерелаOlsson-Strömberg, Ulla. "Clinical and Experimental Studies in Chronic Myeloid Leukemia : Studies of Treatment Outcome, In Vitro Cellular Drug Resistance and Gene Expression." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7841.
Повний текст джерелаThe aims of the studies described in the thesis were to investigate different treatment strategies in chronic myeloid leukemia (CML) patients. Furthermore, activity of imatinib was investigated by in vitro cytotoxicity assay, and the gene expression pattern in interferon treated patients.
In a randomized prospective national study, we examined the influence of busulphan (n=89) versus hydroxyurea (n=90) treatment on time to blast crisis, and survival. There was no significant difference in survival between hydroxyurea and busulphan treated patients; median survival was 3.5 and 3.2 years, respectively. The 26 patients who underwent allogeneic stem cell transplantation had a significantly longer median survival (4.7 years) than those who were not transplanted.
We investigated the feasibility of mobilizing Philadelphia chromosome negative blood stem cells with intensive chemotherapy and lenograstim in CML patients. Twenty-three patients (62%) were successfully mobilized. Twenty-one of these patients underwent autologous stem cell transplantation later on, with a 5-year overall survival at 68%.
Fluorometric Microculture Cytotoxicity Assay was used to analyze 32 tumor cell samples from CML patients, (26 chronic phase and 6 blast crisis). Imatinib showed a higher in vitro activity and more positive drug interactions in cells from blast crisis than from chronic phase. Interferon, daunorubicin and arsenic trioxide had the greatest benefit from a combination with imatinib.
Microarray-based gene expression analyses were performed on diagnostic CML samples prior to interferon treatment. We identified six genes that were differentially expressed in responders and non-responders to interferon. It might prove possible to use gene expression analysis to predict future response to interferon.
Mascarenhas, Cintia do Couto 1982. "Identificação e investigação de genes diferencialmente expressos entre pacientes com leucemia mielóide crônica e indivíduos controle." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308645.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A elucidação dos mecanismos moleculares envolvidos na fisiopatologia e tratamento das doenças hematológicas, bem como no entendimento do perfil de expressão gênica das linhagens celulares leucêmicas, tem sido objeto de numerosas investigações. Com o uso da técnica SSH (Subtractive Supression Hybridization ou Biblioteca Subtrativa Supressiva) foi possível identificar importantes genes que se encontram diferencialmente expressos em granulócitos de pacientes com Leucemia Mielóide Crônica e indivíduos controle. Foram encontrados 39 genes superexpressos e 173 com expressão diminuída em células de LMC. Ao relacionar esses genes com vias metabólicas que estão reguladas positiva (expressão aumentada) ou negativamente (expressão diminuída) nessa doença, verificou-se que a maioria dos genes estavam relacionados com a regulação de NF-kB, AKT, o Interferon e a IL-4 em células de controle. Entre os genes superexpressos encontrados na LMC, foi observado o SEPT5, RUNX1, MIER1, KPNA6 e FLT3, enquanto PAN3, TOB1 e ITCH estavam com expressão diminuída nessa doença em comparação com indivíduos controle. O TOB1 se mostrou promissor, uma vez que é um gene supressor tumoral, pode estar envolvido na proliferação de células leucêmicas e interage com vários outros genes encontrados neste estudo. Assim, devido à grande heterogeneidade de funções relacionadas com a expressão desse gene, foi investigada a relação entre a expressão de mRNA e as respostas aos ITK's na LMC. A avaliação foi realizada por PCR em tempo real em doentes com CCgR, PCgR, MINCgR e NOCgR após tratamento com TKI's e os resultados foram comparados com a expressão em granulócitos de indivíduos controle, observando que os pacientes NOCgR têm uma expressão de TOB1 significativamente inferior em comparação com doadores saudáveis e pacientes que alcançaram RCgC. Ao comparar pacientes não resistentes e resistentes a diferença foi significativa. Esses resultados sugerem que a expressão diminuída de TOB1 em pacientes NOCgR pode ser indicativo de desregulação da apoptose e de vias de sinalização importantes nessa doença incluindo a via da AKT, conduzindo assim a resistência a ITK's nesses pacientes. Outro objetivo deste trabalho foi caracterizar a função dos genes TOB1 e SEPT5 nos processos celulares e vias de sinalização de apoptose, proliferação, migração e ciclo celular em linhagens celulares leucêmicas. Ao realizar o silenciamento desses genes (utilizando partículas lentivirais) notou-se que o silenciamento de TOB1, como já descrito na literatura em outras doenças, interfere na proliferação celular, clonogenicidade, apoptose, ciclo celular e expressão de proteínas importantes da cascata de sinalização, o que salienta sua importância em células BCR-ABL positivas. Já o gene SEPT5 ao ser silenciado leva a algumas alterações como a apoptose e ciclo celular. Nesse contexto, o silenciamento destes genes chama atenção para as possibilidades de controle da proliferação celular, apoptose, ciclo celular e clonogenicidade em células BCR-ABL positivas. Foi realizada a avaliação da expressão desses genes em células de sangue periférico e medula óssea de pacientes com LMC e indivíduos controles, linhagens celulares de câncer humano e linhagens de murino. Os resultados mostraram um aumento significativo na expressão do gene SEPT5 em todos os tipos celulares analisados em pacientes com LMC. O mesmo padrão foi observado em células de murino que possuem a mutação T315I e em células humanas que possuem a translocação t(9;22) e estão relacionadas com a fase blástica da doença [K562, KU812, NALM]. Quando avaliada a expressão do gene TOB1 nota-se diminuição em todos os tipos celulares analisados em pacientes com LMC e em células BaF3T315I. Também foi observada uma baixa expressão em células com a t(9;22) e estão relacionadas com a fase blástica da doença[K562, KU812, NALM] quando comparadas a expressão em medula óssea controle. Outro resultado interessante foi obtido a partir da análise de adesão celular em granulócitos de pacientes com LMC e controles, evidenciando a diminuição da adesão em granulócitos de pacientes com LMC em relação aos de controles, levando a hipótese de que essa alteração nas propriedades adesivas dos granulócitos em pacientes com LMC pode estar diretamente ligada à liberação de células jovens pela matriz da medula óssea. A criação de estratégias que levam ao melhor entendimento da fisiopatologia da doença e avanço no tratamento da LMC deve ser focada em vários genes alvos e não apenas no BCR-ABL, pois no desenvolvimento da LMC há a ativação e desativação de várias vias de sinalização celular. Os resultados deste estudo podem ajudar na melhor compreensão dessas vias e também para identificar outros genes e vias úteis para a melhora no manejo terapêutico e criação de novas drogas para o tratamento dessa doença
Abstract: The elucidation of the molecular mechanisms involved in the pathophysiology and treatment of blood disorders, as well as the understanding of genes expression profiling of leukemia cell lines has been the focus of numerous investigations. The use of the SSH (Suppression Subtractive Hybridization Library or Suppression Subtractive) technique made available the identification of important genes which are differentially expressed in granulocytes from patients with chronic myeloid leukemia (CML) and healthy controls. 39 genes overexpressed were found, and 173 with decreased expression in CML cells. When correlating these genes with metabolic pathways that are regulated positively (increased expression) or negatively (decreased expression) in this disease, it was found that most of the genes were related to the regulation of NF-kB, AKT, Interferon and IL-4 in control cells. The following genes were found overexpressed in CML: SEPT5, RUNX1, MIER1, KPNA6 and FLT3, while PAN3, TOB1 and ITCH were found with decreased expression in this disease compared with controls. The TOB1 gene showed promising since it is a tumor suppressor, may be involved in the proliferation of leukaemic cells and interacts with several others genes found in this study. Thus, due to the great heterogeneity of functions related to this gene, was investigated the relationship between mRNA expression and TKI's responses. The evaluation was performed by real time PCR in patients with CCgR, PCgR, MINCgR and NOCgR after treatment with TKI and healthy controls. Was observed that patients that have NOCgR, the TOB1 expression is significantly lower compared with healthy donors and patients who achieved CCgR. When comparing non-resistant and resistant patients the difference also was significant. These results suggest that reduced expression of TOB1 in NOCgR patients may indicate apoptosis deregulation and changes in important signaling pathways of CML including the Akt pathway, thereby leading to TKI's resistance of these patients. Another aim of this work was to characterize the function of TOB1 and SEPT5 in cellular processes and signaling pathways of apoptosis, proliferation, migration and cell cycle in leukemic cell lines. After the silencing of these genes (using lentiviral particles), was noted that the silencing TOB1 - as described in the literature for other diseases - interferes in cell proliferation, clonogenicity, apoptosis, cell cycle and in expression of important proteins at signaling cascade, which emphasizes its importance in BCR-ABL positive cells. The SEPT5 silencing leads to some changes such as apoptosis and cell cycle. In this context, the silencing of these genes leads to attention of possibilities of control of cell proliferation, apoptosis, cell cycle and cell clonogenicity in BCR-ABL positive cells. Was assessed the expression of these genes in cells from peripheral blood and bone marrow of CML patients and controls, as well in human and murine cell lines. Results showed a significant increase in SEPT5 gene expression in patients with CML in all cell types evaluated. The same profile was observed in murine cells BAF3T315I and in human cells having the translocation t (9; 22) been related to blast crisis [K562, KU812, NALM]. When measuring expression of TOB1, was noted decrease in all cell types studied in CML patients and cells BaF3T315I. Another interesting result was obtained from the analysis of cell adhesion at granulocytes in CML patients and controls which showed decreased adhesion of granulocytes in CML patients compared to controls, leading to the hypothesis that the change in adhesive properties at CML can be directly linked to the release of young cells by bone marrow. The creation of strategies that lead to better understanding of the pathophysiology of the disease and advance in the treatment of CML should be focused on several target genes and not only in BCR-ABL, since in the development of CML there is an activation and deactivation of multiple signaling pathways . The results of this study may help to better understand these pathways and also to identify other genes and pathways useful for improving the management and development of new therapeutic drugs to treat this disease
Doutorado
Clinica Medica
Doutora em Clínica Médica
Küpper, Maja Kim [Verfasser], Wolfgang [Akademischer Betreuer] Wagner, and Gerhard [Akademischer Betreuer] Müller-Newen. "STAT3-mediated therapy resistance of malignant stem cells in chronic myeloid leukemia (CML) / Maja Kim Küpper ; Wolfgang Wagner, Gerhard Müller-Newen." Aachen : Universitätsbibliothek der RWTH Aachen, 2019. http://d-nb.info/1194067107/34.
Повний текст джерелаKatsoulas, Athanasia. "Design and mechanism of action of novel agents termed "combi-molecules" engineered for tandem targeting for Bcr-abl expressing leukemia cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111884.
Повний текст джерелаКниги з теми "Chronic myeloid leukemia gene therapy"
Weinberg, Robert A. (Robert Allan), 1942-, ed. The Philadelphia chromosome: A mutant gene and the quest to cure cancer at the genetic level. New York: The Experiment, LLC, 2013.
Знайти повний текст джерела1947-, Talpaz Moshe, and Kantarjian Hagop 1952-, eds. Medical management of chronic myelogenous leukemia. New York: Dekker, 1998.
Знайти повний текст джерелаWapner, Jessica. The Philadelphia Chromosome: A Mutant Gene and the Quest to Cure Cancer at the Genetic Level. Highbridge Audio and Blackstone Publishing, 2021.
Знайти повний текст джерелаWeinberg, Robert A., and Jessica Wapner. Philadelphia Chromosome: A Genetic Mystery, a Lethal Cancer, and the Improbable Invention of a Lifesaving Treatment. Experiment LLC, The, 2014.
Знайти повний текст джерела(Editor), Jorge Cortes, and Michael Deininger (Editor), eds. Chronic Myeloid Leukemia. Informa Healthcare, 2006.
Знайти повний текст джерелаCortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2006.
Знайти повний текст джерелаCortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2006.
Знайти повний текст джерелаCortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2019.
Знайти повний текст джерелаE, Cortés F. Jorge, and Deininger Michael, eds. Chronic myeloid leukemia. New York: Informa Healthcare, 2007.
Знайти повний текст джерелаCortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2006.
Знайти повний текст джерелаЧастини книг з теми "Chronic myeloid leukemia gene therapy"
Yong, Agnes S. M., and Junia V. Melo. "Pathophysiology of Chronic Myeloid Leukemia." In Leukemias: Principles and Practice of Therapy, 259–70. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327359.ch21.
Повний текст джерелаCastro, Januario E., and Thomas J. Kipps. "Gene Therapy of Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 329–40. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_18.
Повний текст джерелаJabbour, Elias, and Jorge Cortes. "Targeted Therapies in Chronic Myeloid Leukemia." In Targeted Therapy in Translational Cancer Research, 111–20. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118468678.ch11.
Повний текст джерелаCorey, Seth J., and Jorge Cortes. "Chronic Myeloid Leukemia: Pathophysiology and Therapeutics." In Molecularly Targeted Therapy for Childhood Cancer, 139–53. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-69062-9_8.
Повний текст джерелаHochhaus, Andreas. "Therapy of Newly Diagnosed and Chronic-Phase Chronic Myeloid Leukemia." In Leukemias: Principles and Practice of Therapy, 271–80. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327359.ch22.
Повний текст джерелаValencia-Serna, Juliana, Breanne Landry, Xiaoyan Jiang, and Hasan Uludag. "Potential of siRNA Therapy in Chronic Myeloid Leukemia." In Intracellular Delivery II, 435–73. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8896-0_21.
Повний текст джерелаPawelski, S., L. Konopka, K. Szczepanik, and H. Zdziechowska. "Therapy of Blastic Transformation of Chronic Myeloid Leukemia." In Leukemias, 249–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77083-8_45.
Повний текст джерелаHiwase, Devendra K., and Timothy P. Hughes. "Therapy of Advanced-Stage and Resistant Chronic Myeloid Leukemia." In Leukemias: Principles and Practice of Therapy, 281–95. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327359.ch23.
Повний текст джерелаRadich, Jerald. "The Detection and Quantification of bcr-abl in Chronic Myeloid Leukemia Following Marrow Transplantation." In Gene Quantification, 277–93. Boston, MA: Birkhäuser Boston, 1998. http://dx.doi.org/10.1007/978-1-4612-4164-5_16.
Повний текст джерелаLussana, Federico, Tamara Intermesoli, Paola Stefanoni, and Alessandro Rambaldi. "Mechanisms of Resistance to Targeted Therapies in Chronic Myeloid Leukemia." In Mechanisms of Drug Resistance in Cancer Therapy, 231–50. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/164_2017_81.
Повний текст джерелаТези доповідей конференцій з теми "Chronic myeloid leukemia gene therapy"
Bajpai, Prachi, A. Tripathi, and Deepa Agrawal. "Abstract B42: Polymorphism of CYP3A5 gene in Indian chronic myeloid leukemia patients." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-b42.
Повний текст джерелаYi, Bin, Xiaobo Li, Wenjun Du, Gary A. Piazza, and Yaguang Xi. "Abstract 1848: Let-7 brings new insights into chronic myeloid leukemia therapy." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1848.
Повний текст джерелаLaurino, Marco, Maurizio Stano, Monica Betta, Gabriele Pannocchia, and Alberto Landi. "Combining pharmacological therapy and vaccination in Chronic Myeloid Leukemia via model predictive control." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6610403.
Повний текст джерелаBasak, Jayasri, Soma Mukhopadhyay, Sukanta Konar, and Ashis Mukhopadhyay. "Abstract A68: Molecular response of pediatric chronic myeloid leukemia (CML) with imatinib mesylate therapy." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-a68.
Повний текст джерелаPemmaraju, Naveen, Hagop Kantarjian, Susan O'Brien, Raja Luthra, Elias Jabbour, Aflonso Quintas-Cardama, Gautam Borthakur, et al. "Abstract 4715: Dasatinib as initial therapy for patients with chronic myeloid leukemia (CML) in early chronic phase (CP)." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4715.
Повний текст джерелаHostetler, Bryan, Olga Uchakina, and Robert McKallip. "Abstract 3848: Targeting hyaluronidase reduces stromal cell protection of chronic myeloid leukemia to imatinib therapy." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3848.
Повний текст джерелаVolz, C., A. Gottschalk, M. Krumbholz, C. Albert, S. Semper, M. Suttorp, I. Glauche, and M. Metzler. "Therapy assessment of pediatric chronic myeloid leukemia (CML) using combined analyses of RNA/DNA response dynamics." In 33. Jahrestagung der Kind-Philipp-Stiftung für pädiatr. onkolog. Forschung. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1709801.
Повний текст джерелаDufva, Olli, Tiina Kasanen, Mohamed El Missiry, Judith Klievink, Hanna Lähteenmäki, and Satu Mustjoki. "Abstract A115: Tyrosine kinase inhibitor therapy modulates immune checkpoints and TCR repertoire diversity in chronic myeloid leukemia." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a115.
Повний текст джерелаKaehler, Meike, Inga Nagel, Henrike Bruckmueller, Ruwen Boehm, Ole Ammerpohl, and Ingolf Cascorbi. "Abstract 5846: Drug resistance in chronic myeloid leukemia: Impact of methylation on gene expression in imatinib and nilotinib resistance." 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.am2018-5846.
Повний текст джерелаOliveira, Ligia P., Rafael G. Ferro, and Ana CSS Galvão. "Abstract 1846: Gene expression analysis of P-glycoprotein and LMWPTP in chronic myeloid leukemia cells treated with metformin and imatinib mesylate." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1846.
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