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Статті в журналах з теми "BCR-ABL like"
Gross, Alec W., Xiaowu Zhang, and Ruibao Ren. "Bcr-Abl with an SH3 Deletion Retains the Ability To Induce a Myeloproliferative Disease in Mice, yet c-Abl Activated by an SH3 Deletion Induces Only Lymphoid Malignancy." Molecular and Cellular Biology 19, no. 10 (October 1, 1999): 6918–28. http://dx.doi.org/10.1128/mcb.19.10.6918.
Повний текст джерелаCross, Nick. "BCR-ABL Negative CML-Like Disorder." Clinical Lymphoma Myeloma and Leukemia 17 (September 2017): S107—S108. http://dx.doi.org/10.1016/j.clml.2017.08.052.
Повний текст джерелаHe, Yiping, Jason A. Wertheim, Lanwei Xu, Juli P. Miller, Fredrick G. Karnell, John K. Choi, Ruibao Ren, and Warren S. Pear. "The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia–like disease by bcr/abl." Blood 99, no. 8 (April 15, 2002): 2957–68. http://dx.doi.org/10.1182/blood.v99.8.2957.
Повний текст джерелаHao, Sheryl X., and Ruibao Ren. "Expression of Interferon Consensus Sequence Binding Protein (ICSBP) Is Downregulated in Bcr-Abl-Induced Murine Chronic Myelogenous Leukemia-Like Disease, and Forced Coexpression of ICSBP Inhibits Bcr-Abl-Induced Myeloproliferative Disorder." Molecular and Cellular Biology 20, no. 4 (February 15, 2000): 1149–61. http://dx.doi.org/10.1128/mcb.20.4.1149-1161.2000.
Повний текст джерелаZheng, Xiaomin, Saskia Güller, Gesine Bug, Bithia Grace, Roxana Bistrian, Dieter Hoelzer, Oliver G. Ottmann, Reinhard Henschler, and Martin Ruthardt. "The Reciprocal t(9;22)-Translocation Products ABL/BCR Have Leukemogenic Potential Independently from BCR/ABL." Blood 104, no. 11 (November 16, 2004): 214. http://dx.doi.org/10.1182/blood.v104.11.214.214.
Повний текст джерелаMillion, Ryan P., and Richard A. Van Etten. "The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase." Blood 96, no. 2 (July 15, 2000): 664–70. http://dx.doi.org/10.1182/blood.v96.2.664.014k52_664_670.
Повний текст джерелаMillion, Ryan P., and Richard A. Van Etten. "The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase." Blood 96, no. 2 (July 15, 2000): 664–70. http://dx.doi.org/10.1182/blood.v96.2.664.
Повний текст джерелаAlbers, Corinna, Anna L. Illert, Cornelius Miething, Christian Peschel, and Justus Duyster. "Grb10 Mediated Akt Activation Is Required for Induction of CML Like Myeloproliferative Disease in Mice by BCR-ABL." Blood 110, no. 11 (November 16, 2007): 1012. http://dx.doi.org/10.1182/blood.v110.11.1012.1012.
Повний текст джерелаMohi, M. Golam, Wayne W. Chan, Shaoguang Li, Benjamin Neel, and Richard A. Van Etten. "Distinct Gab2-Mediated Signaling Pathways Are Essential for Myeloid or Lymphoid Transformation and Leukemogenesis by BCR-ABL." Blood 112, no. 11 (November 16, 2008): 570. http://dx.doi.org/10.1182/blood.v112.11.570.570.
Повний текст джерелаAlbers, Corinna, Anna Lena Illert, Cornelius Miething, Christian Peschel, and Justus Duyster. "Raf1 Is Required for Induction of a Bcr-Abl Positive CML Like Myeloproliferative Disease in Mice." Blood 112, no. 11 (November 16, 2008): 3207. http://dx.doi.org/10.1182/blood.v112.11.3207.3207.
Повний текст джерелаДисертації з теми "BCR-ABL like"
Drivet, Elsa. "Etude préclinique personnalisée d'une translocation rare T(1 ; 9)(Q24 ; Q34) "PH-LIKE" et perspectives d'optimisation des traitements contre les LAL-B de mauvais pronostic." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0664.
Повний текст джерелаThe t(1;9)(q24;q34) translocation, generating the RCSD1-ABL1 fusion protein, is found in bad prognosis LAL cases. The oncogenic properties of RCSD1-ABL1 are unknown and the structure of the RCSD1 portion as well as its impact on RCSD1-ABL1 activity and signaling is yet to be determined. We recently reported the case of a patient with ALL associated with a RCSD1-ABL1 rearrangement that was resistant or poorly responsive to a large number of TKIs but was sensitive to Ponatinib, with no mutation that could explain this.In order to characterize this fusion protein, understand its response profile to TKI and optimize therapeutic approaches for these patients, we cloned the RCSD1-ABL1 gene from the patient sample and expressed it in the cellular model BaF3. This allowed us to 1) Demonstrate and 2) Study for the first time the oncogenic properties and signaling of the fusion protein, which is partially distinct from that of BCR-ABL1, especially regarding the JAK/STAT pathway; 3) Purify RCSD1-ABL1 and reveal the impact of the RCSD1 N-terminal portion on the enzyme activity and its TKI sensitivity; 4) Integrate this data and demonstrate the potentiating effect of JAT/STAT pathway inhibitors on TIK activity in cells expressing RCSD1-ABL1 but not in cells expressing BCR-ABL1.Finally, the chemo-genomic profiling of samples from three B-ALL t(1;9)(q24 ;q34) allowed us to consolidate our results and to propose preclinical bases for personalized treatments targeting the identified mechanisms
Okada, Masayuki. "A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL positive human leukemic cells : caspase-independent, necrosis-like programmed cell death mediated by serine protease activity." Kyoto University, 2005. http://hdl.handle.net/2433/145297.
Повний текст джерелаBewry, Nadine N. "STAT3 Contributes to Resistance Towards BCR-ABL Inhibitors in a Bone Marrow Microenvironment Model of Drug Resistance in Chronic Myeloid Leukemia Cells." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0002892.
Повний текст джерелаNishihara, Toshio. "Effects of the Tyrosine Kinase Inhibitor, Imatinib Mesylate on a Bcr-Abl-Positive Cell Line : Suppression of Autonomous Cell Growth but No Effect on Decreased Adhesive Property and Morphological Changes." Kyoto University, 2004. http://hdl.handle.net/2433/147461.
Повний текст джерелаHeurteau, Foulon Stéphanie. "Prévalence, qualité de vie et coût de la Leucémie Myéloïde Chronique en France Using healthcare claims data to analyze the prevalence of BCR-ABL-positive chronic myeloid leukemia in France: A nationwide population-based study Health state utility and quality of life measures in patients with chronic myeloid leukemia in France." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS574.
Повний текст джерелаChronic myeloid leukemia (CML) is a rare myeloproliferative neoplasm whose prognosis has been transformed since the 2000s by tyrosine kinase inhibitors (TKI). The dramatic increase in patients' life expectancy has led to an increase in the prevalence of CML. CML has become a chronic disease that requires daily TKI treatment for several years, but which is compatible with a normal life span for the majority of patients. TKI are expensive treatments that, taken over the long term by an increasing number of patients, increase the economic burden of the disease. TKI have side effects that affect patients' quality of life. In France, however, there is little data on the prevalence of CML, on the economic burden and quality of life.The National Health Data System (Système National des Données de Santé, SNDS) is a health care claims database that covers 98,8% of the French population and contains exhaustive data on health cares reimbursed by the Health Insurance. We built and validated an algorithm identifying patients with CML in the SNDS, based on their healthcare consumption and estimated the prevalence of the disease on December 31st, 2014. On the population identified by the algorithm, we estimated the cost of TKI in 2013 and 2014 from a health insurance perspective. We also conducted a survey in CML patients to collect their quality of life data using generic (EuroQol EQ-5D-3L), cancer-specific (EORTC-QLQ-C30) and CML-specific (EORTC-QLQ-CML-24) questionnaires. Utility values in CML patients were assessed using the French EQ-5D-3L value set.The algorithm identified 10,789 patients with CML in France in 2014, corresponding to a crude prevalence of the disease of 16.3 per 100,000 inhabitants [95% confidence interval 16.0-16.6]. In the 10,158 prevalent CML patients in 2013, the reimbursement for TKI amounted to €238 million, all insurance schemes combined. This amount increased to €247 million for the 10,789 patients prevalent in 2014. In 2014, imatinib accounted for about 55% of TKI reimbursements, followed by nilotinib (22%) and dasatinib (22%). The quality of life in CML patients was significantly impaired compared to the general population of the same sex and age, mainly in the dimensions of social functioning, role functioning and cognitive functioning. Fatigue, dyspnea and pain were the symptoms with the highest deviation from general population norms. The mean utility score (standard deviation) was 0.72 (0.25) for patients in chronic phase and 0.84 (0.21) for patients in remission without treatment.Beyond the epidemiological, clinical and economic results, this work demonstrates that using a database such as the SNDS for research is feasible, relevant but also complex in rare diseases such as CML
山本, 起代子, and Kiyoko Yamamoto. "Functionally deregulated AML1/RUNX1 cooperates with BCR-ABL to induce a blastic phase-like phenotype of chronic myelogenous leukemia in mice." Thesis, 2013. http://hdl.handle.net/2237/19156.
Повний текст джерелаCheng, Hao-Yuan, and 鄭皓遠. "Combination of protein tyrosine kinase inhibitor AG1024 with paclitaxel enhances cell program death in BCR-ABL-mediated resistance of K562 cell line." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/30227831001776366712.
Повний текст джерела國立陽明大學
醫學生物技術研究所
93
Chronic myelogenous leukaemia (CML) is a clonal malignancy of the pluripotent haematopoietic stem cell, characterised by an uncontrolled proliferation and expansion of myeloid progenitors expressing a fusion oncogene, BCR-ABL, the molecular counterpart of the Ph1 chromosome. Many evidences showed that the tyrosine kinase activity of BCR-ABL is able to activate several major signalling pathways in malignant cells, including Ras, JAK/STAT and PI3K/Akt and also prevent cells apoptosis under some antineoplastic agents such as paclitaxel. Targeting these abnormalities by blocking tyrosine kinase of BCR-ABL with STI571 provides a promising approach for the therapy of CML. The recent development of resistance to STI571 illustrates, however, that the use of other tyrosine kinase inhibitors could be of major interest for therapeutic purposes. To this end, the tyrosine kinase inhibitor Tyrphostin AG1024 was used to evaluate the effects on regulation of BCR-ABL expression, inhibition of cell proliferation and enhanced Taxol-induced apoptosis in BCR-ABL expressing cell lines, K562. As the result, Tyrphostin AG1024 was shown to downregulate the expression of BCR-ABL and anti-apoptosis factors such as Bcl-2 and Bcl-XL represented downstream of PI3K/Akt pathway in K562 cells. In addition, combination of Tyrphostin AG1024 with Taxol was able to inhibit cell proliferation, and enhance Taxol-induced apoptosis in 24 hours. Therefore, these evidences suggest that Tyrphostin AG1024 could be an enhancer of Taxol-based chemotherapy and provide another ways to fight CML.
Частини книг з теми "BCR-ABL like"
Baccarani, Michele, Fausto Castagnetti, Gabriele Gugliotta, Francesca Palandri, Simona Soverini, and Gianantonio Rosti. "Prognostic factors of chronic myeloid leukaemia." In Oxford Specialist Handbook: Myeloproliferative Neoplasms, 63–78. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0005.
Повний текст джерелаGeyer, Holly L., Deepti Radia, Nicholas Sarlis, and Ruben A. Mesa. "Assessment of disease burden in patients with myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms, 267–85. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0017.
Повний текст джерелаТези доповідей конференцій з теми "BCR-ABL like"
Tostes, Carine Pimenta Maurício Dantas, Kelly Costa De Almeida, Carolina V. A. Lutterbach De Carvalho, Gustavo Manso Fernandes, and Aislan Cristina R. F.Pascoal. "O EFEITO DA HIDROXIUREIA E MESILATO DE IMATINIBE NO TRATAMENTO DA LMC: RELATO DE CASO." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/14.
Повний текст джерелаJesus, Anderson Avelino de, Samuel Santana Moura, Rebeca Santos Da Silva, Raqueline Pastor De Santana E. Santana, and Irlandia Oliveira Almeida. "LEUCEMIA MIELÓIDE CRÔNICA: O CROMOSSOMO PHILADELPHIA E O GENE BCR-ABL." In I Congresso Nacional Multidisciplinar de Oncologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1529.
Повний текст джерелаBosso, Gabriela Jubilato, Letícia Cappellano, Luis Fernando Ventura Vilella, André Viu Matheus, and Ana Paula Pinto Batista. "LEUCEMIA MIELOIDE CRÔNICA EM ADOLESCENTE: RELATO DE CASO." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/28.
Повний текст джерелаSilva, Danielle Cardoso da, Miguel A. Moreira, Raquel C. Maia, and Flavia C. Vasconcelos. "Abstract A58: Bcr-Abl independent activation of Erk1/2 in an imatinib resistant cell line." In Abstracts: AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.tcm17-a58.
Повний текст джерелаLima, Luã De Morais De, and Cássia Bassetto Lorenzoni. "RECOMENDAÇÕES FARMACOLÓGICAS PARA TRATAMENTO DE LEUCEMIA MIELÓIDE CRÔNICA." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/51.
Повний текст джерелаVilella, Luis Fernando Ventura, Gabriela Jubilato Bosso, Leticia Cappellano, Natalia Marques Rodrigues, and André Viu Matheus. "LEUCEMIA MIELOIDE CRÔNICA (LMC) EM ADOLESCENTE DE 13 ANOS: RELATO DE CASO." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/29.
Повний текст джерелаSoverini, Simona, Caterina De Benedittis, Alessandra Gnani, Ilaria Iacobucci, Fausto Castagnetti, Gabriele Gugliotta, Cristina Papayannidis, et al. "Abstract 1884: Resistance to second-line tyrosine kinase inhibitor treatment in imatinib-resistant Philadelphia-positive leukemia patients can be anticipated by ultra-deep sequencing of the BCR-ABL kinase domain using Roche 454 technology." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1884.
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