Study of correlation between imatinib mesylate plasma levels and hematological profile of patients undergoing treatment for chronic myeloid leukemia

Conclusion: There was no correlation between the number of leukocytes, platelets and hemoglobin and the serum level of IM, although there is a trend with respect to hemoglobin (p = 0.062).RESUMO Introdu ção: Leucemia mieloide crônica (LMC) é uma desordem genética de células-tronco hematopoiéticas, resultando em uma expansão mieloproliferativa das células sanguíneas. A LMC está associada à presença do cromossomo Philadelphia (Ph), o que gera um oncogene (BCR-ABL). Atualmente, o tratamen to de primeira escolha é o mesilato de imatinibe (MI). Objetivo: Correlacionar os níveis séricos de MI com parâmetros hematológicos em pacientes com LMC. Método: Estudo transversal retrospectivo em pacientes com LMC em tratamento. O nível sérico de MI foi determinado por um sistema de crom atografia líquida de alta eficiência com detector de arranjo de diodos (CLAE-DAD), e a análise estatística foi realizada no programa SPSS versão 20.0. Resultados: Foram estudados 55 pacientes - 24 homens (43,6%) e 31 mulheres (56,4%) - com média de idade de 54 anos, portadores de LMC que util izavam MI. Destes, 45 encontravam-se em fase crônica (81,6%); sete, em fase acelerada (13,1%) e três, em crise blástica (5,2%). Os pacientes em questão receberam uma média de dose do MI de 434 mg/dia. O n&...
Source: Jornal Brasileiro de Patologia e Medicina Laboratorial - Category: Pathology Source Type: research

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Conclusions The discovery of JAK2V617F mutation in BCR-ABL1-negative MPNs by four different international cooperative groups in 2005 (2–5) led to significant insights on the pathogenesis of these disorders. In fact, this mutation results in a gain-of-function with activation of cytokine and growth factor receptors, and thus of the downstream JAK-STAT pathway (79, 95–98). The JAK2 point mutation in exon 12, present in a small percentage of patients with PV, is able to induce the MPN phenotype through the same pathogenic mechanism (6, 7). In 2006 the MPLW515L/K was reported in ET and PMF patients (44, 45) and d...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research
Authors: Aladağ E, Haznedaroğlu İC Abstract With an annual incidence of 1-2 in a million, Ph*(+) chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disease that makes myeloid neoplastic cells breed out of control. This BCR-ABL(+) myeloproliferative disease makes up about 15%-20% of all leukemia cases in adults. CML is seen more in males than females, with a rate of three to two. However, it does not show differences in prevalence in terms of age. CML consists of three clinical phases. The first one is the chronic phase, defined by rising white blood cell levels and also by myeloid proliferation a...
Source: Turkish Journal of Medical Sciences - Category: General Medicine Tags: Turk J Med Sci Source Type: research
Conditions:   Acute Bilineal Leukemia;   Minimal Residual Disease;   Myelodysplastic/Myeloproliferative Neoplasm;   Myelodysplastic/Myeloproliferative Neoplasm, Unclassifiable;   Myeloproliferative Neoplasm;   Recurrent Acute Biphenotypic Leukemia;   Recurrent Acute Lymphoblastic Leukemia;   Recurrent Acute Myeloid Leukemia;   Recurrent Blastic Plasmacytoid Dendritic Cell Neoplasm;   Recurrent Chronic Lymphocytic Leukemia;   Recurrent Chronic Myelogenous Leukemia, BCR-ABL1 Positiv...
Source: ClinicalTrials.gov - Category: Research Source Type: clinical trials
ConclusionOur first-in-human clinical trial demonstrates promising efficacy of cCAR therapy in treating patients with relapsed/ refractory AML. cCAR is able to eradicate leukemia blasts and leukemia stem cells, exerting a profound tumor killing effect that is superior to single target CAR T cell therapies. cCAR is also shown to induce total myeloid ablation in bone marrow, suggesting that it may act as a safer alternative to avoid the severe toxicities caused by standard bone marrow ablation regimens without sacrificing the anti-tumor efficacy. This strategy will likely benefit patients who are unable to tolerate total bod...
Source: Blood - Category: Hematology Authors: Tags: 616. Acute Myeloid Leukemia: Novel Therapy, excluding Transplantation: Immunotherapy Source Type: research
Post-transplant lymphoproliferative disorder (PTLD) following hematopoietic stem cell transplantation (HSCT) is a rare, but life-threatening complication. PTLD typically develops within 6-12 months of HSCT, which is before the reconstitution of EBV-specific cytotoxic T-cell immunity. Several risk factors for developing PTLD have been reported in the literature, including the use of antithymocyte globulin (ATG) and ex vivo T-cell depletion (TCD). However, only a few large-scale retrospective studies have been conducted and risk scores have not yet been well defined. Therefore, to further evaluate the probability of and risk...
Source: Blood - Category: Hematology Authors: Tags: 723. Clinical Allogeneic and Autologous Transplantation: Late Complications and Approaches to Disease Recurrence: HSCT Late Effects and Disease Monitoring Source Type: research
Chromosomal rearrangements resulting in generation of novel fusion oncogenes are common in hematologic malignancies. These disease drivers are key therapeutic targets and form the basis of animal model development for preclinical studies. For example, retroviral introduction of the chronic myeloid leukemia (CML) fusion BCR-ABL to hematopoietic stem cells (HSCs) results in a myeloproliferative disease similar to accelerated-phase human CML when transplanted to recipient mice. This model and many others are established traditionally through retroviral or germline introduction of human fusion oncogenes to the murine genome. R...
Source: Blood - Category: Hematology Authors: Tags: 622. Lymphoma Biology-Non-Genetic Studies: Other Lymphoma Types Source Type: research
Conclusion.We show that both mouse and human MPNs have higher Dusp1 expression irrespective of MPN drivers (JAK2, MPL, and CALR). Jak2V617F is uniquely addicted to the Dusp1 expression, where genetic deletion of Dusp1 is lethal to Jak2V617F expressing cells, but not to the other MPN drivers, such as, MPLW515L. Thus, providing a rationale for targeting the Dusp1 in Jak2 mutated MPNs to eliminate the mutant clones and cure the disease.DisclosuresNo relevant conflicts of interest to declare.
Source: Blood - Category: Hematology Authors: Tags: 635. Myeloproliferative Syndromes: Basic Science: Identification of Novel Therapeutic Targets Source Type: research
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