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white/tyrosine

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Chronic Myloid Leukemic Patients Treated With Tyrosine Kinase Inhibitor

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Chronic myelogenous leukemia (CML) is a myeloproliferative disorder in which leukemic cells display the Philadelphia chromosome generated from a reciprocal t(9:22) (q34:q11) translocation.1 The chromosome 9 and chromosome 22 transposal of t (9:22) and (q34:q11) causes the cancer gene C-ABL at 9q34

Tyrosine Kinase Inhibition to Treat Myeloid Hypereosinophilic Syndrome

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This study will evaluate the safety and effectiveness of imatinib mesylate in reducing the number of eosinophils (a type of white blood cell) in patients with hypereosinophilic syndrome (HES). Patients with HES have elevated counts of eosinophils in the blood and body tissues, which can cause damage

Epidemiology: Oxidative Stress and Early Atherosclerosis

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BACKGROUND: Low blood antioxidant concentrations are associated with several major degenerative diseases including cardiovascular disease and cancer. Animal, cellular and chemical experiments have elucidated biologic mechanisms consistent with antioxidant protection against several disease
PRIMARY OBJECTIVES: I. To determine the maximum tolerated dose of clofarabine in combination with 2, 3, or 4 Gy TBI in preparation for hematopoietic cell transplantation (HCT) from human leukocyte antigen (HLA)-identical related and HLA-matched unrelated donors in patients with AML. (Part 1) II. To

Efficacy and Safety Study of Dasatinib in Patients With Chronic Myeloid Leukemia

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Primary Objective: 1. To assess the efficacy of Dasatinib therapy in chronic and accelerated phase BCR-ABL (+) (Ph + and Ph -) CML patients that undergo molecular, cytogenetic or haematological relapse following SCT. Secondary Objective(s): 1. To assess the impact of Dasatinib therapy on patient
PRIMARY OBJECTIVES: I. Determine if monoclonal antibody Ch14.18 (dinutuximab) + cytokines + isotretinoin (13-cis-retinoic acid, or RA) improves event free survival after myeloablative therapy and stem cell rescue as compared to RA alone, in high risk neuroblastoma patients who have achieved a

Explore the Synergy of Combination TKI Therapy

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If the subjects qualify to take part in this research study, they will undergo the following procedures. Subjects will be asked to abstain from alcoholic beverages (24 hours), grapefruit products, herbal supplements/teas, and over-the-counter medications (48 hours) prior to the study visits. There

KISS Study: Kinase Inhibition With Sprycel Start up

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The KISS Study is a Phase II, multicentre, open-label, prospective non-randomised study of treatment modification in response to maintenance of MR3.0 at 12 months. Patients must be newly diagnosed with chronic phase CML (CML-CP) (<3 months) and previously untreated with the exception of
Phenylketonuria (PKU, OMIM 261600), an autosomal recessive disorder, affects approximately 1:11,000 individuals in the United States. In PKU, mutations in the gene responsible for the liver enzyme phenylalanine hydroxylase (PAH) result in reduced or absent conversion of phenylalanine (Phe) to
OUTLINE: This is a multi-center study. Phase I: Patients will be accrued in the classic 3 patients per dose per cohort design, 21-day cycle - Dose Level 1 Everolimus 10 mg BNC105P 4.2 mg/m2 - Dose Level 2 Everolimus 10 mg BNC105P 8.4 mg/m2 - Dose Level 3 Everolimus 10 mg BNC105P 12.6 mg/m2 - Dose
Phenylketonuria (PKU) is an autosomal recessive disorder resulting from a deficiency of phenylalanine hydroxylase, which converts phenylalanine to tyrosine. Phenylalanine hydroxylase is one of the three aromatic amino acid hydroxylases that utilizes tetrahydrobiopterin (BH4) as cofactor. The

AZD2171 to Treat Prostate Cancer

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Background: - AZD2171 (Cediranib) is an oral potent inhibitor of receptor tyrosine kinases which impact vascular endothelial growth factor-A (VEGF). - VEGF appears important in blood vessel formation and disease progression in prostate cancer. - No known effective therapy in patients with

Use of SV40 Vectors to Treat Chronic Myeloid Leukemia (CML)

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A novel methodology that facilitates specific silencing of genes has recently been developed. The method is based on the property of small molecules of nucleic acids (RNA) to specifically repress expression of targeted genes. These small interfering RNA (siRNA) molecules were recently demonstrated
All of the included patients underwent: (1) A complete clinical evaluation; (2) Laboratory investigations: CBC, liver profile, viral markers (HBs Ag, HB core Ab, HCV Ab) using the ELISA technique; (3) Thrombophilia workup to clarify the underlying etiology of vascular liver disease. It was done only
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