Roles for deregulated receptor tyrosine kinases and their downstream signaling molecules in hematologic malignancies

Matsumura, Itaru; Mizuki, Masao; Kanakura, Yuzuru

doi:10.1111/j.1349-7006.2007.00717.x

Cited by 38 publications

(38 citation statements)

References 61 publications

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“…Finally, to explain the possible relationship of leptin and NGAL levels with imatinib therapy, we have to bear in mind that imatinib modulates several signal pathways such as Kit, PDGFRs, MEK/MAPK and others [28,29,30,31], while NGAL and leptin regulate these pathways, and their expression could be regulated by the same pathways [32,33,34,35]. …”

Section: Discussionmentioning

confidence: 99%

Imatinib Mesylate Therapy Induces Reduction in Neutrophil Gelatinase-Associated Lipocalin Serum Levels and Increase in Leptin Concentrations in Chronic Myeloid Leukemia Patients in Molecular Remission

Alonci

Allegra²,

Russo³

et al. 2011

Acta Haematol

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The aim of the present study was to determine serum levels of neutrophil gelatinase-associated lipocalin (NGAL) and leptin in patients with chronic myeloid leukemia (CML) at diagnosis and after imatinib therapy when patients achieved a complete molecular remission. The study was conducted on 22 patients with CML in the chronic phase and 10 healthy subjects. The median serum NGAL levels in CML patients at diagnosis were significantly higher compared to age-matched controls. After imatinib therapy, all patients achieved complete molecular remission and NGAL levels decreased and were found significantly lower with respect to the baseline. No significant correlations were found between NGAL levels and other disease parameters. Before imatinib therapy, the median blood leptin levels were not significantly different from those of controls. After therapy with imatinib, all patients in molecular remission presented an increase in leptin levels. Future research is eagerly awaited as it may demonstrate the real role of NGAL and leptin in the onset and progression of CML.

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Section: Discussionmentioning

confidence: 99%

Imatinib Mesylate Therapy Induces Reduction in Neutrophil Gelatinase-Associated Lipocalin Serum Levels and Increase in Leptin Concentrations in Chronic Myeloid Leukemia Patients in Molecular Remission

Alonci

Allegra²,

Russo³

et al. 2011

Acta Haematol

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“…There are two PDGF-receptor subunits (PDGFRA,PDGFRB) can associate as three dimer forms (alpha/alpha,alpha/beta,beta/beta) with variable binding specificity for the PDGF ligand dimers. Oncogenic receptor tyrosine kinase (RTKs) or also oncogenic receptor PDGFRA and PDGFRB mutants and/or fusions have been detected in many malignancies (for instances glioma, GIST and chronic eosinophilic leukemia) and their target therapy [2][3][4][5][6].…”

Section: Discussionmentioning

confidence: 99%

Use of traditional medicine in severe edema amelioration of refractory congestive heart failure - case report

Zhu¹

2018

Blood Heart Circ

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The main treatment to congestive heart failure is common source of western medicine. Here, a refractory heart failure was treated following traditional medicine with potential therapeutic benefits, suggesting its role of traditional medicine in heart disease especially in another myocardial infarction (for instance Suxiao Jiuxin pill, compound Danshen dripping pill DSP). In discussion, controlled delivery of injectable nanofibers with PDGFs and bFGF preserve myocardial function, which currently the care.

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“…This mutation enables the active configuration of c-kit, responsible for the aberrant constitutive activation of RTK, associated with malignant transformation in human mast cell leukemia [20]. Constitutive activation of PI3K was found in more than 50% of AML cases, and the activation of Akt was significantly higher in spontaneously proliferating AML cells [17].…”

Section: Introductionmentioning

confidence: 99%

Translational research in complex etiopathogenesis and therapy of hematological malignancies: the specific role of tyrosine kinases signaling and inhibition

Stankov

Popovic

2008

Med Oncol

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During the recent genomics and proteomics era, high-resolution, genome-wide approaches have revealed numerous promising new drug targets and disease biomarkers, accelerating and emphasizing the need for targeted molecular therapy compounds. Significant progress has been made in understanding the pathogenesis of hematological malignancies there by, revealing new drug targets. Introduction of multiple new technologies in cancer research have significantly improved the drug discovery process, leading to key success in targeted cancer therapeutics, including tyrosine kinase inhibitors. The studies of receptor tyrosine kinases and their role in malignant transformation are already translated from the preclinical level (cell-based and animal models) to clinical studies, enabling the more complete understanding of tumor cell biology and improvement of tumor therapy.

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Roles for deregulated receptor tyrosine kinases and their downstream signaling molecules in hematologic malignancies

Cited by 38 publications

References 61 publications

Imatinib Mesylate Therapy Induces Reduction in Neutrophil Gelatinase-Associated Lipocalin Serum Levels and Increase in Leptin Concentrations in Chronic Myeloid Leukemia Patients in Molecular Remission

Imatinib Mesylate Therapy Induces Reduction in Neutrophil Gelatinase-Associated Lipocalin Serum Levels and Increase in Leptin Concentrations in Chronic Myeloid Leukemia Patients in Molecular Remission

Use of traditional medicine in severe edema amelioration of refractory congestive heart failure - case report

Translational research in complex etiopathogenesis and therapy of hematological malignancies: the specific role of tyrosine kinases signaling and inhibition

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