ReviewCancer science2008
Roles for deregulated receptor tyrosine kinases and their downstream signaling molecules in hematologic malignancies.
Review in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- The role of PIK3CA gene mutations in colorectal cancer and the selection of treatment strategies.Frontiers in pharmacology · 2024Review
- Novel biomolecules in targeted cancer therapy: a new approach towards precision medicine.Medical oncology (Northwood, London, England) · 2023Review
- Article
- Emerging findings into molecular mechanism of brain metastasis.Cancer medicine · 2018Review
- Article
- Effects of inhibitors of vascular endothelial growth factor receptor 2 and downstream pathways of receptor tyrosine kinases involving phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin or mitogen-activated protein kinase in canine hemangiosarcoma cell lines.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2016Article
- Immunohistochemical detection of a potential molecular therapeutic target for canine hemangiosarcoma.The Journal of veterinary medical science · 2016Article
- Class III Receptor Tyrosine Kinases in Acute Leukemia - Biological Functions and Modern Laboratory Analysis.Biomarker insights · 2015Review
- Modular nanotransporters for targeted intracellular delivery of drugs: folate receptors as potential targets.Current pharmaceutical design · 2015Review
- Functional characterization of a novel FGFR1OP-RET rearrangement in hematopoietic malignancies.Molecular oncology · 2014Article
- Article
- Tandutinib inhibits the Akt/mTOR signaling pathway to inhibit colon cancer growth.Molecular cancer therapeutics · 2013Article
- Analysis of activated platelet-derived growth factor β receptor and Ras-MAP kinase pathway in equine sarcoid fibroblasts.BioMed research international · 2013Article
- Leptin modification in chronic myeloid leukemia patients treated with imatinib: An emerging effect of targeted therapy.Leukemia research reports · 2013Article
- Constitutive phosphorylation of the mTORC2/Akt/4E-BP1 pathway in newly derived canine hemangiosarcoma cell lines.BMC veterinary research · 2012Article
- [Research progress in non-small cell lung cancer with concomitant EML4-ALK fusion gene and EGFR gene mutation].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2011Review
- Distinct involvement of the Gab1 and Grb2 adaptor proteins in signal transduction by the related receptor tyrosine kinases RON and MET.The Journal of biological chemistry · 2011Article
- Involvement of Grb2 adaptor protein in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated signaling and anaplastic large cell lymphoma growth.The Journal of biological chemistry · 2010Article
- Translational research in complex etiopathogenesis and therapy of hematological malignancies: the specific role of tyrosine kinases signaling and inhibition.Medical oncology (Northwood, London, England) · 2009Article
- Novel benzylidene-thiazolidine-2,4-diones inhibit Pim protein kinase activity and induce cell cycle arrest in leukemia and prostate cancer cells.Molecular cancer therapeutics · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth, survival and differentiation of hematopoietic cells are regulated by the interactions between hematopoietic growth factors and their receptors. The defect in these interactions results in a failure of hematopoiesis, while aberrantly elevated and/or sustained activation of these signals cause hematologic malignancies. Among them, constitutively activating mutations of the receptor tyrosine kinases (RTKs), such as c-Kit, platelet-derived growth factor receptor (PDGFR) and FLT3, are often involved in the pathogenesis of various types of hematologic malignancies. Constitutive activation of RTKs is provoked by several mechanisms including chromosomal translocations and various mutations involving their regulatory regions. Chromosomal translocations commonly generate chimeric proteins consisting of the cytoplasmic domain of RTKs and the dimerization or multimerization motif of the fusion partner, resulting in the constitutive dimerization of RTKs. On the other hand, missense, insertion or deletion mutations in the regulatory regions, such as juxtamembrane domain, activation loop, and extracellular domain, also cause constitutive activation of RTKs mainly by preventing the auto-inhibitory regulation. Oncogenic RTKs activate downstream signaling molecules such as Ras/MAPK, PI3-K/Akt/mTOR, and STATs as well as ligand-activated wild type RTKs. However, their signals are quantitatively and qualitatively different from wild type RTKs. Based on these findings, several agents that target oncogenic RTKs or their downstream molecules have been developed: imatinib and FLT3 inhibitors for RTKs themselves, farnesyltransferase inhibitors, mTOR inhibitors and MEK inhibitors for the downstream signaling molecules. As promising results have been obtained in several clinical trials using these agents, the establishment of these molecular targeted agents is expected.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.