Signal transduction therapy of colon tumors with multiple target kinase inhibitors

Tyrosine kinases play key roles in cell proliferation, survival and differentiation. Their aberrant activation, caused either by the formation of fusion genes by chromosome translocation or by intragenic changes, such as point mutations or internal duplications, is of major importance in the development of many haematological malignancies. An understanding of the mechanisms by which BCR-ABL contributes to the pathogenesis of chronic myeloid leukaemia led to the development of imatinib, the first of several tyrosine kinase inhibitors to enter clinical trials. Although the development of resistance has been problematic, particularly in aggressive disease, the development of novel inhibitors and combination with other forms of therapy shows promise.

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Kinase Inhibitors in Signal Transduction Therapy

Protein Kinases as Drug Targets - Methods and Principles in Medicinal Chemistry ◽

10.1002/9783527633470.ch5 ◽

2011 ◽

pp. 115-144

Author(s):

György Kéri ◽

László Őrfi ◽

Gábor Németh

Keyword(s):

Signal Transduction ◽

Kinase Inhibitors ◽

Signal Transduction Therapy

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Rap/B-Raf signal transduction is activated in neuroendocrine tumors of the digestive tract and may be effectively inhibited by Raf-kinase inhibitors

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/s-2005-862850 ◽

2005 ◽

Vol 113 (S 1) ◽

Author(s):

D Karhoff ◽

J Schrader ◽

R Göke ◽

R Arnold

Keyword(s):

Signal Transduction ◽

Digestive Tract ◽

Neuroendocrine Tumors ◽

Kinase Inhibitors ◽

Raf Kinase

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Withdrawn: Automated Diagnosis of Glaucoma Using Deep Neural Network Classifier

Current Signal Transduction Therapy ◽

10.2174/1574362414666190906112910 ◽

2019 ◽

Vol 14 ◽

Author(s):

M. Madhumalini ◽

T. Meera Devi

Keyword(s):

Neural Network ◽

Signal Transduction ◽

Deep Neural Network ◽

Neural Network Classifier ◽

Current Signal ◽

Automated Diagnosis ◽

Signal Transduction Therapy ◽

Copyright Permission ◽

Legal Right

The article has been withdrawn on the request of the authors and the editor of the journal Current Signal Transduction Therapy. Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused. BENTHAM SCIENCE DISCLAIMER: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers, if and when the article is accepted for publication.

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Leukocyte response integrin and integrin-associated protein act as a signal transduction unit in generation of a phagocyte respiratory burst.

Journal of Experimental Medicine ◽

10.1084/jem.178.4.1165 ◽

1993 ◽

Vol 178 (4) ◽

pp. 1165-1174 ◽

Cited By ~ 81

Author(s):

M Zhou ◽

E J Brown

Keyword(s):

Signal Transduction ◽

Membrane Protein ◽

Respiratory Burst ◽

Kinase Inhibitors ◽

Solid Phase ◽

Enhanced Sensitivity ◽

Basement Membrane Protein ◽

Coated Surfaces ◽

Leukocyte Response ◽

Distinct Membrane

The leukocyte response integrin (LRI) is a phagocyte integrin which recognizes the basement membrane protein entactin and the synthetic peptide Lys-Gly-Ala-Gly-Asp-Val (KGAGDV). The function of LRI is intimately associated with that of a distinct membrane protein, integrin-associated protein (IAP), as antibodies which recognizes IAP can inhibit all known functions of LRI. When adherent to surface, the LRI ligands entactin and KGAGDV activate the respiratory burst in polymorphonuclear leukocytes (PMN) and monocytes, as do monoclonal antibodies (mAb) directed at either LRI or IAP. When added in solution, peptides and antibodies specific for LRI, and some, but not all, anti-IAP antibodies, can inhibit the respiratory burst activated by any of these surface-adherent ligands. Only monoclonal anti-IAP antibodies which can inhibit LRI function when added in solution are competent to activate the respiratory burst when adherent to a surface. KGAGDV peptide and anti-LRI added in solution can inhibit anti-IAP-stimulated respiratory burst. The LRI-IAP-initiated respiratory burst is independent of CD18, as judged by: (a) blockade of inhibition by anti-CD18 mAb with the protein kinase A inhibitor HA1004; (b) enhanced sensitivity of CD18-dependent respiratory burst compared with LRI/IAP-dependent respiratory burst to the tyrosine kinase inhibitors genestein and herbimicin; and (c) generation of a respiratory burst in response to KGAGDV, anti-LRI, and anti-IAP coated surfaces in PMN from a patient with LAD. Despite its apparent CD18 independence, LRI/IAP-initiated respiratory burst requires a solid phase ligand and is sensitive to cytochalasin B. These data suggest a model in which LRI and IAP act together as a single signal transduction unit to activate the phagocyte respiratory burst, in a manner that requires CD18-independent cell adhesion.

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Signal Transduction Therapy of Diabetic Vascular Complication

Current Signal Transduction Therapy ◽

10.2174/157436207779317100 ◽

2007 ◽

Vol 2 (1) ◽

pp. 91-100

Author(s):

Sho-ichi Yamagishi ◽

Kazuo Nakamura ◽

Takanori Matsui ◽

Yumiko Yoshida ◽

Katsuhiko Takenaka ◽

...

Keyword(s):

Signal Transduction ◽

Vascular Complication ◽

Diabetic Vascular Complication ◽

Signal Transduction Therapy

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ROLE OF SERIN/ THREONINE KINASE INHIBITOR IN THERAPY NON-ALCOHOLIC STEATOHEPATITIS AND ALCOHOLIC HEPATITIS

Jurnal Kedokteran dan Kesehatan Publikasi Ilmiah Fakultas Kedokteran Universitas Sriwijaya ◽

10.32539/jkk.v6i3.7744 ◽

2019 ◽

Vol 6 (3) ◽

pp. 101-109

Author(s):

Novriantika Lestari

Keyword(s):

Signal Transduction ◽

Liver Fibrosis ◽

Kinase Inhibitors ◽

Kinase Inhibitor ◽

Binding Activity ◽

Serine Threonine Kinase ◽

Threonine Kinase ◽

Receptor Binding Activity ◽

Marked Accumulation

Liver fibrosis is a reversible response to a wound healing with marked accumulation of extracellular matrix which caused by injury to the liver. Liver fibrosis can be caused by various factors including alcohol and non-alcohol steatohepatitis. The process of fibrosis serves to localize the inflammation during chronic exposure. The hepatic stem cell (HSC) has a key role in the pathogenesis of liver fibrosis. The HSC activation is characterized by increased profibrogenic mediators including members of the TGF-? superfamily. In order to enable signal transduction, the mediator needs to bind to its receptors. The serine/ threonine kinase receptor is a receptor that binds to the TGF-? superfamily ligand, including TGF-?, BMP, activin and other mediators. The ligand receptor-binding activity will stimulate signal transduction that will translocate into the nucleus and phosphorylate various transcription factors that play a role in cell proliferation, differentiation, or apoptosis. There is currently no standard therapy for liver fibrosis. Based on the central role of the serine/ threonine kinase receptor in the pathogenesis of liver fibrosis, it is thought that the use of serine/ threonine kinase inhibitors is a promising therapy.

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