scholarly journals Molecular Therapeutic Targets for Glioma Angiogenesis

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Shingo Takano ◽  
Toshiharu Yamashita ◽  
Osamu Ohneda
Keyword(s):  
Endothelial Cells ◽  
Antiangiogenic Therapy ◽  
Malignant Gliomas ◽  
Therapeutic Targets ◽  
Molecular Targets ◽  
Endogenous Inhibitors ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets ◽  
The Brain ◽  
Induced Proteins

Due to the prominent angiogenesis that occurs in malignant glioma, antiangiogenic therapy has been attempted. There have been several molecular targets that are specific to malignant gliomas, as well as more broadly in systemic cancers. In this review, I will focus on some topics related to molecular therapeutic targets for glioma angiogenesis. First, important angiogenic factors that could be considered molecular targets are VEGF, VEGF-induced proteins on endothelial cells, tissue factor, osteopontin, integrin, and thymidine phosphorylase as well as endogenous inhibitors, soluble Flt1, and thrombospondin 1. Second, hypoxic areas are also decreased by metronomic CPT11 treatment as well as temozolomide. Third, glioma-derived endothelial cells that are genetically and functionally distinct from normal endothelial cells should be targeted, for example, with SDF-1 and CXCR7 chemokine. Fourth, endothelial progenitor cells (EPCs) likely contribute towards glioma angiogenesis in the brain and could be useful as a drug delivery tool. Finally, blockade of delta-like 4 (Dll4) results in a nonfunctioning vasculature and could be another important target distinct from VEGF.

Molecular Therapeutic Targets in Tobacco-Induced Lung Pathology

2019 ◽  
pp. 477-491
Author(s):  
Pramod K. Avti ◽  
Krishan L. Khanduja
Keyword(s):  
Therapeutic Targets ◽  
Lung Pathology ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets

FTO Gene Affects Obesity and Breast Cancer Through Similar Mechanisms: A New Insight into the Molecular Therapeutic Targets

2017 ◽  
Vol 70 (1) ◽  
pp. 30-36 ◽  
Author(s):  
M. E. Akbari ◽  
M. Gholamalizadeh ◽  
S. Doaei ◽  
F. Mirsafa
Keyword(s):  
Breast Cancer ◽  
Therapeutic Targets ◽  
Fto Gene ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets ◽  
Insight Into

scholarly journals Rac Guanosine Triphosphatases Represent Integrating Molecular Therapeutic Targets for BCR-ABL-Induced Myeloproliferative Disease

Cancer Cell ◽  
2007 ◽  
Vol 12 (5) ◽  
pp. 467-478 ◽  
Author(s):  
Emily K. Thomas ◽  
Jose A. Cancelas ◽  
Hee-Don Chae ◽  
Adrienne D. Cox ◽  
Patricia J. Keller ◽  
...  
Keyword(s):  
Therapeutic Targets ◽  
Myeloproliferative Disease ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets

scholarly journals Molecular genetics of medullary thyroid carcinoma: the quest for novel therapeutic targets

2009 ◽  
Vol 43 (4) ◽  
pp. 143-155 ◽  
Author(s):  
Aniello Cerrato ◽  
Valentina De Falco ◽  
Massimo Santoro
Keyword(s):  
Thyroid Carcinoma ◽  
Medullary Thyroid Carcinoma ◽  
Therapeutic Targets ◽  
C Cells ◽  
Rare Tumour ◽  
Medullary Thyroid ◽  
Early Evidence ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets ◽  
Novel Therapeutic

Medullary thyroid carcinoma (MTC) is a rare tumour arising from neural crest-derived parafollicular C-cells. Metastatic MTC patients are incurable because the cancer does not respond to radiotherapy or chemotherapy. The REarranged during Transfection (RET) proto-oncogene plays a key role in the development of MTC. However, one-half of the sporadic MTC do not carry RET mutations. Mice models and early evidence obtained in human samples suggest that other genes, including those encoding components of the RB1 (retinoblastoma) and TP53 tumour-suppressor pathways, may be involved in MTC formation. Here, we review the data on the involvement of genes acting in the RET and RB1/TP53 pathways in MTC. Understanding genetic lesions that occur in MTC is a prerequisite to identifying molecular therapeutic targets in MTC and in improving the efficacy of RET-targeted therapies.

Tissue fibrosis and carcinogenesis: Divergent or successive pathways dictate multiple molecular therapeutic targets for oligo decoy therapies

2006 ◽  
Vol 97 (6) ◽  
pp. 1161-1174 ◽  
Author(s):  
Kenneth R. Cutroneo ◽  
Sheryl L. White ◽  
Jen-Fu Chiu ◽  
H. Paul Ehrlich
Keyword(s):  
Therapeutic Targets ◽  
Tissue Fibrosis ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets

scholarly journals Emerging molecular therapeutic targets for cholangiocarcinoma

2017 ◽  
Vol 67 (3) ◽  
pp. 632-644 ◽  
Author(s):  
Sumera Rizvi ◽  
Gregory J. Gores
Keyword(s):  
Therapeutic Targets ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets

scholarly journals Cytochrome P450 eicosanoids and cerebral vascular function

2011 ◽  
Vol 13 ◽  
Author(s):  
John D. Imig ◽  
Alexis N. Simpkins ◽  
Marija Renic ◽  
David R. Harder
Keyword(s):  
Blood Flow ◽  
Cytochrome P450 ◽  
Vascular Function ◽  
Therapeutic Targets ◽  
Vascular Diseases ◽  
Cell Types ◽  
Cellular Mechanisms ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets ◽  
Cerebral Vascular

The eicosanoids 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs), which are generated from the metabolism of arachidonic acid by cytochrome P450 (CYP) enzymes, possess a wide array of biological actions, including the regulation of blood flow to organs. 20-HETE and EETs are generated in various cell types in the brain and cerebral blood vessels, and contribute significantly to cerebral blood flow autoregulation and the coupling of regional brain blood flow to neuronal activity (neurovascular coupling). Investigations are beginning to unravel the molecular and cellular mechanisms by which these CYP eicosanoids regulate cerebral vascular function and the changes that occur in pathological states. Intriguingly, 20-HETE and the soluble epoxide hydrolase (sEH) enzyme that regulates EET levels have been explored as molecular therapeutic targets for cerebral vascular diseases. Inhibition of 20-HETE, or increasing EET levels by inhibiting the sEH enzyme, decreases cerebral damage following stroke. The improved outcome following cerebral ischaemia is a consequence of improving cerebral vascular structure or function and protecting neurons from cell death. Thus, the CYP eicosanoids are key regulators of cerebral vascular function and novel therapeutic targets for cardiovascular diseases and neurological disorders.

DUAL SPECIFICITY PROTEIN PHOSPHATASES: Therapeutic Targets for Cancer and Alzheimer's Disease

2005 ◽  
Vol 45 (1) ◽  
pp. 725-750 ◽  
Author(s):  
Alexander P. Ducruet ◽  
Andreas Vogt ◽  
Peter Wipf ◽  
John S. Lazo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Drug Discovery ◽  
Therapeutic Targets ◽  
Dual Specificity ◽  
Complete Sequencing ◽  
Dual Specificity Phosphatases ◽  
Molecular Therapeutic ◽  
Specificity Protein ◽  
Molecular Therapeutic Targets

The complete sequencing of the human genome is generating many novel targets for drug discovery. Understanding the pathophysiological roles of these putative targets and assessing their suitability for therapeutic intervention has become the major hurdle for drug discovery efforts. The dual-specificity phosphatases (DSPases), which dephosphorylate serine, threonine, and tyrosine residues in the same protein substrate, have important roles in multiple signaling pathways and appear to be deregulated in cancer and Alzheimer's disease. We examine the potential of DSPases as new molecular therapeutic targets for the treatment of human disease.

Molecular therapeutic targets for bladder cancer

2007 ◽  
Vol 7 (12) ◽  
pp. 1691-1693
Author(s):  
Evangelos Zacharakis ◽  
Mahmoud Monem ◽  
Jean V Joseph ◽  
Hiten RH Patel
Keyword(s):  
Bladder Cancer ◽  
Therapeutic Targets ◽  
Molecular Therapeutic ◽  
Molecular Therapeutic Targets
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