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

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.

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

scholarly journals Weighted Gene Co-expression Network Analysis Reveals ALDH1B1 As a Prognositc Biomarker Involved in Gastric Cancer Development

2021 ◽  
Author(s):  
Yi Li ◽  
Ke Pu ◽  
Yuping Wang ◽  
Yongning Zhou
Keyword(s):  
Gastric Cancer ◽  
Network Analysis ◽  
Drug Treatment ◽  
Therapeutic Targets ◽  
Cancer Drug ◽  
Hub Genes ◽  
Hub Gene ◽  
Molecular Therapeutic ◽  
Cancer Drug Treatment ◽  
Molecular Therapeutic Targets

Abstract BackgroundGastric cancer (GC) is one of the leading cancers associated with high mortality and poor prognosis mainly due to its relatively late diagnosis and the limited therapeutic options. Consequently, screening for prognostic GC biomarkers and novel molecular therapeutic targets is necessary to promote patient outcomes. Methods Weighted gene co-expression network analysis (WGCNA), a systems biology approach, was applied to analyze the mRNA sequencing data and clinical information of GC patients obtained from The Cancer Genome Atlas (TCGA). Gene modules and clinical traits were constructed according to the Pearson correlation analysis, and the gene ontology (GO) and functional enrichment analysis of meaningful modules were carried out. Hub genes from meaningful modules were screened out by two approaches: the intra-modular and protein-protein interaction (PPI) analysis methods. Next, through upstream regulatory analysis, hub genes with high connectivity degree were further validated with differential expression analysis, Kaplan-Meier survival analysis, and the Cox regression model. ResultsWe found that seven modules were associated with the following clinical traits: anatomical location of gastric adenocarcinoma, histological type, histological grade, and pathological stage. The hub gene ALDH1B1 was found to have potential as a biomarker for gastric cancer cells, the relationship between this hub gene and gastric cancer drug treatment is also worthy of attention.Conclusion These findings may contribute to understanding the GC tumourigenic mechanisms, as well as provide new potential prognostic factors and molecular therapeutic targets for GC. The ALDH1B1 hub gene also provides a new vantage point for further clinical experiments and large-scale cohort studies to validate its association with GC patient survival, and provide a new direction for the research of gastric cancer drug treatment.

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