Novel Cancer Therapies by Molecular Targeting Distinct Growth Factor Pathways and Drug Resistance-Associated Molecules in Cancer- and Metastasis-Initiating Cells

2016 ◽  
pp. 213-240
Keyword(s):  
Drug Resistance ◽  
Growth Factor ◽  
Molecular Targeting ◽  
Cancer Therapies ◽  
Growth Factor Pathways

Genetic and Epigenetic Modulation of Drug Resistance in Cancer: Challenges and Opportunities

2020 ◽  
Vol 20 (14) ◽  
pp. 1114-1131 ◽  
Author(s):  
Kanisha Shah ◽  
Rakesh M. Rawal
Keyword(s):  
Drug Resistance ◽  
Drug Targets ◽  
Complex Disease ◽  
Cancer Therapies ◽  
Altered Expression ◽  
Acquired Drug Resistance ◽  
Challenges And Opportunities ◽  
Chemotherapeutic Treatment ◽  
Epigenetic Modulation ◽  
Targeted Drug Therapies

Cancer is a complex disease that has the ability to develop resistance to traditional therapies. The current chemotherapeutic treatment has become increasingly sophisticated, yet it is not 100% effective against disseminated tumours. Anticancer drugs resistance is an intricate process that ascends from modifications in the drug targets suggesting the need for better targeted therapies in the therapeutic arsenal. Advances in the modern techniques such as DNA microarray, proteomics along with the development of newer targeted drug therapies might provide better strategies to overcome drug resistance. This drug resistance in tumours can be attributed to an individual’s genetic differences, especially in tumoral somatic cells but acquired drug resistance is due to different mechanisms, such as cell death inhibition (apoptosis suppression) altered expression of drug transporters, alteration in drug metabolism epigenetic and drug targets, enhancing DNA repair and gene amplification. This review also focusses on the epigenetic modifications and microRNAs, which induce drug resistance and contributes to the formation of tumour progenitor cells that are not destroyed by conventional cancer therapies. Lastly, this review highlights different means to prevent the formation of drug resistant tumours and provides future directions for better treatment of these resistant tumours.

Dynamic Expression of TRPV3 and Integrated Signaling with Growth Factor Pathways During Lung Epithelial Wound Repair Following Wood Smoke Particle and Other Forms of Lung Cell Injury

2021 ◽  
pp. MOLPHARM-AR-2021-000280
Author(s):  
Katherine L. Burrell ◽  
Nam D. Nguyen ◽  
Cassandra E. Deering-Rice ◽  
Tosifa A. Memon ◽  
Marysol Almestica-Roberts ◽  
...  
Keyword(s):  
Growth Factor ◽  
Wound Repair ◽  
Cell Injury ◽  
Wood Smoke ◽  
Smoke Particle ◽  
Dynamic Expression ◽  
Lung Epithelial ◽  
Growth Factor Pathways

scholarly journals Patient-derived models of acquired resistance can identify effective drug combinations for cancer

Science ◽  
2014 ◽  
Vol 346 (6216) ◽  
pp. 1480-1486 ◽  
Author(s):  
Adam S. Crystal ◽  
Alice T. Shaw ◽  
Lecia V. Sequist ◽  
Luc Friboulet ◽  
Matthew J. Niederst ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kinase Inhibitors ◽  
Acquired Resistance ◽  
Growth Factor Receptor ◽  
Drug Combinations ◽  
Effective Drug ◽  
Cancer Therapies ◽  
Lung Cancer Patients ◽  
Anaplastic Lymphoma ◽  
Culture Models

Targeted cancer therapies have produced substantial clinical responses, but most tumors develop resistance to these drugs. Here, we describe a pharmacogenomic platform that facilitates rapid discovery of drug combinations that can overcome resistance. We established cell culture models derived from biopsy samples of lung cancer patients whose disease had progressed while on treatment with epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors and then subjected these cells to genetic analyses and a pharmacological screen. Multiple effective drug combinations were identified. For example, the combination of ALK and MAPK kinase (MEK) inhibitors was active in an ALK-positive resistant tumor that had developed a MAP2K1 activating mutation, and the combination of EGFR and fibroblast growth factor receptor (FGFR) inhibitors was active in an EGFR mutant resistant cancer with a mutation in FGFR3. Combined ALK and SRC (pp60c-src) inhibition was effective in several ALK-driven patient-derived models, a result not predicted by genetic analysis alone. With further refinements, this strategy could help direct therapeutic choices for individual patients.

scholarly journals Epidermal Growth Factor Receptor Expression in the Corneal Epithelium

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2409
Author(s):  
Joanne L. Peterson ◽  
Brian P. Ceresa
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Corneal Epithelium ◽  
Growth Factor Receptor ◽  
Receptor Expression ◽  
Cancer Therapies ◽  
Anterior Portion ◽  
Increased Risk ◽  
Epidermal Growth

A properly functioning cornea is critical to clear vision and healthy eyes. As the most anterior portion of the eye, it plays an essential role in refracting light onto the retina and as an anatomical barrier to the environment. Proper vision requires that all layers be properly formed and fully intact. In this article, we discuss the role of the epidermal growth factor receptor (EGFR) in maintaining and restoring the outermost layer of the cornea, the epithelium. It has been known for some time that the addition of epidermal growth factor (EGF) promotes the restoration of the corneal epithelium and patients using EGFR inhibitors as anti-cancer therapies are at increased risk of corneal erosions. However, the use of EGF in the clinic has been limited by downregulation of the receptor. More recent advances in EGFR signaling and trafficking in corneal epithelial cells have provided new insights in how to overcome receptor desensitization. We examine new strategies for overcoming the limitations of high ligand and receptor expression that alter trafficking of the ligand:receptor complex to sustain receptor signaling.

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