Efficient and economical electrical therapy for pancreatic cancers

Background:: Cancer is one of the significant causes of morbidity and mortality in patients globally. Lung cancer, among other cancers, remains to be one of the principal causes of deaths in both men and women. The most common type of lung cancer is the non-small-cell lung cancer (NSCLC). Apart from lung cancer, pancreatic cancer is also one of the common cancers currently. Objective:: The assessment of QoL in erlotinib-treated patients can also prove to be very useful in the establishment of this drug as the main treatment option for the patients with pancreatic and lung cancer. Methods:: Therapies that target EGFR-mediated signalling are the latest keystones for treating these two types of cancers. They comprise of two main treatment modalities: firstly, against the extracellular fields, that include monoclonal antibodies and secondly, mechanisms that create interferences in the signalling pathways, primarily the small molecule tyrosine kinase inhibitors. Results:: Quality of life (QoL) is one of the key advantages in erlotinib therapy over chemotherapy. Conclusion:: The present review reports the role of erlotinib in improving the quality of life of cancer patients especially in NSCLC and pancreatic cancers. The studies or trials establishing the relations between erlotinib and QoL are discussed in detail in this review.

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The Eccentric Engineer - Electrical Therapy. James Graham: a wannabe electrical engineer and doctor

Engineering & Technology ◽

10.1049/et.2019.0135 ◽

2019 ◽

Vol 14 (1) ◽

pp. 90-90

Author(s):

J. Pollard

Keyword(s):

Electrical Engineer ◽

Electrical Therapy

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Macropinocytosis requires Gal-3 in a subset of patient-derived glioblastoma stem cells

Communications Biology ◽

10.1038/s42003-021-02258-z ◽

2021 ◽

Vol 4 (1) ◽

Author(s):

Laetitia Seguin ◽

Soline Odouard ◽

Francesca Corlazzoli ◽

Sarah Al Haddad ◽

Laurine Moindrot ◽

...

Keyword(s):

Stem Cells ◽

Cell Survival ◽

Small Gtpases ◽

Molecular Signature ◽

Carbohydrate Binding ◽

Pancreatic Cancers ◽

Galectin 3 ◽

Pharmacologic Inhibition

AbstractRecently, we involved the carbohydrate-binding protein Galectin-3 (Gal-3) as a druggable target for KRAS-mutant-addicted lung and pancreatic cancers. Here, using glioblastoma patient-derived stem cells (GSCs), we identify and characterize a subset of Gal-3high glioblastoma (GBM) tumors mainly within the mesenchymal subtype that are addicted to Gal-3-mediated macropinocytosis. Using both genetic and pharmacologic inhibition of Gal-3, we showed a significant decrease of GSC macropinocytosis activity, cell survival and invasion, in vitro and in vivo. Mechanistically, we demonstrate that Gal-3 binds to RAB10, a member of the RAS superfamily of small GTPases, and β1 integrin, which are both required for macropinocytosis activity and cell survival. Finally, by defining a Gal-3/macropinocytosis molecular signature, we could predict sensitivity to this dependency pathway and provide proof-of-principle for innovative therapeutic strategies to exploit this Achilles’ heel for a significant and unique subset of GBM patients.

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GSK-3β Can Regulate the Sensitivity of MIA-PaCa-2 Pancreatic and MCF-7 Breast Cancer Cells to Chemotherapeutic Drugs, Targeted Therapeutics and Nutraceuticals

Cells ◽

10.3390/cells10040816 ◽

2021 ◽

Vol 10 (4) ◽

pp. 816

Author(s):

Stephen L. Abrams ◽

Shaw M. Akula ◽

Akshaya K. Meher ◽

Linda S. Steelman ◽

Agnieszka Gizak ◽

...

Keyword(s):

Breast Cancer ◽

Signal Transduction ◽

Cancer Cells ◽

Mitochondrial Respiration ◽

Breast Cancer Cells ◽

Chemotherapeutic Drugs ◽

Pancreatic Cancers ◽

Signal Transduction Inhibitors ◽

Gsk 3Β ◽

Mcf 7

Glycogen synthase kinase-3 (GSK-3) is a regulator of signaling pathways. KRas is frequently mutated in pancreatic cancers. The growth of certain pancreatic cancers is KRas-dependent and can be suppressed by GSK-3 inhibitors, documenting a link between KRas and GSK-3. To further elucidate the roles of GSK-3β in drug-resistance, we transfected KRas-dependent MIA-PaCa-2 pancreatic cells with wild-type (WT) and kinase-dead (KD) forms of GSK-3β. Transfection of MIA-PaCa-2 cells with WT-GSK-3β increased their resistance to various chemotherapeutic drugs and certain small molecule inhibitors. Transfection of cells with KD-GSK-3β often increased therapeutic sensitivity. An exception was observed with cells transfected with WT-GSK-3β and sensitivity to the BCL2/BCLXL ABT737 inhibitor. WT-GSK-3β reduced glycolytic capacity of the cells but did not affect the basal glycolysis and mitochondrial respiration. KD-GSK-3β decreased both basal glycolysis and glycolytic capacity and reduced mitochondrial respiration in MIA-PaCa-2 cells. As a comparison, the effects of GSK-3 on MCF-7 breast cancer cells, which have mutant PIK3CA, were examined. KD-GSK-3β increased the resistance of MCF-7 cells to chemotherapeutic drugs and certain signal transduction inhibitors. Thus, altering the levels of GSK-3β can have dramatic effects on sensitivity to drugs and signal transduction inhibitors which may be influenced by the background of the tumor.

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