Results 101 to 110 of about 1,787,106 (336)

TRPM8 levels determine tumor vulnerability to channel agonists

open access: yesMolecular Oncology, EarlyView.
TRPM8 is a Ca2+ permissive channel. Regardless of the amount of its transcript, high levels of TRPM8 protein mark different tumors, including prostate, breast, colorectal, and lung carcinomas. Targeting TRPM8 with channel agonists stimulates inward calcium currents followed by emptying of cytosolic Ca2+ stores in cancer cells.
Alessandro Alaimo   +18 more
wiley   +1 more source

The anticancer effect of the HDAC inhibitor belinostat is enhanced by inhibitors of Bcl‐xL or Mcl‐1 in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
The pan‐HDAC inhibitor belinostat increases the expression of the pro‐apoptotic proteins Bim, Puma, and Noxa and induces apoptosis in ovarian cancer cell lines and patient‐derived tumor organoids when used at high concentrations. Moreover, inhibiting the anti‐apoptotic proteins Bcl‐xL or Mcl‐1 sensitizes these preclinical models to the cytotoxic effect
Cécilia Thomine   +10 more
wiley   +1 more source

Dose‐dependent induction of epithelial‐mesenchymal transition in 3D melanoma models by non‐thermal plasma treatment

open access: yesMolecular Oncology, EarlyView.
Non‐thermal plasma treatment of melanoma cells induced epithelial‐mesenchymal transition (EMT) in a dose‐dependent fashion. This report highlights the critical need to further investigate potential adverse effects of non‐thermal plasma for cancer therapy and to optimize treatment parameters for clinical translation. Despite the promising results of non‐
Eline Biscop   +10 more
wiley   +1 more source

Identification of Risk Factors for Gliptin-associated Bullous Pemphigoid among Diabetic Patients

open access: yesActa Dermato-Venereologica
Drug-associated bullous pemphigoid has been shown to follow long-term gliptin (dipeptidyl-peptidase 4 inhibitors) intake. This study aimed at identifying risk factors for gliptin-associated bullous pemphigoid among patients with type 2 diabetes.
Dana Shalmon   +7 more
doaj   +1 more source

A nucleotide‐independent, pan‐RAS‐targeted DARPin elicits anti‐tumor activity in a multimodal manner

open access: yesMolecular Oncology, EarlyView.
We report a Designed Ankyrin Repeat Protein that binds and inhibits RAS proteins, which serve as central cell signaling hubs and are essential for the progression of many cancers. Its unique feature is that it does not discriminate between different RAS isoforms or mutations and is capable of binding to RAS in both its active (GTP‐bound) and inactive ...
Jonas N. Kapp   +13 more
wiley   +1 more source

Therapeutic applications of a novel humanized monoclonal antibody targeting chemokine receptor CCR9 in pancreatic cancer

open access: yesMolecular Oncology, EarlyView.
C–C chemokine receptor type 9 (CCR9) is an immune checkpoint in pancreatic ductal adenocarcinoma (PDAC). Novel anti‐CCR9 antibody SRB2 was evaluated in combination with cytotoxic chemotherapy in PDAC cells, patient‐derived organoids, patient‐derived xenografts, and humanized mouse models.
Hannah G. McDonald   +18 more
wiley   +1 more source

BMP antagonist CHRDL2 enhances the cancer stem‐cell phenotype and increases chemotherapy resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Overexpression of CHRDL2 in colon cancer cells makes them more stem‐like and resistant to chemo‐ and radiotherapy. CHRDL2‐high cells have upregulation of the WNT pathway, genes involved in the DNA damage response (DDR) pathway and epithelial‐to‐mesenchymal transition (EMT). This leads to quicker repair of damaged DNA and more cell migration.
Eloise Clarkson, Annabelle Lewis
wiley   +1 more source

Exploring antibiotic safety: A prospective observational study from a tertiary care public sector hospital

open access: yesClinical Epidemiology and Global Health
Background: Antibiotics are the most commonly used drugs to treat bacterial infections; however, these life-saving drugs can also cause adverse drug reactions.
Garapati Pavan   +5 more
doaj  

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