Results 1 to 10 of about 585,532 (315)

Does Porphyromonas gingivalis truly inhibit the oral carcinogenesis?

open access: yesMolecular Oncology, EarlyView.
 
Chen‐xi Li, Zhong‐cheng Gong
wiley   +1 more source

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

Cross-reactions between rheumatoid factor and IgM SARS-CoV-2. [PDF]

open access: yesMed Clin (Engl Ed), 2020
Vinyé Bausà M   +2 more
europepmc   +2 more sources

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

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

CROSS-REACTIONS AMONG GROUP A STREPTOCOCCI [PDF]

open access: green, 1968
Grove G. Wiley, Pauline N. Bruno
openalex   +1 more source

Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis

open access: yesMolecular Oncology, EarlyView.
TRIM24 and TRIM28 are androgen receptor (AR) coregulators which exhibit increased expression with cancer progression. Both TRIM24 and TRIM28 combine to influence the response of castrate‐resistant prostate cancer (CRPC) cells to AR inhibitors by mediating AR signalling, regulation of MYC and upregulating VEGF to promote angiogenesis. Castrate‐resistant
Damien A. Leach   +8 more
wiley   +1 more source

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