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Confounding Effects of Tamoxifen: Cautionary and Practical Considerations for the Use of Tamoxifen-Inducible Mouse Models in Atherosclerosis Research
CONCLUSIONS: In this study, we establish that tamoxifen administration results in decreased serum cholesterol, decreased plaque formation, and increased hepatic lipid accumulation. These alterations represent significant confounding variables in atherosclerosis research, and we urge future investigators to take these findings into consideration when planning and executing their own atherosclerosis experiments.PMID:37706321 | DOI:10.1161/ATVBAHA.123.319922
Source: Arteriosclerosis, Thrombosis and Vascular Biology - September 14, 2023 Category: Cardiology Authors: Allison M Dubner Sizhao Lu Austin J Jolly Tysen Noble Tyler Hinthorn Raphael A Nemenoff Karen S Moulton Mark W Majesky Mary C M Weiser-Evans Source Type: research

A comparative study of the ability of recombinant oncolytic adenovirus, doxorubicin and tamoxifen to inhibit the proliferation of breast cancer cells
In this study, we compared the inhibitory effects of recombinant oncolytic adenovirus (Ad-apoptin-hTERTp-E1a, Ad-VT) with that of doxorubicin (DOX), a first-line chemotherapy drug, and tamoxifen (TAM), an endocrine therapy drug, on the proliferation of breast cancer cells. We found that Ad-VT could effectively inhibit the proliferation of breast cancer cells (p < 0.01); the inhibition rate of Ad-VT on normal mammary epithelial MCF-10A cells was less than 20%. DOX can effectively inhibit the proliferation of breast cancer cells and also has a strong inhibitory effect on MCF-10A cells (p < 0.01). TAM also has a strong ...
Source: J Cell Mol Med - September 23, 2022 Category: Molecular Biology Authors: Shanzhi Li Zhuoxin Li Yiquan Li Yilong Zhu Jicheng Han Wenjie Li Ningyi Jin Jinbo Fang Xiao Li Guangze Zhu Source Type: research

Fibroblast GSK-3 α Promotes Fibrosis via RAF-MEK-ERK Pathway in the Injured Heart
CONCLUSIONS: GSK-3α-mediated MEK-ERK activation is a critical profibrotic signaling circuit in the injured heart, which operates independently of the canonical TGF-β1-SMAD3 pathway. Therefore, strategies to inhibit the GSK-3α-MEK-ERK signaling circuit could prevent adverse fibrosis in diseased hearts.PMID:36052698 | DOI:10.1161/CIRCRESAHA.122.321431
Source: Cell Research - September 2, 2022 Category: Cytology Authors: Prachi Umbarkar Sultan Tousif Anand P Singh Joshua C Anderson Qinkun Zhang Michelle D Tallquist James Woodgett Hind Lal Source Type: research

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