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Lorne J. Hofseth

Researcher at University of South Carolina

Publications -  92
Citations -  9892

Lorne J. Hofseth is an academic researcher from University of South Carolina. The author has contributed to research in topics: Colitis & Inflammation. The author has an hindex of 50, co-authored 92 publications receiving 8977 citations. Previous affiliations of Lorne J. Hofseth include National Institutes of Health.

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Radical causes of cancer

TL;DR: Understanding the association between chronic inflammation and cancer provides insights into the molecular mechanisms involved and highlights the interaction between nitric oxide and p53 as a crucial pathway in inflammatory-mediated carcinogenesis.
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p53: 25 years after its discovery.

TL;DR: The first 25 years of research on p53 are reviewed, which shows how this molecule continues to be studied intensively in biomedical research, including the fields of toxicology and pharmacology.
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p53-induced up-regulation of MnSOD and GPx but not catalase increases oxidative stress and apoptosis.

TL;DR: A novel mechanism of p53-dependent apoptosis is identified in which p 53-mediated up-regulation of MnSOD and GPx, but not CAT, produces an imbalance in antioxidant enzymes and oxidative stress.
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Hormone replacement therapy with estrogen or estrogen plus medroxyprogesterone acetate is associated with increased epithelial proliferation in the normal postmenopausal breast.

TL;DR: It is shown that postmenopausal HRT with E+P was associated with greater breast epithelial cell proliferation and breast epithelium density than E alone or no HRT, and breast proliferation was localized to the terminal duct-lobular unit of the breast, which is the site of development of most breast cancers.
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Nitric oxide-induced cellular stress and p53 activation in chronic inflammation.

TL;DR: In noncancerous colon tissues from patients with ulcerative colitis, inducible NO synthase protein levels were positively correlated with p53 serine 15 phosphorylation levels, and Immunostaining of HDM-2 and p21WAF1 was consistent with transcriptionally active p53.