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Melanie S. Flint

Researcher at University of Brighton

Publications -  52
Citations -  1132

Melanie S. Flint is an academic researcher from University of Brighton. The author has contributed to research in topics: Cancer & DNA damage. The author has an hindex of 19, co-authored 47 publications receiving 912 citations. Previous affiliations of Melanie S. Flint include National Institute for Occupational Safety and Health & East Sussex County Council.

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Induction of DNA damage, alteration of DNA repair and transcriptional activation by stress hormones

TL;DR: Data show that stress hormones can increase DNA damage and transformation and alter transcriptional regulation of the cell cycle.
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Glucocorticoids induce production of reactive oxygen species/reactive nitrogen species and DNA damage through an iNOS mediated pathway in breast cancer.

TL;DR: It is demonstrated that glucocorticoids may interact with iNOS in a non-genomic manner to produce damaging levels of RNS, thus allowing an insight into the potential mechanisms by which psychological stress may impact breast cancer.
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Stress hormones reduce the efficacy of paclitaxel in triple negative breast cancer through induction of DNA damage.

TL;DR: A novel mechanism through which stress hormones can induce drug resistance to paclitaxel is described, which may have profound implications for treating drug resistance in patients with TNBC.
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C57BL/6 mice are resistant to acute restraint modulation of cutaneous hypersensitivity.

TL;DR: Combined application of acute restraint and corticosterone prior to chemical challenge significantly enhanced the ear swelling response in C57BL/6 wild-type mice and demonstrates that stress-resistance is not conferred exclusively through the glucocorticoid pathways.
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Chronic exposure to stress hormones promotes transformation and tumorigenicity of 3T3 mouse fibroblasts

TL;DR: In summary, incubation of 3T3 cells with catecholamines results in long-term DNA damage as measured by increased transformed phenotypes and tumor progression, indicating that they are important mediators of stress effects on genomic instability and vulnerability to tumor formation.