Publications by authors named "Cydney Dennis"
Studies have evaluated vitamin D's therapeutic potential in estrogen-responsive cancers, with conflicting findings. We have shown that the proliferation of breast cancer cells is regulated by 24R,25-dihydroxyvitamin D (24R,25(OH)D) depending on estrogen receptor alpha 66 (ERα66) expression, suggesting that this could also be the case for estrogen-sensitive laryngeal cancer cells. Accordingly, we examined levels of ERα isoforms in ERα66-positive UM-SCC-12 and ERα66-negative UM-SCC-11A cells and their response to 24R,25(OH)D.
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- Triple-negative breast cancer (TNBC) lacks estrogen receptor alpha 66 (ERα66) and is resistant to hormone therapy, but a variant called ERα36 has been found in TNBC cells that responds to estrogen (E).
- Research using the MDA-MB-231 TNBC cell line shows that E can lead to bone osteolysis by activating osteoclasts, with effects that can be blocked by anti-ERα36 antibodies.
- In mouse models, treatment with estrogen and tamoxifen increased osteolytic lesions and bone breakdown in TNBC tumors, highlighting ERα36 as a potential target for therapy in TNBC patients.
Local production of active vitamin D metabolites in breast cancer cells by CYP24A1 and CYP27B1.
J Steroid Biochem Mol Biol
September 2023
The role of vitamin D and its metabolites in cancer and especially as a treatment option has been widely disputed. Clinicians noting low serum 25-hydroxyvitamin D [25(OH)D] levels in their patients, recommend vitamin D supplementation as a method of reducing the risk of cancer; however, data supporting this are inconsistent. These studies rely on systemic 25(OH)D as an indicator of hormone status, but 25(OH)D is further metabolized in the kidney and other tissues under regulation by several factors.
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