D
Dawn Holt
Researcher at University of Maryland, Baltimore
Publications - 10
Citations - 641
Dawn Holt is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Receptor & Metastasis. The author has an hindex of 7, co-authored 10 publications receiving 565 citations.
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CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model
Xinrong Ma,Kelly Norsworthy,Namita Kundu,William H. Rodgers,Phyllis A. Gimotty,Olga Goloubeva,Michael M. Lipsky,Yanchun Li,Dawn Holt,Amy M. Fulton +9 more
TL;DR: The relationship of CXCR3 expression to clinical outcome in 75 women diagnosed with early-stage breast cancer and the antimetastatic effect of CxCR3 gene silencing was compromised in mice depleted of Natural Killer cells or with mutations in IFN-γ, suggest that the role of C XCR3 is not simply to mediate tumor cell trafficking.
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Prostaglandin E2 EP receptors as therapeutic targets in breast cancer
TL;DR: While preclinical and epidemiological data support the use of nonsteroidal anti-inflammatory drugs and selective COX-2 inhibitors (COXibs) for the prevention and treatment of malignancy, toxicities due to COXIBs as well as less than promising results from clinical trials have laboratories seeking alternative targets.
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Prostaglandin E(2) (PGE (2)) suppresses natural killer cell function primarily through the PGE(2) receptor EP4.
TL;DR: A mechanism whereby inhibiting PGE2 production or preventing signaling through the EP4 receptor may prevent suppression of NK functions that are critical to the control of breast cancer metastasis is supported.
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A prostaglandin E (PGE) receptor EP4 antagonist protects natural killer cells from PGE2-mediated immunosuppression and inhibits breast cancer metastasis
TL;DR: The findings reveal that EP4 antagonism prevents tumor-mediated NK-cell immunosuppression and demonstrates the anti-metastatic activity of a novel EP4 antagonist, which support the investigation of EP4 antagonists in clinical trials.
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Modulation of host natural killer cell functions in breast cancer via prostaglandin E2 receptors EP2 and EP4.
TL;DR: It is shown that NK functions are depressed in tumor-bearing hosts relative to normal NK cells and that PGE2 suppresses NK functions by acting on EP2 and EP4 receptors.