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Melissa S. Simper

Researcher at University of Texas MD Anderson Cancer Center

Publications -  12
Citations -  273

Melissa S. Simper is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Receptor & Prostaglandin E2. The author has an hindex of 7, co-authored 10 publications receiving 235 citations.

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The role of the EP receptors for prostaglandin E2 in skin and skin cancer.

TL;DR: Current studies are focused on identifying which of the G protein-coupled EP receptors mediate the tumor promotion/progression activities of PGE2 and the signaling pathways involved.
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DMBA induced mouse mammary tumors display high incidence of activating Pik3caH1047 and loss of function Pten mutations.

TL;DR: Long latency DMBA induced mouse mammary tumors reproduce the molecular profile of human luminal breast carcinomas representing an excellent preclinical model for the testing of PIK3CA/Akt/mTOR pathway inhibitory therapies and a good platform for the developing of additional preclinical tools such as syngeneic transplants in immunocompetent hosts.
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The chemopreventive efficacies of nonsteroidal anti-inflammatory drugs: the relationship of short-term biomarkers to long-term skin tumor outcome.

TL;DR: This study compared the efficacy of several NSAIDs and NO-NSAIDs on UV-induced NMSC in SKH-1 hairless mice and determined whether various short-term biomarkers were predictive of long-term tumor outcome with these agents.
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Systematic evaluation of RNA-Seq preparation protocol performance

TL;DR: At the manufacturers’ recommended input RNA levels, all the RNA-Seq library preparation protocols evaluated were suitable for distinguishing between experimental groups, and the TruSeq Stranded mRNA kit was universally applicable to studies focusing on protein-coding gene profiles.
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Protection against 2-chloroethyl ethyl sulfide (CEES)-induced cytotoxicity in human keratinocytes by an inducer of the glutathione detoxification pathway.

TL;DR: CDDO-Me is a promising chemopreventive agent for SM toxicity in the skin and 2,6-dithiopurine (DTP), a nucleophilic scavenging agent, is suggested to increase the viability of keratinocytes exposed to CEES.