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Author

Doris M. Benbrook

The University of Oklahoma Health Sciences Center, United States
3 articles in our journals

Articles where this person is an author, newest first. People are matched by their name as printed (no ORCID iD is recorded for them), not by name alone; search the name as text to find namesakes too.

Research ArticleOpen accessRetinoids Chemosensitize Ovarian Cancer Cell Lines to Cisplatin Independent of Nuclear Receptors and p53Suresh Guruswamy, Doris M. BenbrookTreatment of ovarian cancer with cisplatin-based chemotherapy is highly toxic and is often followed by cancer recurrence. Repeated treatments with cisplatin frequently result in the development of resistance to this drug. Drugs with low toxicity that could enhance the tumor cell killing effects of cisplatin could potentially reduce the toxicity and enhance the efficacy of cisplatin. The mechanism of cell … …American Journal of Pharmacology and Toxicology, Vol. 1, Issue 4 · 31 Dec 2006 · 6,958 accessesView PDFCite
Research ArticleOpen accessSensitivities of Uterine Adenocarcinoma, Mixed Mullerian Tumor (MMT) and Sarcoma Cell Lines to Chemotherapeutic Agents and a Flex-Het DrugJohnny Hyde, Doris M. BenbrookThe administration and combination of a variety of chemotherapeutic agents for treatment of advanced or recurrent uterine cancer of different histologies is under current debate. Mixed Mullerian Tumors (MMTs), which contain both adenocarcinoma and sarcoma components, are the most rate histologic type and it is therefore difficult to conduct clinical trials to determine if they should be treated like endometrial … …American Journal of Pharmacology and Toxicology, Vol. 1, Issue 4 · 31 Dec 2006 · 7,460 accessesView PDFCite
Research ArticleOpen accessRole of AP-1 Antagonism in Growth Inhibition of Cervical Cancer Cell Lines by RetinoidsShennan Lu, Doris M. BenbrookRetinoid compounds induce multiple molecular effects that need to be taken into consideration in the development of theses agents as pharmaceuticals for cancer chemoprevention. Inhibition of cancer cell growth by retinoids is thought to occur through at least two mechanisms of transcriptional regulation resulting from direct binding of retinoids to nuclear retinoid receptors (RARs and RXR’s). First, the nuclear receptors … …American Journal of Pharmacology and Toxicology, Vol. 1, Issue 3 · 30 Sep 2006 · 7,477 accessesView PDFCite