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Alice P. Pentland, M.D.
Alice P. Pentland, M.D.

Alice P. Pentland, M.D.

Dermatology — General — Dermatology

Accepting New Patients

Alice P. Pentland, M.D.

Dermatology — General — Dermatology

Accepting New Patients


400 Red Creek, Suite 200
Rochester, NY 14623
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(585) 275-7546



(585) 273-1346

About Me

Dr. Pentland, an expert in photobiology and skin cancer, specializes in the treatment of Bullous diseases, such as pemphigus and severe psoriasis. Dr. Pentland has dedicated her career to bringing state-of-the-art technology to support individual health and to creating a rich interdisciplinary environment within the department. She received her undergraduate and medical degrees from the University of Michigan.



MD | University of Michigan Medical School — 1978

Post-doctoral Training & Residency:

Internship in Internal Medicine at North Carolina Memorial Hospital — 1978 - 1979
Residency in Dermatology at University Of Michigan — 1979 - 1983
Fellowship in Dermatology at Washington University School of Medicine — 1983 - 1986


Research in the Pentland Lab addresses the role of prostaglandins in skin carcinogenesis and in cell differentiation. The role of these lipid mediators in the induction of squamous cell carcinoma of the skin is being studied in the context of ultraviolet light injury. Recent work has shown that significant contributions to tumor initiation and promotion may be made by eicosanoids (arachidonic acid and its metabolites). Most importantly, non-steroidal anti-inflammatory drugs (NSAIDs), which are inhibitors of prostaglandin synthesis, have been shown to have anti-tumor properties in humans. Unfortunately, NSAIDs chemoprevention is limited by NSAID side effects. However, new data shows the hormone metabolizing enzyme aldo-keto reductase AKR1C3 is also inhibited by most NSAIDs, begging the question whether cyclooxygenase inhibition is actually the key target through which NSAIDs produce their cancer prevention effects. A potential role in cancer for AKR1C3 has been shown in many tumor types. AKR1C3 metabolizes the cyclooxygenase product PGH2 into PGF2alpha, as well as transforming PGD2 into 9alpha11betaPGF2. This activity can shunt prostaglandin metabolism away from pro-differentiation, pro-apoptotic mediators such as PGJ2. AKR1C3 is also the primary enzyme responsible for synthesis of 17Beta-estradiol and testosterone from their respective less active precursors, supporting its role in hormone sensitive tumors. Lastly, AKR1C3 is capable of supporting redox cycling, which can produce mutations that could promote carcinogenesis.

We are testing the hypothesis that AKR1C3 is an important therapeutic target regulating SCC growth, due to PGF2alpha mediated signaling, redox and hormonal metabolic effects on SCC apoptosis, proliferation or invasion. We seek to determine whether this action is distinct from cancer reduction produced by cyclooxygenase. Current work addresses whether AKR1C3 expression is correlated with degree of tumor malignancy, and examines the relative importance of prostanoid metabolism, hormones and oxidative stress in human SCC-derived cell lines. In vivo models are also in use to understand the relative importance of these AKR1C3 activities.


Oleksyn D, Zhao J, Vosoughi A, Zhao JC, Misra R, Pentland AP, Ryan D, Anolik J, Ritchlin C, Looney J, Anandarajah AP, Schwartz G, Calvi LM, Georger M, Mohan C, Sanz I, Chen L. "PKK deficiency in B cells prevents lupus development in Sle lupus mice." Immunology letters.. 2017 May 0; 185:1-11. Epub 2017 Mar 06.

Barlow ML, Cummings RJ, Pentland AP, Love TM, Haidaris CG, Ryan JL, Lord EM, Gerber SA. "Total-Body Irradiation Exacerbates Dissemination of Cutaneous Candida Albicans Infection." Radiation research.. 2016 Nov 0; 186(5):436-446. Epub 2016 Oct 06.

Chen L, Oleksyn D, Pulvino M, Sanz I, Ryan D, Ryan C, Lin CS, Poligone B, Pentland AP, Ritchlin C, Zhao J. "A critical role for the protein kinase PKK in the maintenance of recirculating mature B cells and the development of B1 cells." Immunology letters.. 2016 Apr 0; 172:67-78. Epub 2016 Feb 26.

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