Clara N Curiel
Director, Cutaneous Oncology Program
Interim Chief, Division of Dermatology
Professor, BIO5 Institute
Professor, Medicine - (Tenure Track)
Primary Department
Department Affiliations
(520) 626-0307
Research Interest
Clara Curiel-Lewandroski, PhD, is the director of the Pigmented Lesion Clinic and Multidisciplinary Cutaneous Oncology Program, both part of the University of Arizona Cancer Center Skin Cancer Institute. She completed two research fellowships, the first in the Department of Dermatology at Harvard Medical School, and the second at the Ludwig Boltzman Institute and Immunobiology of the Skin at Miinster University in Germany. Dr. Curiel is certified by the American Board of Dermatology.Dr. Curiel-Lewandroski’s research focus is on melanoma chemoprevention, early detection of melanoma, cutaneous T cell lymphomas and skin cancer. She studied the extended use of non-steroidal anti-inflammatory drugs, particularly aspirin, and their ability to possibly decrease the risk of cutaneous medanoma (CM) development. CM is responsible for more than 77 percent of skin cancer deaths.

Publications

Curiel, C. N. (1999). Atypical fibroxanthoma vs malignant fibrohistiocytoma. Dermatology & Cosmetics, 9, 67-9.
Kurtzman, D. J., Oulton, J., Erickson, C., & Curiel-Lewandrowski, C. (2017). Everolimus-Induced Symmetrical Drug-Related Intertriginous and Flexural Exanthema (SDRIFE). Dermatitis : contact, atopic, occupational, drug, 27(2), 76-7.
Finnane, A., Curiel-Lewandrowski, C., Wimberley, G., Caffery, L., Katragadda, C., Halpern, A., Marghoob, A. A., Malvehy, J., Kittler, H., Hofmann-Wellenhof, R., Abraham, I., Soyer, H. P., & , I. S. (2017). Proposed Technical Guidelines for the Acquisition of Clinical Images of Skin-Related Conditions. JAMA dermatology, 153(5), 453-457.

Standardizing dermatological imaging is important to improve monitoring of skin lesions and skin conditions, ensure the availability of high-quality images for teledermatology, and contribute to the development of a robust archive of skin images to be used for research.

Bermudez, Y., Stratton, S. P., Curiel-Lewandrowski, C., Warneke, J., Hu, C., Bowden, G. T., Dickinson, S. E., Dong, Z., Bode, A. M., Saboda, K., Brooks, C. A., Petricoin, E. F., Hurst, C. A., Alberts, D. S., & Einspahr, J. G. (2015). Activation of the PI3K/Akt/mTOR and MAPK Signaling Pathways in Response to Acute Solar-Simulated Light Exposure of Human Skin. Cancer prevention research (Philadelphia, Pa.), 8(8), 720-8.
BIO5 Collaborators
Clara N Curiel, Chengcheng Hu

The incidence of skin cancer is higher than all other cancers and continues to increase, with an average annual cost over $8 billion in the United States. As a result, identifying molecular pathway alterations that occur with UV exposure to strategize more effective preventive and therapeutic approaches is essential. To that end, we evaluated phosphorylation of proteins within the PI3K/Akt and MAPK pathways by immunohistochemistry in sun-protected skin after acute doses of physiologically relevant solar-simulated ultraviolet light (SSL) in 24 volunteers. Biopsies were performed at baseline, 5 minutes, 1, 5, and 24 hours after SSL irradiation. Within the PI3K/Akt pathway, we found activation of Akt (serine 473) to be significantly increased at 5 hours while mTOR (serine 2448) was strongly activated early and was sustained over 24 hours after SSL. Downstream, we observed a marked and sustained increase in phospho-S6 (serine 235/S236), whereas phospho-4E-BP1 (threonines 37/46) was increased only at 24 hours. Within the MAPK pathway, SSL-induced expression of phospho-p38 (threonine 180/tyrosine 182) peaked at 1 to 5 hours. ERK 1/2 was observed to be immediate and sustained after SSL irradiation. Phosphorylation of histone H3 (serine 10), a core structural protein of the nucleosome, peaked at 5 hours after SSL irradiation. The expression of both p53 and COX-2 was increased at 5 hours and was maximal at 24 hours after SSL irradiation. Apoptosis was significantly increased at 24 hours as expected and indicative of a sunburn-type response to SSL. Understanding the timing of key protein expression changes in response to SSL will aid in development of mechanistic-based approaches for the prevention and control of skin cancers.

Leachman, S., Jetter, J., Curiel-Lewandrowski, C., Swetter, S., & Cassidy, P. (2017). Chemoprevention Agents for Melanoma: Moving candidates forward into Phase 3 Clinical Trials. Cancer.