Clara N Curiel

Photo of Clara N Curiel

Clara N Curiel

Director, Cutaneous Oncology Program
Division Chief, Dermatology
Member of the Graduate Faculty
Professor, BIO5 Institute
Professor, Medicine - (Tenure Track)
Primary Department
Medicine
Department Affiliations
Medicine
BIO5 Institute
Contact
(520) 626-0307
ccuriel@arizona.edu

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

Kurtzman, D. J., Thiede, R., Erickson, C., & Curiel-Lewandrowski, C. (2016). An abrupt onset pustular eruption. Journal of the American Academy of Dermatology, 75(2), e45-6.
Lee, M., Lim, D. o., Kim, D., Lee, D., Shin, D., Kim, D., Kim, D., Kim, D., Jung, D., Yao, D., Kundu, D., Lee, D., Lee, D., Dickinson, D., Alberts, D., Bowden, D., Stratton, D., Curiel, D., Einspahr, D., , Bode, D., et al. (2015). Genetic ablation of caspase-7 promotes solar-simulated light-induced mouse skin carcinogenesis: the involvement of keratin-17. Carcinogenesis, 36(11), 1372-80.

Solar ultraviolet irradiation is an environmental carcinogen that causes skin cancer. Caspase-7 is reportedly expressed at reduced levels in many cancers. The present study was designed to examine the role of caspase-7 in solar-simulated light (SSL)-induced skin cancer and to elucidate its underlying molecular mechanisms. Our study revealed that mice with genetic deficiency of caspase-7 are highly susceptible to SSL-induced skin carcinogenesis. Epidermal hyperplasia, tumor volume and the average number of tumors were significantly increased in caspase-7 knockout (KO) mice compared with SKH1 wild-type mice irradiated with SSL. The expression of cell proliferation markers, such as survivin and Ki-67, was elevated in SSL-irradiated skin of caspase-7 KO mice compared with those observed in SSL-exposed wild-type SKH1 mouse skin. Moreover, SSL-induced apoptosis was abolished in skin from caspase-7 KO mice. Two-dimensional gel electrophoresis, followed by matrix-assisted laser desorption/ionization-time-of-flight analysis of skin tissue lysates from SSL-irradiated SKH1 wild-type and caspase-7 KO mice revealed an aberrant induction of keratin-17 in caspase-7 KO mice. Immunohistochemical analysis of skin tumors also showed an increase of keratin-17 expression in caspase-7 KO mice compared with SKH1 wild-type mice. The expression of keratin-17 was also elevated in SSL-irradiated caspase-7 KO keratinocytes as well as in human basal cell carcinomas. The in vitro caspase activity assay showed keratin-17 as a substrate of caspase-7, but not caspase-3. Overall, our study demonstrates that genetic loss of caspase-7 promotes SSL-induced skin carcinogenesis by blocking caspase-7-mediated cleavage of keratin-17.

Krase, I. Z., Cavanaugh, K., & Curiel-Lewandrowski, C. (2016). A case of rupioid syphilis. JAAD case reports, 2(2), 141-3.
Curiel, C. N., Martinez, R., Pinto, V., Rosales, A., & Sanchez de Leon, R. (1995). Increase in cardiac output and PEEP as mechanism of pulmonary optimization. Rev Fisiol Esp, 51(1), 7-15.
Marghoob, A. A., & , I. S. (2015). Standards in Dermatologic Imaging. JAMA dermatology, 151(8), 819-21.

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