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
Department Affiliations
Contact
(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. (2016). Everolimus-Induced Symmetrical Drug-Related Intertriginous and Flexural Exanthema (SDRIFE).. Dermatitis, 27(2), 76-7.
Einspahr, J. G., Thomas, T. M., Saboda, K., Nickoloff, B. J., & Curiel-Lewandrowski, C. N. (2007). Expression of VEGF and microvessel density counts in cutaneous melanocytic lesion progression. Cancer, 110(11), 2519-27.
Tuzova, M., Richmond, J., Wolpowitz, D., Curiel-Lewandrowski, C., Chaney, K., Kupper, T., & Cruikshank, W. (2015). CCR4+T cell recruitment to the skin in mycosis fungoides: potential contributions by thymic stromal lymphopoietin and interleukin-16. Leukemia & lymphoma, 56(2), 440-9.

Mycosis fungoides (MF) is characterized by skin accumulation of CCR4+CCR7- effector memory T cells; however the mechanism for their recruitment is not clearly identified. Thymic Stromal Lymphopoietin (TSLP) is a keratinocyte-derived cytokine that triggers Th2 immunity and is associated with T cell recruitment to the skin in atopic dermatitis. Interleukin-16 (IL-16) is a chemoattractant and growth factor for CD4+T cells. We hypothesized that TSLP and IL-16 could contribute to recruitment of malignant T cells in MF. We found elevated TSLP and IL-16 in very early stage patients' plasma and skin biopsies, prior to elevation in CCL22. Both TSLP and IL-16 induced migratory responses of CCR4+TSLPR+CD4+CCR7-CD31+cells, characteristic of malignant T cells in the skin. Co-stimulation also resulted in significant proliferative responses. We conclude that TSLP and IL-16, expressed at early stages of disease, function to recruit malignant T cells to the skin and contribute to their enhanced proliferation.

Kim, C. C., Swetter, S. M., Curiel-Lewandrowski, C., Grichnik, J. M., Grossman, D., Halpern, A. C., Kirkwood, J. M., Leachman, S. A., Marghoob, A. A., Ming, M. E., Nelson, K. C., Veledar, E., Venna, S. S., & Chen, S. C. (2015). Addressing the knowledge gap in clinical recommendations for management and complete excision of clinically atypical nevi/dysplastic nevi: Pigmented Lesion Subcommittee consensus statement. JAMA dermatology, 151(2), 212-8.

The management of clinically atypical nevi/dysplastic nevi (CAN/DN) is controversial, with few data to guide the process. Management recommendations for DN with positive histologic margins were developed by the Delphi method to achieve consensus among members of the Pigmented Lesion Subcommittee (PLS) of the Melanoma Prevention Working Group (MPWG) after reviewing the current evidence.

Krase, I. Z., Cavanaugh, K., & Curiel-Lewandrowski, C. (2015). Treatment of Refractory Pityriasis Rubra Pilaris With Novel Phosphodiesterase 4 (PDE4) Inhibitor Apremilast. JAMA dermatology, 1-2.