Clara N Curiel

Clara N Curiel

Professor, Medicine - (Tenure Track)
Director, Cutaneous Oncology Program
Interim Chief, Division of Dermatology
Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-0307

Research Interest

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

Engelhardt, C., Curiel-Lewandrowski, C., Warneke, J., & Cranmer, L. (2011). Metastatic cutaneous squamous cell carcinoma responding to erlotinib therapy. Journal of the American Academy of Dermatology, 65(1), 237-8.
Leachman, S. A., Cassidy, P. B., Chen, S. C., Curiel, C., Geller, A., Gareau, D., Pellacani, G., Grichnik, J. M., Malvehy, J., North, J., Jacques, S. L., Petrie, T., Puig, S., Swetter, S. M., Tofte, S., & Weinstock, M. A. (2016). Methods of Melanoma Detection. Cancer treatment and research, 167, 51-105.

Detection and removal of melanoma, before it has metastasized, dramatically improves prognosis and survival. The purpose of this chapter is to (1) summarize current methods of melanoma detection and (2) review state-of-the-art detection methods and technologies that have the potential to reduce melanoma mortality. Current strategies for the detection of melanoma range from population-based educational campaigns and screening to the use of algorithm-driven imaging technologies and performance of assays that identify markers of transformation. This chapter will begin by describing state-of-the-art methods for educating and increasing awareness of at-risk individuals and for performing comprehensive screening examinations. Standard and advanced photographic methods designed to improve reliability and reproducibility of the clinical examination will also be reviewed. Devices that magnify and/or enhance malignant features of individual melanocytic lesions (and algorithms that are available to interpret the results obtained from these devices) will be compared and contrasted. In vivo confocal microscopy and other cellular-level in vivo technologies will be compared to traditional tissue biopsy, and the role of a noninvasive "optical biopsy" in the clinical setting will be discussed. Finally, cellular and molecular methods that have been applied to the diagnosis of melanoma, such as comparative genomic hybridization (CGH), fluorescent in situ hybridization (FISH), and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), will be discussed.

Einspahr, J., Bowden, G. T., Alberts, D. S., McKenzie, N., & Curiel, C. N. (2008). Cross-validation of murine UVB signal transduction pathways in human skin. Photochem Photobiol;, 84(2), 463-76.
Curiel, C. N., Wiliams, C. M., Swindells, K. J., Tahan, S. R., & Astner, S. (2004). Use of in vivo confocal microscopy in malignant melanoma: an aid in diagnosis and assessment of surgical and non-surgical therapeutic approaches. Arch Dermatol, 140(9), 1127-32.
Leachman, S. A., Carucci, J., Kohlmann, W., Banks, K. C., Asgari, M. M., Bergman, W., Bianchi-Scarrà, G., Brentnall, T., Bressac-de Paillerets, B., Bruno, W., Curiel-Lewandrowski, C., de Snoo, F. A., Debniak, T., Demierre, M., Elder, D., Goldstein, A. M., Grant-Kels, J., Halpern, A. C., Ingvar, C., , Kefford, R. F., et al. (2009). Selection criteria for genetic assessment of patients with familial melanoma. Journal of the American Academy of Dermatology, 61(4), 677.e1-14.

Approximately 5% to 10% of melanoma may be hereditary in nature, and about 2% of melanoma can be specifically attributed to pathogenic germline mutations in cyclin-dependent kinase inhibitor 2A (CDKN2A). To appropriately identify the small proportion of patients who benefit most from referral to a genetics specialist for consideration of genetic testing for CDKN2A, we have reviewed available published studies of CDKN2A mutation analysis in cohorts with invasive, cutaneous melanoma and found variability in the rate of CDKN2A mutations based on geography, ethnicity, and the type of study and eligibility criteria used. Except in regions of high melanoma incidence, such as Australia, we found higher rates of CDKN2A positivity in individuals with 3 or more primary invasive melanomas and/or families with at least one invasive melanoma and two or more other diagnoses of invasive melanoma and/or pancreatic cancer among first- or second-degree relatives on the same side of the family. The work summarized in this review should help identify individuals who are appropriate candidates for referral for genetic consultation and possible testing.