Clinical Focus

  • Dermatology
  • Precision Dermatology
  • Skin Cancers
  • Genetic Skin Disease

Academic Appointments

Administrative Appointments

  • Clinical Assistant Professor in Dermatology, Stanford University Medical Center (2013 - Present)
  • Clinical Instructor in Dermatology, Stanford University Medical Center (2012 - 2013)

Honors & Awards

  • Medical Dermatology Career Development Award, Dermatology Foundation (2014-2017)
  • F32 NRSA Ruth L. Kirschstein National Research Service Award, National Institutes of Health (2013-2014)
  • Translational Research and Medicine Award, Stanford University (2013-2014)
  • Scholar Travel Award, American Association of Cancer Research (2006)
  • Medical Scientist Training Program Scholarship, National Institutes of Health (2000-2008)
  • 1st Place Award for Human-Computer Interaction (Senior Thesis Project), Stanford University (2000)
  • President's Scholar, Stanford University (1996-2000)
  • Unsung Hero Award, NBC (1996)

Boards, Advisory Committees, Professional Organizations

  • Fellow, American Academy of Dermatology (2009 - Present)
  • Member, Society of Investigative Dermatology (2014 - Present)
  • Member, Dermatology Foundation (2014 - Present)

Professional Education

  • Board Certification: Dermatology, American Board of Dermatology (2012)
  • Internship:Santa Clara Valley Medical Center (2009) CA
  • Residency:Stanford University - Dept of Dermatology (2012) CA
  • Medical Education:Stanford University Medical Center (2008) CA
  • PhD, Stanford University- Dept of Genetics, CA (2006)
  • BS, Stanford University- Computer Science, CA (2000)

Research & Scholarship

Current Research and Scholarly Interests

My research encompasses two main areas: 1) Using next-generation RNA, whole genome, and exome sequencing, we are investigating the genetic alterations involved in skin cancer progression, response to therapy, and other clinical outcomes and 2) We are developing and implementing genome-wide genetic risk prediction assessments for skin cancer into clinical use and studying the impact of this information on patient care.

Clinical Trials

  • Analysis of Cutaneous and Hematologic Disorders by High-Throughput Nucleic Acid Sequencing Recruiting

    The goal of this study is to identify genetic changes associated with the initiation, progression, and treatment response of response of cutaneous and hematologic disorders using recently developed high-throughput sequencing technologies. The improved understanding of the genetic changes associated with cutaneous and hematologic disorders may lead to improved diagnostic, prognostic and therapeutic options for these disorders.

    View full details


  • Genetic alterations in vismodegib resistant basal cell carcinomas, Stanford University (July 2014 - June 2017)

    The goal of this project is to identify genetic alterations that confer resistance to Smoothened inhibitor therapy in basal cell carcinoma.


    Stanford University

  • Development and implementation of a Genetic Risk SCore for skin cancer prediction, Stanford University (September 2013 - 12/2014)

    The study aims to develop, implement and assess the impact of a genetic risk score to predict skin cancer risk based on genotypic data with the goal of understanding the barriers and benefits of implementing genetic risk analysis into clinical care


    Stanford University


Journal Articles

  • Activating HRAS Mutation in Nevus Spilus. journal of investigative dermatology Sarin, K. Y., McNiff, J. M., Kwok, S., Kim, J., Khavari, P. A. 2014; 134 (6): 1766-1768

    View details for DOI 10.1038/jid.2014.6

    View details for PubMedID 24390138

  • Dermatomyositis associated with capecitabine in the setting of malignancy JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY Chen, F. W., Zhou, X., Egbert, B. M., Swetter, S. M., Sarin, K. Y. 2014; 70 (2): E47-E48

    View details for DOI 10.1016/j.jaad.2013.10.025

    View details for Web of Science ID 000329851500013

    View details for PubMedID 24438983

  • Dermatological Applications of Direct to Consumer Genomic Analysis Journal of the American Academy of Dermatology Fogel, A., Azizi, N., Tang, J., Sarin, K. 2014: in press
  • Activating HRAS mutation in agminated Spitz nevi arising in a nevus spilus. JAMA dermatology Sarin, K. Y., Sun, B. K., Bangs, C. D., Cherry, A., Swetter, S. M., Kim, J., Khavari, P. A. 2013; 149 (9): 1077-1081


    IMPORTANCE Spitz nevi are benign melanocytic proliferations that can sometimes be clinically and histopathologically difficult to distinguish from melanoma. Agminated Spitz nevi have been reported to arise spontaneously, in association with an underlying nevus spilus, or after radiation or chemotherapy. However, to our knowledge, the genetic mechanism for this eruption has not been described. OBSERVATIONS We report a case of agminated Spitz nevi arising in a nevus spilus and use exome sequencing to identify a clonal activating point mutation in HRAS (GenBank 3265) (c.37G→C) in the Spitz nevi and underlying nevus spilus. We also identify a secondary copy number increase involving HRAS on chromosome 11p, which occurs during the development of the Spitz nevi. CONCLUSIONS AND RELEVANCE Our results reveal an activating HRAS mutation in a nevus spilus that predisposes to the formation of Spitz nevi. In addition, we demonstrate a copy number increase in HRAS as a "second hit" during the formation of agminated Spitz nevi, which suggests that both multiple Spitz nevi and solitary Spitz nevi may arise through similar molecular pathways. In addition, we describe a unique investigative approach for the discovery of genetic alterations in Spitz nevi.

    View details for DOI 10.1001/jamadermatol.2013.4745

    View details for PubMedID 23884457

  • Mosaic Activating RAS Mutations in Nevus Sebaceus and Nevus Sebaceus Syndrome JOURNAL OF INVESTIGATIVE DERMATOLOGY Sun, B. K., Saggini, A., Sarin, K. Y., Kim, J., Benjamin, L., LeBoit, P. E., Khavari, P. A. 2013; 133 (3): 824-827

    View details for DOI 10.1038/jid.2012.377

    View details for Web of Science ID 000315008500032

    View details for PubMedID 23096709

  • Molecular Profiling to Diagnose a Case of Atypical Dermatomyositis. The Journal of investigative dermatology Sarin, K. Y., Chung, L., Kim, J., Higgs, B. W., Jallal, B., Yao, Y., Fiorentino, D. F. 2013

    View details for PubMedID 23732751

  • Treatment of Recalcitrant Eosinophilic Cellulitis With Adalimumab ARCHIVES OF DERMATOLOGY Sarin, K. Y., Fiorentino, D. 2012; 148 (9): 990-992

    View details for Web of Science ID 000308883500002

    View details for PubMedID 22986848

  • Reversible cell-cycle entry in adult kidney podocytes through regulated control of telomerase and Wnt signaling NATURE MEDICINE Shkreli, M., Sarin, K. Y., Pech, M. F., Papeta, N., Chang, W., Brockman, S. A., Cheung, P., Lee, E., Kuhnert, F., Olson, J. L., Kuo, C. J., Gharavi, A. G., D'Agati, V. D., Artandi, S. E. 2012; 18 (1): 111-119


    Mechanisms of epithelial cell renewal remain poorly understood in the mammalian kidney, particularly in the glomerulus, a site of cellular damage in chronic kidney disease. Within the glomerulus, podocytes--differentiated epithelial cells crucial for filtration--are thought to lack substantial capacity for regeneration. Here we show that podocytes rapidly lose differentiation markers and enter the cell cycle in adult mice in which the telomerase protein component TERT is conditionally expressed. Transgenic TERT expression in mice induces marked upregulation of Wnt signaling and disrupts glomerular structure, resulting in a collapsing glomerulopathy resembling those in human disease, including HIV-associated nephropathy (HIVAN). Human and mouse HIVAN kidneys show increased expression of TERT and activation of Wnt signaling, indicating that these are general features of collapsing glomerulopathies. Silencing transgenic TERT expression or inhibiting Wnt signaling through systemic expression of the Wnt inhibitor Dkk1 in either TERT transgenic mice or in a mouse model of HIVAN results in marked normalization of podocytes, including rapid cell-cycle exit, re-expression of differentiation markers and improved filtration barrier function. These data reveal an unexpected capacity of podocytes to reversibly enter the cell cycle, suggest that podocyte renewal may contribute to glomerular homeostasis and implicate the telomerase and Wnt-β-catenin pathways in podocyte proliferation and disease.

    View details for DOI 10.1038/nm.2550

    View details for Web of Science ID 000299018600036

  • TERT promotes epithelial proliferation through transcriptional control of a Myc- and Wnt-related developmental program PLOS GENETICS Choi, J., Southworth, L. K., Sarin, K. Y., Venteicher, A. S., Ma, W., Chang, W., Cheung, P., Jun, S., Artandi, M. K., Shah, N., Kim, S. K., Artandi, S. E. 2008; 4 (1)


    Telomerase serves a critical role in stem cell function and tissue homeostasis. This role depends on its ability to synthesize telomere repeats in a manner dependent on the reverse transcriptase (RT) function of its protein component telomerase RT (TERT), as well as on a novel pathway whose mechanism is poorly understood. Here, we use a TERT mutant lacking RT function (TERT(ci)) to study the mechanism of TERT action in mammalian skin, an ideal tissue for studying progenitor cell biology. We show that TERT(ci) retains the full activities of wild-type TERT in enhancing keratinocyte proliferation in skin and in activating resting hair follicle stem cells, which triggers initiation of a new hair follicle growth phase and promotes hair synthesis. To understand the nature of this RT-independent function for TERT, we studied the genome-wide transcriptional response to acute changes in TERT levels in mouse skin. We find that TERT facilitates activation of progenitor cells in the skin and hair follicle by triggering a rapid change in gene expression that significantly overlaps the program controlling natural hair follicle cycling in wild-type mice. Statistical comparisons to other microarray gene sets using pattern-matching algorithms revealed that the TERT transcriptional response strongly resembles those mediated by Myc and Wnt, two proteins intimately associated with stem cell function and cancer. These data show that TERT controls tissue progenitor cells via transcriptional regulation of a developmental program converging on the Myc and Wnt pathways.

    View details for DOI 10.1371/journal.pgen.0040010

    View details for Web of Science ID 000255378700011

    View details for PubMedID 18208333

  • Aging, graying and loss of melanocyte stem cells STEM CELL REVIEWS Sarin, K. Y., Artandi, S. E. 2007; 3 (3): 212-217


    Hair graying is one of the prototypical signs of human aging. Maintenance of hair pigmentation is dependent on the presence and functionality of melanocytes, neural crest derived cells which synthesize pigment for growing hair. The melanocytes, themselves, are maintained by a small number of stem cells which reside in the bulge region of the hair follicle. The recent characterization of the melanocyte lineage during aging has significantly accelerated our understanding of how age-related changes in the melanocyte stem cell compartment contribute to hair graying. This review will discuss our current understanding of hair graying, drawing on evidence from human and mouse studies, and consider the contribution of melanocyte stem cells to this process. Furthermore, using the melanocyte lineage as an example, it will discuss common theories of tissue and stem cell aging.

    View details for DOI 10.1007/s12015-007-0028-0

    View details for Web of Science ID 000249929800004

    View details for PubMedID 17917134

  • Conditional telomerase induction causes proliferation of hair follicle stem cells NATURE Sarin, K. Y., Cheung, P., Gilison, D., Lee, E., Tennen, R. I., Wang, E., Artandi, M. K., Oro, A. E., Artandi, S. E. 2005; 436 (7053): 1048-1052


    TERT, the protein component of telomerase, serves to maintain telomere function through the de novo addition of telomere repeats to chromosome ends, and is reactivated in 90% of human cancers. In normal tissues, TERT is expressed in stem cells and in progenitor cells, but its role in these compartments is not fully understood. Here we show that conditional transgenic induction of TERT in mouse skin epithelium causes a rapid transition from telogen (the resting phase of the hair follicle cycle) to anagen (the active phase), thereby facilitating robust hair growth. TERT overexpression promotes this developmental transition by causing proliferation of quiescent, multipotent stem cells in the hair follicle bulge region. This new function for TERT does not require the telomerase RNA component, which encodes the template for telomere addition, and therefore operates through a mechanism independent of its activity in synthesizing telomere repeats. These data indicate that, in addition to its established role in extending telomeres, TERT can promote proliferation of resting stem cells through a non-canonical pathway.

    View details for DOI 10.1038/nature03836

    View details for Web of Science ID 000231263900057

    View details for PubMedID 16107853


  • Protect Your Skin This Summer

    Learn about your different sunscreen options. Find out what ingredients and SPF are most effective. Get informed on skin cancer risk and how to use "ABCDE" for self-awareness. Discover foods and lifestyle practices to prevent skin damage, and understand the BRCA and melanoma correlation.

    Time Period

    August 27, 2014

    Presented To

    Stanford University


    2335 El Camino Real

  • Prevent Defense: Practical Preventative Applications for Primary Care Physicians - A Panel Discussion

    preventative medicine panel for primary care physicians

    Time Period

    September 14, 2014

    Presented To

    Levi's Stadium sponsored by Stanford Health Care


    Levi's Stadium

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