About

Dekker Deacon, MD, PhD, FAAD, completed his residency in dermatology at the University of Utah. He has a special interest in the genetics of skin cancer and skin cancer treatment, including Basal Cell Carcinoma, Squamous Cell Carcinoma, Melanoma, and other skin cancers. He is a member of the Melanoma Disease Center and participates in a weekly melanoma multidisciplinary treatment planning conference. Dr. Deacon treats skin cancer at both The Huntsman Cancer Institute and the University of Utah Hospital clinics. In addition to skin cancer, he sees general dermatology patients for a wide range of conditions including Actinic Keratoses, Acne, Warts, Psoriasis, Dermatitis, Rosacea, Hives, Rashes, Skin Lesions, Cysts, Skin Infections, Excessive Sweating, Hair and Nail Disease, and Drug Reactions.

Research topics

• Medicine
• Internal medicine
• Intensive care medicine
• Oncology
• Cancer research
• Immunology
• Biology
• Medical emergency
• Virology
• Family medicine
• Dermatology
• Pathology

Selected publications

• Abstract IA006: Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi- Selective Inhibitors in NRAS-Mutated Melanoma

  Cancer Research · 2026-03-05

  article

  Abstract Most patients with advanced BRAF or NRAS-driven melanoma receive front-line immunotherapy. However, if immunotherapy fails, BRAF-mutated patients have effective second-line therapies, whereas NRAS-mutated patients lack pathway-targeted options. Recently, RAS(ON) multi-selective inhibitors like RMC-7977, and the investigational agent daraxonrasib, were described that, in partnership with cyclophilin-A (CYPA), inhibit RAS[GTP] signaling. Both compounds demonstrate potent anti- proliferative activity against NRAS-mutated melanoma cell lines and robust anti-tumor activity against preclinical melanoma models. However, in preclinical models, resistance to RMC-7977 monotherapy arose through mutations in Ppia (encoding CYPA) or Map2k1 (encoding MEK1). Moreover, two clinical case studies in patients with NRAS-mutated melanoma treated with daraxonrasib demonstrated clear anti-tumor activity in one patient, but progressive disease in another with co-occurring NRAS and MAP2K1 mutations at baseline. These findings support the potential for daraxonrasib in treatment of patients with NRAS-mutated melanoma, and reveal candidate mechanisms of monotherapy resistance, underscoring the need for combination therapies to improve outcomes. Citation Format: Mona Foth, Wontak Kim, Kayla O'Toole, Brandon Murphy, Montserrat Justo-Garrido, Sanjana Boggaram, Phaedra Ghazi, Euan Brennan, Isaac Wright, Tate Shepherd, Emilio Cortes-Sanchez, Yingyun Wang, Jennifer Roth, Matthew Rees, Melissa Ronan, Jingjing Jiang, Ursula Wasko, Amanda Jiang, Carly Becker, Dekker Deacon, Siwen Hu-Lieskovan, Conan Kinsey, Jeffery Russell, Aparna Hegde, Ignacio Garrido-Laguna, Matthew Holderfield, Mallika Singh, Martin McMahon. Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi- Selective Inhibitors in NRAS-Mutated Melanoma [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: RAS Oncogenesis and Therapeutics; 2026 Mar 5-8; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(5_Suppl_1):Abstract nr IA006.

  PublisherDOI

• CIT tumor lines: A series of immunogenic murine cutaneous squamous cell carcinoma cell lines derived from chemical carcinogenesis

  JID Innovations · 2026-04-15

  articleOpen access
  PublisherDOI

• Genetic Drivers of Sensitivity or Resistance to RAS(ON) Multi-Selective Inhibitors in NRAS-Mutated Melanoma

  Cancer Research · 2026-05-22

  article

  Most patients with advanced BRAF or NRAS-driven melanoma receive front-line immunotherapy. However, if immunotherapy fails, BRAF-mutated patients have effective second-line therapies, whereas NRAS-mutated patients lack pathway-targeted options. Recently, RAS(ON) multi-selective inhibitors like RMC-7977, and the investigational agent daraxonrasib, were described that inhibit RAS[GTP] signaling in partnership with cyclophilin A (CYPA). Here, we found that both compounds demonstrated potent anti-proliferative activity against NRAS-mutated melanoma cell lines and robust anti-tumor activity against preclinical melanoma models. However, in preclinical models, resistance to RMC-7977 monotherapy arose through mutations in Ppia (encoding CYPA) or Map2k1 (encoding MEK1). Moreover, two clinical case studies in patients with NRAS-mutated melanoma treated with daraxonrasib demonstrated clear anti-tumor activity in one patient, but progressive disease in another with co-occurring NRAS and MAP2K1 mutations at baseline. These findings support the potential for daraxonrasib in treatment of patients with NRAS-mutated melanoma, and reveal candidate mechanisms of monotherapy resistance, underscoring the need for combination therapies to improve outcomes.

  PublisherDOI

• Ancestry and somatic profile indicate acral melanoma origin and prognosis

  Nature · 2026-02-18

  articleOpen access

  Abstract Acral melanoma, which is not ultraviolet-associated, is the type of melanoma reported most commonly in several non-European-descent populations 1–3 , including in Mexican people 4 . Latin American samples are substantially under-represented in global cancer genomics studies 5 , which directly affects patients in these regions as it is known that cancer risk and incidence may be influenced by ancestry and environmental exposures 6–8 . To address this, we characterized the genome and transcriptome of 123 acral melanoma tumours from 92 Mexican patients—a population notable because of its genetic admixture 9 . Compared with other studies of melanoma, we found fewer mutations in classical driver genes such as BRAF , NRAS or NF1 . Although most patients had predominantly Amerindian genetic ancestry, those with higher European ancestry had increased frequency of BRAF mutations. The tumours with activating BRAF mutations had a transcriptional profile more similar to cutaneous non-volar melanocytes, indicating that acral melanomas in these patients may arise from a distinct cell of origin compared with other tumours arising in these locations. Transcriptional profiling defined three expression clusters; these characteristics were associated with recurrence-free and overall survival. Our study enhances knowledge of this understudied disease and underscores the importance of including samples from diverse ancestries in cancer genomics studies.

  PublisherDOI

• Non‐invasive adhesive patch microRNA assay recapitulates tissue biomarkers for melanoma

  Clinical and Translational Medicine · 2026-02-01

  articleOpen access

  Dear Editor: We show that microRNAs (miRNAs) are substantially more stable than long RNAs in tape-stripped skin samples and can be robustly quantified by digital polymerase chain reaction (dPCR). Using this approach, a miRNA ratio previously validated in tissue specimens retains its ability to distinguish melanocytic nevi (MN) from invasive melanoma (IM) when measured non-invasively. Many clinically suspicious pigmented skin lesions are biopsied to exclude melanoma, yet the vast majority prove to be benign (e.g. MN), resulting in substantial over-biopsy and patient burden1. This reflects an unmet need for objective, molecular pre-biopsy triage tools to help prioritise lesions for histopathologic evaluation. Existing non-invasive approaches, including image-based and RNA-based tape stripping (TS) assays, have shown promise but are limited by variability, technical failure rates, low specificity, or dependence on degradation-prone RNA species.2, 3 A barrier to broader translation has been the lack of molecular biomarkers that are both biologically informative and analytically robust when collected non-invasively. TS uses an adhesive patch to collect stratum corneum material for analysis (Figure 1A). Current TS RNA assays are designed for use by dermatologists to help prioritise ambiguous pigmented lesions2 (Figure 1B). These assays suffer relatively high technical failure rates—up to ∼14% of tests yield invalid results3—likely due to degradation of the long RNA targets. As miRNAs are inherently more resistant to degradation than mRNAs4, we hypothesised that using more stable short RNA biomarkers could improve the reliability of TS-based tests. We first determined that intact miRNAs are collected in TS samples and can be sensitively quantified by dPCR. TapeStation analysis confirmed that long RNA was largely degraded in TS-derived RNA (Figure 1C). Small RNA sequencing of the preserved fraction predominantly mapped to annotated miRNAs (Figure 1D,E). Several miRNA expression ratios (miR-21-5p:miR-125b-5p and miR-21-5p:miR-211-5p) were previously discovered in tissue specimens and later confirmed across large meta-analyses to consistently distinguish melanoma from nevi.5-7 Those studies were performed on miRNAs isolated from formalin-fixed, paraffin-embedded tissue sections from archival specimens. Here, we evaluate whether these previously established miRNA ratios remain diagnostic when measured non-invasively using TS samples. We developed a multiplex dPCR assay to quantify TS-derived miRNAs, using TaqMan Advanced miRNA probe/primer sets for three targets (miR-125b-5p, miR-21-5p, and miR-211-5p). An input dilution series for the miR-125b-5p dPCR assay revealed a limit of quantification (LOQ) of approximately 9.62 pg RNA, corresponding to ∼7.3 copies/µL (cp/µL) (Figure 1F). Outputs for miR-125b-5p and the commonly used loading control miR-16-5p were linearly related over a wide range, supporting the use of miR-125b-5p as a reference (Figure 1g). We excluded the miR-211-5p assay from quantitative analysis because its endpoint dPCR amplitude distribution lacked a discrete positive cloud, precluding objective thresholding and Poisson-based quantification, consistent with inefficient assay performance rather than biological absence of signal (Figure 2). We prospectively collected TS samples from 177 clinically suspicious pigmented lesions (in 168 patients) immediately before biopsy (Table S1). Each TS sample's miRNA profile was later matched to the lesion's histopathologic diagnosis, which included 80 MNs, 36 IMs, and 61 melanomas in situ (MIS). Patient age, sex, and anatomic distribution were consistent with expected clinical patterns across diagnostic categories (Figure 3A,B). Signals exceeded the LOQ in 96.61% of specimens (171/177) and did not correlate with cohort features (Figure S1). Consistent with prior tissue-based studies, the miR-21-5p:miR-125b-5p ratio was significantly higher in IM than in MN (p < 0.0001; Figure 3C). Receiver operating characteristic analysis demonstrated discrimination between IM and MN with an area under the curve (AUC) of 79.6% (95% bootstrap confidence interval [CI] 69.3%–89.8%) (Figure 3D). Using repeated 10-fold cross-validation (200 iterations), a cut point yielded a sensitivity of 69.4% (95% CI 63.9%–75.0%) and specificity of 80.0% (95% CI 80.0%–82.5%) when sensitivity and specificity were equally weighted. Weighting sensitivity twice as important increased sensitivity to 75.0% with reduced specificity (66.3%). MIS, which had not been previously evaluated using this ratio, showed intermediate values between MN and IM, differing significantly from MN, while remaining lower than IM (Figure 3C). When IM and MIS were combined, discrimination from MN was preserved (Figure 3E, AUC = 70.0%, 95% CI 62.3%–77.9%), with expected trade-offs between sensitivity and specificity depending on weighting. In the subset of samples with sufficient RNA yield to perform both assays, miRNA ratio performance compared favourably to TS mRNA markers (PRAME and LINC00518), demonstrating higher sensitivity and specificity and reinforcing the analytic robustness of the miRNA-based approach (Figure 3F,G). To assess assay robustness under extreme handling conditions, matched triads of tape-strip specimens from adjacent skin were either immediately processed or processed after 3 days at room temperature with and without 12 hours at high temperature (HT, 49°C) (Figure 3H). Resulting miR-21-5p:miR-125b-5p ratios showed acceptable precision (mean CV = 11.99%), indicating stable miRNA ratio signal preservation across these conditions. Conclusion: We demonstrate that a TS patch can collect stable miRs from skin lesions and that a miR-21-5p:miR-125b-5p ratio derived from these samples differentiates melanoma from MN with good discriminatory performance. This non-invasive approach recapitulates a melanoma-associated biomarker previously established in tissue within a real-world prospective cohort, supporting its potential utility for prioritising lesions for biopsy rather than for definitive diagnosis. Performance estimates were derived using conservative cross-validation, and confidence intervals remain relatively wide, reflecting the sample size and underscoring the need for larger, independent cohorts to further refine these metrics. The present study focuses on melanocytic lesions, which represent the primary source of diagnostic ambiguity prompting melanoma biopsy, rather than non-melanocytic skin tumours that are typically clinically distinct. While digital PCR provides high analytic sensitivity and precision, future validation studies will need to consider factors such as cost, throughput, reproducibility and platform selection. Importantly, the reported sensitivity indicates that not all melanomas would be identified by this approach, emphasising that it is not intended to exclude melanoma or replace biopsy, but rather to inform prioritisation of lesions for timely clinical evaluation. With further validation, such a strategy could help improve early melanoma detection, particularly in settings with limited access to dermatologic care. Conceptualization: DEKKER C. DEACON, DOUGLAS GROSSMAN and ROBERT L. JUDSON-TORRES. Formal analysis: CARLY A. BECKER, ROBERT L. JUDSON-TORRES, KENNETH M. BOUCHER and CHRIS J. STUBBEN. Funding acquisition: DOUGLAS GROSSMAN and ROBERT L. JUDSON-TORRES. Investigation: CARLY A. BECKER, DAVIDW.N. MWELWA, AMANDA Z. JIANG and ANNABELLE HUNTSMAN. Methodology: DOUGLAS GROSSMAN and ROBERT L. JUDSON-TORRES. Supervision: ROBERT L. JUDSON-TORRES. Original draft preparation: ROBERT L. JUDSON-TORRES. Writing—reviewing and editing: CARLY A. BECKER, ERIC A. SMITH, DEKKER C. DEACON, DOUGLAS GROSSMAN and ROBERT L. JUDSON-TORRES. We would like to thank the patients who consented and participated in this study. We thank Tristan Smart and Lisa West-Kincaid for assistance in collecting TS samples. We acknowledge the DNA Sequencing Core at the University of Utah and thank Derek Warner for their assistance. We acknowledge the High-Throughput Genomics Core at Huntsman Cancer Institute and thank Brian Dalley for their assistance. This work was supported by the National Cancer Institute (R01CA229896 to Robert L. Judson-Torres), the V Foundation (Translational Research Award T2022-007 to Douglas Grossman), and by direct support from the Huntsman Cancer Institute Melanoma Research Centre. Additional support was provided by the National Cancer Institute of the National Institutes of Health under Award Number P30CA042014 and the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number T32TR004392. The authors declare no conflict of interest. This study was approved by the University of Utah IRB (protocol #156786). All subjects provided written informed consent prior to participation. All primary data in the study are available upon request from the corresponding author. The sequencing data discussed in this publication have been deposited in NCBI's Gene Expression Omnibus (GEO) and are accessible through GEO Series accession number GSE286566. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

  PublisherOA PDFDOI

• 367 Landscape and Molecular/Clinical Correlates of Pathogenic Gene Fusions in Melanoma: A Comprehensive Molecular Profiling Study

  Laboratory Investigation · 2026-03-01

  article
  PublisherDOI

• Recurrent melanoma presenting as a rash: a case report

  Skin Health and Disease · 2025-09-04

  articleOpen accessSenior author

  Melanoma is the most aggressive form of common skin cancer and recurrence, while rare, typically presents as pigmented papules or nodules near the primary site. Here, we describe a case of a woman with stage IIIC melanoma undergoing intralesional talimogene laherparepvec (T-VEC) therapy who developed a spreading erythematous rash on her left leg, accompanied by fatigue and leg swelling. Skin biopsy revealed recurrent melanoma, with SOX10 and Melan-A positivity, and imaging showed features concerning for multifocal disease recurrence in the left popliteal fossa. This case highlights an unusual presentation of melanoma recurrence and underscores the importance of biopsy in -evaluating new skin findings in patients with a history of melanoma.

  PublisherOA PDFDOI

• Data from Assessing &lt;i&gt;MC1R&lt;/i&gt; Variants in Lentigo Maligna Melanoma within the Utah Population

  2025-07-28

  preprintOpen accessSenior author

  &lt;div&gt;Abstract&lt;p&gt;Lentigo maligna (LM) and lentigo maligna melanoma (LMM) arise from chronically sun-damaged skin. LM/LMM incidence continues to increase, particularly in Utah, where melanoma rates are twice the national average. The melanocortin-1 receptor (&lt;i&gt;MC1R&lt;/i&gt;) has been studied in melanocyte pigmentation and DNA repair but has yet to be thoroughly investigated in LM/LMM. We investigated allele and genotype frequencies of germline &lt;i&gt;MC1R&lt;/i&gt; variants among 175 Utah patients diagnosed with LM/LMM and 402 Utah reference individuals. The comparative analysis demonstrated an increased frequency of the D294H allele (0.046; &lt;i&gt;P&lt;/i&gt; = 0.0042) and a decreased frequency of the V60L allele (0.074; &lt;i&gt;P&lt;/i&gt; = 0.034) in patients with LM/LMM. The LM/LMM group demonstrated a higher OR compared with the Utah reference group associated with R151C homozygosity compared with heterozygous R151C [OR = 5.6; 95% confidence interval (CI), 0.98–32; &lt;i&gt;P&lt;/i&gt; = 0.052] and R151C homozygosity compared with wild type (OR = 5.7; 95% CI, 1.1–30; &lt;i&gt;P&lt;/i&gt; = 0.042). D294H heterozygosity was strongly associated with LM/LMM (OR = 3.8; 95% CI, 1.3–11; &lt;i&gt;P&lt;/i&gt; = 0.014). Conversely, V60L heterozygosity was less strongly associated with LM/LMM (OR = 0.52; 95% CI, 0.26–1.1; &lt;i&gt;P&lt;/i&gt; = 0.072). Stratified analyses showed no significant differences in age or gender across the key &lt;i&gt;MC1R&lt;/i&gt; variants studied. These data highlight significant differences in &lt;i&gt;MC1R&lt;/i&gt; allele frequencies in patients with LM/LMM, demonstrating that D294H is associated with increased LM/LMM risk, whereas the V60L variant is inversely associated with risk. This study provides the first comprehensive analysis of specific high-risk &lt;i&gt;MC1R&lt;/i&gt; variants in patients with LM/LMM in Utah.&lt;/p&gt;Significance:&lt;p&gt;Our study is the first comprehensive analysis of &lt;i&gt;MC1R&lt;/i&gt; germline variants in patients with LM/LMM in Utah, a region with an exceptionally high melanoma incidence. We draw new risk associations in LM/LMM, identifying an increased risk with the D294H and R151C variants. We also describe a novel inverse association for V60L, warranting further investigation. This study contributes to improved targeted risk stratification and an increased understanding of an understudied melanoma subtype.&lt;/p&gt;&lt;/div&gt;

  PublisherDOI

• A BRN2:MYC transcriptional axis regulates interconversion between therapy-resistant and tumorigenic phenotypes in melanoma

  Cell Reports · 2025-12-01

  articleOpen access

  Metastatic spread and therapeutic resistance are the principal causes of cancer mortality. For melanoma, these processes rely on the capacity of cells to switch between transcriptional states. Although targeting transcriptional states pharmacologically is promising, the mechanisms by which melanoma cells switch between states-and how these processes differ from melanocytes-remain poorly understood. Here, we isolate distinct melanoma states with unique phenotypes: a MYC-driven state, essential for tumor initiation yet sensitive to BRAF inhibition, and a dedifferentiated, invasive BRN2-high state enriched in therapy-resistant cells but not directly tumorigenic. Transitions between phenotypes occur through intermediate, more differentiated states. Unexpectedly, the BRN2-high state is also present in melanocytes, whereas the MYC state is exclusive to melanoma. Melanoma cells also exhibit an increased frequency of transitions across states. These findings highlight that accelerated phenotypic switching, rather than mere state diversity, is a defining feature of melanoma progression.

  PublisherDOI

• Clinicopathologic Correlation in a Case of Scurvy

  American Journal of Dermatopathology · 2025-12-22

  articleSenior author

  ABSTRACT: Scurvy is an uncommon diagnosis in developed countries, yet it remains an important clinical consideration in patients with restrictive diets. In this study, we report a case of a male patient with a history of sclerosing mesenteritis and chronic dietary restriction who presented with bilateral leg purpura, perifollicular hemorrhage, and gingival bleeding. His cutaneous findings initially raised concern for vasculitis or coagulopathy. However, histopathology revealed classic features of scurvy and an undetectable vitamin C level confirmed the diagnosis. Oral vitamin C supplementation led to rapid clinical improvement. This case emphasizes the importance of a thorough dietary history and skin examination in patients presenting with mucocutaneous bleeding.

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Frequent coauthors

• Robert L. Judson‐Torres

  University of Utah

  20 shared

• Douglas Grossman

  University of Utah

  11 shared

• R.L. Belote

  Huntsman Cancer Institute

  9 shared

• John Hyngstrom

  University of Utah

  8 shared

• Kenneth M. Boucher

  8 shared

• Chris Stubben

  Huntsman Cancer Institute

  8 shared

• C. Neil

  University of California, San Diego

  8 shared

• Eric Adler

  UC San Diego Health System

  7 shared

Education

• M.D.

  University of Utah