About

Dr. Robert L. Judson-Torres is a professor at the Spencer Fox Eccles School of Medicine, affiliated with the Department of Dermatology and the Huntsman Cancer Institute at the University of Utah. He earned his Ph.D. from the University of California, San Francisco in Biomedical Sciences in 2012, where he discovered and mechanistically dissected microRNAs that mediate somatic cell reprogramming. His early career was marked by receiving the NIH Director’s Early Independence Award and initiating an independent research program as a Sandler Fellow at UCSF. From 2014 to 2019, he led a research group at UCSF's Helen Diller Family Comprehensive Cancer Center, pioneering the use of CRISPR/Cas9 engineering in primary human melanocytes to model melanoma initiation and focusing on identifying transcriptional programs that precede tumorigenesis. His research aims to understand the dynamic transcriptional and epigenetic programs regulating human melanocytes and how disruptions in these programs contribute to early melanoma development. His laboratory employs techniques such as single-cell sequencing, live quantitative phase imaging, and CRISPR/Cas9-based precision engineering to study primary human melanocytes and melanoma cell lines. His translational work includes identifying transcriptional programs as potential biomarkers for early melanoma diagnosis and discovering compounds that alter the probability of transformation. Dr. Judson-Torres is also dedicated to mentoring students across various educational levels and emphasizes the importance of community service, participating in career development workshops, university committees, and organizing symposia related to his field.

Selected publications

• Figure 2 from Assessing <i>MC1R</i> Variants in Lentigo Maligna Melanoma within the Utah Population

  2025-07-28

  preprintOpen access

  <p>Specific <i>MC1R</i> genotypes confer an increased risk of developing LM/LMM. The heatmaps display the percentage frequencies of <i>MC1R</i> genotypes within two cohorts: (<b>A</b>) Mohs LM/LMM cohort and (<b>B</b>) the Utah reference group. The heatmaps are color-coded to reflect genotype percentages, with red indicating higher frequencies and green indicating lower frequencies. This comparison highlights the differential distribution of <i>MC1R</i> genotypes between patients with LM/LMM and the Utah reference group. * denotes samples for which we calculated an OR compared with WT or heterozygous/homozygous genotypes.</p>

  PublisherDOI

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

  Cell Reports · 2025-12-01

  articleOpen accessSenior author

  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

• Table 1 from Assessing <i>MC1R</i> Variants in Lentigo Maligna Melanoma within the Utah Population

  2025-07-28

  preprintOpen access

  <p>Key demographic characteristics of patients with LM/LMM in the study (<i>n</i> = 175)</p>

  PublisherDOI

• Data from Assessing <i>MC1R</i> Variants in Lentigo Maligna Melanoma within the Utah Population

  2025-07-28

  preprintOpen access

  <div>Abstract<p>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 (<i>MC1R</i>) 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 <i>MC1R</i> 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; <i>P</i> = 0.0042) and a decreased frequency of the V60L allele (0.074; <i>P</i> = 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; <i>P</i> = 0.052] and R151C homozygosity compared with wild type (OR = 5.7; 95% CI, 1.1–30; <i>P</i> = 0.042). D294H heterozygosity was strongly associated with LM/LMM (OR = 3.8; 95% CI, 1.3–11; <i>P</i> = 0.014). Conversely, V60L heterozygosity was less strongly associated with LM/LMM (OR = 0.52; 95% CI, 0.26–1.1; <i>P</i> = 0.072). Stratified analyses showed no significant differences in age or gender across the key <i>MC1R</i> variants studied. These data highlight significant differences in <i>MC1R</i> 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 <i>MC1R</i> variants in patients with LM/LMM in Utah.</p>Significance:<p>Our study is the first comprehensive analysis of <i>MC1R</i> 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.</p></div>

  PublisherDOI

• The miR-290 and miR-302 clusters are essential for reprogramming of fibroblasts to induced pluripotent stem cells

  Stem Cells · 2025-02-01 · 4 citations

  articleOpen access

  The miR-290 and miR-302 clusters of microRNAs are highly expressed in naïve and primed pluripotent stem cells, respectively. Ectopic expression of the embryonic stem cell (ESC)-specific cell cycle regulating family of microRNAs arising from these two clusters dramatically enhances the reprogramming of both mouse and human somatic cells to induced pluripotency. Here, we used genetic knockouts to dissect the requirement for the miR-290 and miR-302 clusters during the reprogramming of mouse fibroblasts into induced pluripotent stem cells (iPSCs) with retrovirally introduced Oct4, Sox2, and Klf4. Knockout of either cluster alone did not negatively impact the efficiency of reprogramming. Resulting cells appeared identical to their ESC microRNA cluster knockout counterparts. In contrast, the combined loss of both clusters blocked the formation of iPSCs. While rare double knockout clones could be isolated, they showed a dramatically reduced proliferation rate, a persistent inability to fully silence the exogenously introduced pluripotency factors, and a transcriptome distinct from individual miR-290 or miR-302 mutant ESC and iPSCs. Taken together, our data show that miR-290 and miR-302 are essential yet interchangeable in reprogramming to the induced pluripotent state.

  PublisherOA PDFDOI

• Assessing <i>MC1R</i> Variants in Lentigo Maligna Melanoma within the Utah Population

  Cancer Research Communications · 2025-07-01

  articleOpen access

  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 (MC1R) 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 MC1R 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; P = 0.0042) and a decreased frequency of the V60L allele (0.074; P = 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; P = 0.052] and R151C homozygosity compared with wild type (OR = 5.7; 95% CI, 1.1-30; P = 0.042). D294H heterozygosity was strongly associated with LM/LMM (OR = 3.8; 95% CI, 1.3-11; P = 0.014). Conversely, V60L heterozygosity was less strongly associated with LM/LMM (OR = 0.52; 95% CI, 0.26-1.1; P = 0.072). Stratified analyses showed no significant differences in age or gender across the key MC1R variants studied. These data highlight significant differences in MC1R 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 MC1R variants in patients with LM/LMM in Utah. SIGNIFICANCE: Our study is the first comprehensive analysis of MC1R 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.

  PublisherOA PDFDOI

• Supplementary Table 2 from Assessing &lt;i&gt;MC1R&lt;/i&gt; Variants in Lentigo Maligna Melanoma within the Utah Population

  2025-07-28

  supplementary-materialsOpen access

  &lt;p&gt;Table of the Utah reference group data&lt;/p&gt;

  PublisherDOI

• Recent advances in gene delivery for melanocyte-associated disorders

  Advanced Drug Delivery Reviews · 2025-10-04

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Rapid activation of ARF6 after RAF inhibition augments BRAFV600E and promotes therapy resistance

  Research Square · 2025-08-27

  preprintOpen access
  PublisherOA PDFDOI

• Subclinical fields of <i>BRAF</i> V600E-mutant melanocytes populate human skin and are enriched around melanoma and naevi

  British Journal of Dermatology · 2025-10-17 · 2 citations

  articleOpen access

  BACKGROUND: The origins of cutaneous melanoma are often traced to visible precursor lesions (e.g. melanocytic naevi), but approximately two-thirds of melanomas arise from clinically healthy skin with no detectable precursor lesion. The BRAF V600E mutation drives melanoma and naevus formation, but eruptive naevi syndromes and the disproportionate role early-life ultraviolet exposure plays in melanoma risk suggest the presence of a hidden field of oncogene-mutant melanocytes in clinically healthy skin, which may represent an earlier step in tumorigenesis. OBJECTIVES: To determine whether BRAF V600E-mutant melanocytes were commonly present in nonlesional skin from adults at high risk of melanoma. METHODS: We examined BRAF V600E mutations in 97 histologically and clinically healthy, nonlesional skin samples from an Australian cohort of individuals at high risk of melanoma. The skin selected was adjacent to a naevus or a prior melanoma site; photodamaged skin proximal (approximately 5 cm) from melanoma excision; photoprotected skin distant from lesions; and low-risk neonatal foreskin-derived melanoblasts. We used immunohistochemistry to locate BRAF V600E-mutant cells in histopathology sections; droplet digital polymerase chain reaction to determine the fractional abundance of BRAF V600E in whole skin; and single-cell RNA sequencing to confirm cells as melanocytes and detect their transcriptional programmes. RESULTS: We identified BRAF V600E-mutant melanocytes in skin surrounding naevi and primary melanomas, even years after tumour excision. Fields of BRAF V600E-mutant melanocytes were commonly found in the skin of patients at high risk for melanoma and were up to 20-fold denser and 50% more frequent in tumour-adjacent skin. Field cells exhibited a gene expression profile characteristic of BRAF V600E-induced growth arrest, consistent with dormant yet genetically primed cells. CONCLUSIONS: There is a reservoir of oncogene-harbouring melanocytes in normal skin. Our findings challenge the prevailing notion that melanocyte expression of BRAF V600E is inherently tumorigenic. The presence of such fields suggests that the scope of melanoma detection and prevention efforts might be extended beyond visible lesions, to encompass potentially precancerous fields of driver-mutant cells. An author video to accompany this article is available online.

  PublisherDOI

Awards & honors

• NIH Director’s Early Independence Award
• Sandler Fellow in the UCSF Program for Breakthrough Biomedic…