Bio
A native of Queens, New York, Dr. Carolyn Lee joined the Stanford Dermatology faculty in February of 2016 as a specialist in the management of patients at a high risk for developing skin cancer. This year, she has been a featured presenter at both the Society for Investigative Dermatology Annual Meeting and the Gordon Research Conference on Epithelial Differentiation and Keratinization. Dr. Lee graduated with honors from Yale University in 1998 with a BS in Biology and received her MD and PhD from Georgetown University with a specialty in tumor biology in 2006. She completed her Dermatology residency at Stanford in 2010 and a Postdoctoral Fellowship in epithelial biology in the lab of Dr. Paul Khavari in December of 2015. Dr. Lee possesses a strong interest in understanding the mechanisms of high-risk non-melanoma skin cancer and is currently a member of Stanford’s High-Risk Non-Melanoma Skin Cancer Working Group.
Clinical Focus
- Dermatology
- General Dermatology
- Skin cancer
- Cutaneous oncology
- Transplant Dermatology
- Squamous cell carcinoma
- Basal Cell Carcinoma
Academic Appointments
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Assistant Professor, Dermatology
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Member, Bio-X
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Member, Stanford Cancer Institute
Honors & Awards
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Academic Research Award, Women’s Dermatologic Society (2009)
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F32 Ruth L. Kirschstein National Research Service Award, National Institutes of Health (2010-2013)
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K08 Mentored Clinical Scientist Development Award, National Institutes of Health (2013-2018)
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Research Grant, Dermatology Foundation (2016)
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Kimmel Scholar Award, Sidney Kimmel Foundation (2017-2019)
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Milstein Research Scholar Award in Melanoma/Non-Melanoma Skin Cancer, American Skin Association (2018)
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Clinical Scientist Development Award, Doris Duke Charitable Foundation (2018-2021)
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SPARK Project Grant, SPARK Translational Research Program at Stanford (2019-2021)
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Scholar-Innovator Award, Harrington Discovery Institute (2022-2024)
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Award for Excellence, SPARK Translational Research Program at Stanford (2023)
Professional Education
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Medical Education: Georgetown University School of Medicine (2006) DC
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Internship: Saint Joseph Mercy Ann Arbor Transitional Year (2007) MI
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Residency: Stanford University Dermatology Residency (2010) CA
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Board Certification: American Board of Dermatology, Dermatology (2010)
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Bachelor of Science, Yale University, Biology, CT (1998)
Clinical Trials
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Analysis of Cutaneous and Hematologic Disorders by High-Throughput Nucleic Acid Sequencing
Not 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.
Stanford is currently not accepting patients for this trial. For more information, please contact Alexander Ungewickell, 650-723-6661.
All Publications
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Gene expression landscape of cutaneous squamous cell carcinoma progression.
The British journal of dermatology
2024
Abstract
Cutaneous squamous cell carcinomas (SCC) are the second most common human cancer and have been characterized by RNA sequencing (RNA-Seq); however, the transferability of findings from individual studies may be limited by small sample sizes and diverse analysis protocols.To define the transcriptome landscape at different stages in the progression of normal skin to SCC through a meta-analysis of publicly available RNA-Seq samples.Whole-transcriptome data from 73 normal skin samples, 46 actinic keratoses (AK), 16 in situ SCC, 13 keratoacanthomas (KA), and 147 SCC (including 30 SCC from immunocompromised patients and 8 SCC from individuals with recessive dystrophic epidermolysis bullosa [RDEB]) was uniformly processed to harmonize gene expression. Differential expression, fusion detection, and cell-type deconvolution analyses were performed.Individual RNA-Seq studies of SCC demonstrated study-specific clustering and varied widely in their differential gene expression detection. Following batch correction, we defined a consensus set of differentially expressed genes (DEGs), including those altered in the preinvasive stages of SCC development, and used single-cell RNA-Seq data to demonstrate that DEGs are often, but not always, expressed by tumor-specific keratinocytes (TSKs). Analysis of the cellular composition of SCC, KA, and RDEB-SCC identified an increase in differentiated keratinocytes in KA, while RDEB-SCC contained the most TSKs. Compared to SCC arising in immunocompetent patients, SCC from immunosuppressed individuals demonstrated fewer memory B cells and CD8 T cells. A comprehensive and unbiased search for fusion transcripts in SCC and intermediate disease stages identified few candidates that recur in >1% of all specimens, suggesting most SCC are not driven by oncogenic gene fusions. Finally, using GTEx data, we distilled a novel 300-gene signature of chronic sun exposure that affirms greater cumulative ultraviolet (UV) exposure in later stages of SCC development.Our results define the gene expression landscape of SCC progression, characterize cell subpopulation heterogeneity in SCC subtypes that contribute to their distinct clinical phenotypes, demonstrate that gene fusions are not a common cause of SCC, and identify UV-responsive genes associated with SCC development.
View details for DOI 10.1093/bjd/ljae249
View details for PubMedID 38867481
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Unravelling the landscape of skin cancer through single-cell transcriptomics.
Translational oncology
2022; 27: 101557
Abstract
The human skin is a complex organ that forms the first line of defense against pathogens and external injury. It is composed of a wide variety of cells that work together to maintain homeostasis and prevent disease, such as skin cancer. The exponentially rising incidence of skin malignancies poses a growing public health challenge, particularly when the disease course is complicated by metastasis and therapeutic resistance. Recent advances in single-cell transcriptomics have provided a high-resolution view of gene expression heterogeneity that can be applied to skin cancers to define cell types and states, understand disease evolution, and develop new therapeutic concepts. This approach has been particularly valuable in characterizing the contribution of immune cells in skin cancer, an area of great clinical importance given the increasing use of immunotherapy in this setting. In this review, we highlight recent skin cancer studies utilizing bulk RNA sequencing, introduce various single-cell transcriptomics approaches, and summarize key findings obtained by applying single-cell transcriptomics to skin cancer.
View details for DOI 10.1016/j.tranon.2022.101557
View details for PubMedID 36257209
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MAB21L4 deficiency drives squamous cell carcinoma via activation of RET.
Cancer research
2022
Abstract
Epithelial squamous cell carcinomas (SCC) most commonly originate in the skin, where they display disruptions in the normally tightly regulated homeostatic balance between keratinocyte proliferation and terminal differentiation. We performed a transcriptome-wide screen for genes of unknown function that possess inverse expression patterns in differentiating keratinocytes compared to cutaneous SCC (cSCC), leading to the identification of MAB21L4 (C2ORF54) as an enforcer of terminal differentiation that suppresses carcinogenesis. Loss of MAB21L4 in human cSCC organoids increased expression of RET to enable malignant progression. In addition to transcriptional upregulation of RET, deletion of MAB21L4 preempted recruitment of the CacyBP-Siah1 E3 ligase complex to RET and reduced its ubiquitylation. In SCC organoids and in vivo tumor models, genetic disruption of RET or selective inhibition of RET with BLU-667 (pralsetinib) suppressed SCC growth while inducing concomitant differentiation. Overall, loss of MAB21L4 early during SCC development blocks differentiation by increasing RET expression. These results suggest that targeting RET activation is a potential therapeutic strategy for treating SCC.
View details for DOI 10.1158/0008-5472.CAN-22-0047
View details for PubMedID 35705526
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Recurrent bilateral cutaneous squamous cell carcinoma arising within pretibial hypertrophic lichen planus with metastasis while on cemiplimab
Journal of the American Academy of Dermatology Case Reports
2022
View details for DOI 10.1016/j.jdcr.2022.08.046
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Mutant collagen COL11A1 enhances cancerous invasion.
Oncogene
2021
Abstract
Collagens are the most abundant proteins in the body and comprise the basement membranes and stroma through which cancerous invasion occurs; however, a pro-neoplastic function for mutant collagens is undefined. Here we identify COL11A1 mutations in 66 of 100 cutaneous squamous cell carcinomas (cSCCs), the second most common U.S. cancer, concentrated in a triple helical region known to produce trans-dominant collagens. Analysis of COL11A1 and other collagen genes found that they are mutated across common epithelial malignancies. Knockout of mutant COL11A1 impairs cSCC tumorigenesis in vivo. Compared to otherwise genetically identical COL11A1 wild-type tissue, gene-edited mutant COL11A1 skin is characterized by induction of beta1 integrin targets and accelerated neoplastic invasion. In mosaic tissue, mutant COL11A1 cells enhanced invasion by neighboring wild-type cells. These results suggest that specific collagens are commonly mutated in cancer and that mutant collagens may accelerate this process.
View details for DOI 10.1038/s41388-021-02013-y
View details for PubMedID 34584216
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Molecular Profiling of Cutaneous C-Group Non-Langerhans Cell Histiocytoses
SPRINGERNATURE. 2021: 319
View details for Web of Science ID 000629690900270
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Molecular Profiling of Cutaneous C-Group Non-Langerhans Cell Histiocytoses
SPRINGERNATURE. 2021: 319
View details for Web of Science ID 000629694100270
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PD-L1 Expression and Tumor-Infiltrating Lymphocytes in High-Risk and Metastatic Cutaneous Squamous Cell Carcinoma
OTOLARYNGOLOGY-HEAD AND NECK SURGERY
2019; 160 (1): 93–99
View details for DOI 10.1177/0194599818788057
View details for Web of Science ID 000454870600012
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PD-L1 Expression and Tumor-Infiltrating Lymphocytes in High-Risk and Metastatic Cutaneous Squamous Cell Carcinoma.
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
2018: 194599818788057
Abstract
Objective To characterize programmed death-ligand 1 (PD-L1) expression and tumor-infiltrating lymphocyte (TIL) positivity for locally aggressive or regionally metastatic cutaneous head and neck squamous cell carcinoma (cHNSCC). Study Design Retrospective chart review, followed by immunohistochemical staining of archived tumor specimens. Setting Tertiary academic medical center. Subjects and Methods After identification of 101 patients treated surgically for locally advanced or regionally metastatic cHNSCC, archived tissue was stained and graded for PD-L1 expression in addition to TIL presence. Cross-tabulation was performed to examine the association between either of these variables and clinicopathologic features and outcomes. Results A total of 101 patients met inclusion criteria, but archived tissue was available only for 83 (31 primaries, 52 metastases). The majority of primary tumors demonstrated grade 1 PD-L1 staining, while grade 2 staining was more likely for metastases. Neither high- nor low-grade PD-L1 expression correlated with any clinicopathologic variable for primary tumors. However, for metastases, high-grade staining was significantly associated with regional recurrence (15 of 19, P = .02). TILs were present for 65% of primary tumors and 90% of regional metastases but did not correlate with any clinicopathologic variables. Conclusion Diffuse expression of PD-L1 in this study highlights the possibility of using immunotherapy in the form of programmed death 1/PD-L1 blockade to improve treatment for this devastating disease. However, further studies are needed to clarify the significance of PD-L1 expression and TIL positivity for locally advanced or regionally metastatic cHNSCC.
View details for PubMedID 30012051
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Cancer-Associated Long Noncoding RNA SMRT-2 Controls Epidermal Differentiation
JOURNAL OF INVESTIGATIVE DERMATOLOGY
2018; 138 (6): 1445–49
View details for PubMedID 29360484
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Node-positive cutaneous squamous cell carcinoma of the head and neck: Survival, high-risk features, and adjuvant chemoradiotherapy outcomes.
Head & neck
2017
Abstract
Data lacks to guide treatment of regionally metastatic cutaneous head and neck squamous cell carcinoma (HNSCC).We conducted a retrospective review of 80 patients treated for regionally metastatic cutaneous HNSCC. The effect of various clinicopathologic variables on overall survival (OS) was investigated, in addition to outcomes by treatment modality.On multivariate regression, cutaneous primary >2 cm (p = .03) and extracapsular spread (ECS; p = .01) were significantly associated with decreased OS. Location of regional metastasis (neck vs parotid vs both) had no effect on OS (p = .2), nor did the presence of a cutaneous primary at the time of presentation (p = .9). The 3-year survival was 43%, 52%, and 49% for surgery alone, adjuvant radiation, and adjuvant chemoradiation, respectively. Fifty-one percent of patients had a recurrence of their disease.Regionally metastatic cutaneous HNSCC is an aggressive disease associated with high recurrence rates. Patients with tumors >2 cm and ECS have poorer OS despite adjuvant therapy. © 2017 Wiley Periodicals, Inc. Head Neck 39: 881-885, 2017.
View details for DOI 10.1002/hed.24692
View details for PubMedID 28252823
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Factors That May Promote an Effective Local Research Environment
JOURNAL OF INVESTIGATIVE DERMATOLOGY
2016; 136 (8): 1529–31
View details for PubMedID 27450496
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Skin Cancer Prevention and Treatment in Solid Organ Transplant Patients: A Survey of the International Transplant Skin Cancer Collaborative.
Dermatologic surgery
2016; 42 (5): 682-683
View details for DOI 10.1097/DSS.0000000000000668
View details for PubMedID 27045747
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Mutations in the Kinetochore Gene KNSTRN in Basal Cell Carcinoma.
journal of investigative dermatology
2015; 135 (12): 3197-3200
View details for DOI 10.1038/jid.2015.339
View details for PubMedID 26348826
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Genomic analysis of mycosis fungoides and Sézary syndrome identifies recurrent alterations in TNFR2.
Nature genetics
2015; 47 (9): 1056-1060
Abstract
Mycosis fungoides and Sézary syndrome comprise the majority of cutaneous T cell lymphomas (CTCLs), disorders notable for their clinical heterogeneity that can present in skin or peripheral blood. Effective treatment options for CTCL are limited, and the genetic basis of these T cell lymphomas remains incompletely characterized. Here we report recurrent point mutations and genomic gains of TNFRSF1B, encoding the tumor necrosis factor receptor TNFR2, in 18% of patients with mycosis fungoides and Sézary syndrome. Expression of the recurrent TNFR2 Thr377Ile mutant in T cells leads to enhanced non-canonical NF-κB signaling that is sensitive to the proteasome inhibitor bortezomib. Using an integrative genomic approach, we additionally discovered a recurrent CTLA4-CD28 fusion, as well as mutations in downstream signaling mediators of these receptors.
View details for DOI 10.1038/ng.3370
View details for PubMedID 26258847
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Genomic analysis of mycosis fungoides and Sezary syndrome identifies recurrent alterations in TNFR2
NATURE GENETICS
2015; 47 (9): 1056-?
Abstract
Mycosis fungoides and Sézary syndrome comprise the majority of cutaneous T cell lymphomas (CTCLs), disorders notable for their clinical heterogeneity that can present in skin or peripheral blood. Effective treatment options for CTCL are limited, and the genetic basis of these T cell lymphomas remains incompletely characterized. Here we report recurrent point mutations and genomic gains of TNFRSF1B, encoding the tumor necrosis factor receptor TNFR2, in 18% of patients with mycosis fungoides and Sézary syndrome. Expression of the recurrent TNFR2 Thr377Ile mutant in T cells leads to enhanced non-canonical NF-κB signaling that is sensitive to the proteasome inhibitor bortezomib. Using an integrative genomic approach, we additionally discovered a recurrent CTLA4-CD28 fusion, as well as mutations in downstream signaling mediators of these receptors.
View details for DOI 10.1038/ng.3370
View details for Web of Science ID 000360394100016
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Recurrent point mutations in the kinetochore gene KNSTRN in cutaneous squamous cell carcinoma
NATURE GENETICS
2014; 46 (10): 1060-1062
Abstract
Here we report the discovery of recurrent mutations concentrated at an ultraviolet signature hotspot in KNSTRN, which encodes a kinetochore protein, in 19% of cutaneous squamous cell carcinomas (SCCs). Cancer-associated KNSTRN mutations, most notably those encoding p.Ser24Phe, disrupt chromatid cohesion in normal cells, occur in SCC precursors, correlate with increased aneuploidy in primary tumors and enhance tumorigenesis in vivo. These findings suggest a role for KNSTRN mutagenesis in SCC development.
View details for DOI 10.1038/ng.3091
View details for Web of Science ID 000342554100007
View details for PubMedCentralID PMC4324615
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Recurrent point mutations in the kinetochore gene KNSTRN in cutaneous squamous cell carcinoma.
Nature genetics
2014; 46 (10): 1060-1062
Abstract
Here we report the discovery of recurrent mutations concentrated at an ultraviolet signature hotspot in KNSTRN, which encodes a kinetochore protein, in 19% of cutaneous squamous cell carcinomas (SCCs). Cancer-associated KNSTRN mutations, most notably those encoding p.Ser24Phe, disrupt chromatid cohesion in normal cells, occur in SCC precursors, correlate with increased aneuploidy in primary tumors and enhance tumorigenesis in vivo. These findings suggest a role for KNSTRN mutagenesis in SCC development.
View details for DOI 10.1038/ng.3091
View details for PubMedID 25194279
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Control of somatic tissue differentiation by the long non-coding RNA TINCR.
Nature
2013; 493 (7431): 231-235
Abstract
Several of the thousands of human long non-coding RNAs (lncRNAs) have been functionally characterized; however, potential roles for lncRNAs in somatic tissue differentiation remain poorly understood. Here we show that a 3.7-kilobase lncRNA, terminal differentiation-induced ncRNA (TINCR), controls human epidermal differentiation by a post-transcriptional mechanism. TINCR is required for high messenger RNA abundance of key differentiation genes, many of which are mutated in human skin diseases, including FLG, LOR, ALOXE3, ALOX12B, ABCA12, CASP14 and ELOVL3. TINCR-deficient epidermis lacked terminal differentiation ultrastructure, including keratohyalin granules and intact lamellar bodies. Genome-scale RNA interactome analysis revealed that TINCR interacts with a range of differentiation mRNAs. TINCR-mRNA interaction occurs through a 25-nucleotide 'TINCR box' motif that is strongly enriched in interacting mRNAs and required for TINCR binding. A high-throughput screen to analyse TINCR binding capacity to approximately 9,400 human recombinant proteins revealed direct binding of TINCR RNA to the staufen1 (STAU1) protein. STAU1-deficient tissue recapitulated the impaired differentiation seen with TINCR depletion. Loss of UPF1 and UPF2, both of which are required for STAU1-mediated RNA decay, however, did not have differentiation effects. Instead, the TINCR-STAU1 complex seems to mediate stabilization of differentiation mRNAs, such as KRT80. These data identify TINCR as a key lncRNA required for somatic tissue differentiation, which occurs through lncRNA binding to differentiation mRNAs to ensure their expression.
View details for DOI 10.1038/nature11661
View details for PubMedID 23201690
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Control of somatic tissue differentiation by the long non-coding RNA TINCR
NATURE
2013; 493 (7431): 231-U245
Abstract
Several of the thousands of human long non-coding RNAs (lncRNAs) have been functionally characterized; however, potential roles for lncRNAs in somatic tissue differentiation remain poorly understood. Here we show that a 3.7-kilobase lncRNA, terminal differentiation-induced ncRNA (TINCR), controls human epidermal differentiation by a post-transcriptional mechanism. TINCR is required for high messenger RNA abundance of key differentiation genes, many of which are mutated in human skin diseases, including FLG, LOR, ALOXE3, ALOX12B, ABCA12, CASP14 and ELOVL3. TINCR-deficient epidermis lacked terminal differentiation ultrastructure, including keratohyalin granules and intact lamellar bodies. Genome-scale RNA interactome analysis revealed that TINCR interacts with a range of differentiation mRNAs. TINCR-mRNA interaction occurs through a 25-nucleotide 'TINCR box' motif that is strongly enriched in interacting mRNAs and required for TINCR binding. A high-throughput screen to analyse TINCR binding capacity to approximately 9,400 human recombinant proteins revealed direct binding of TINCR RNA to the staufen1 (STAU1) protein. STAU1-deficient tissue recapitulated the impaired differentiation seen with TINCR depletion. Loss of UPF1 and UPF2, both of which are required for STAU1-mediated RNA decay, however, did not have differentiation effects. Instead, the TINCR-STAU1 complex seems to mediate stabilization of differentiation mRNAs, such as KRT80. These data identify TINCR as a key lncRNA required for somatic tissue differentiation, which occurs through lncRNA binding to differentiation mRNAs to ensure their expression.
View details for DOI 10.1038/nature11661
View details for Web of Science ID 000313259600041
View details for PubMedID 23201690
View details for PubMedCentralID PMC3674581
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Transcriptome sequencing in Sezary syndrome identifies Sezary cell and mycosis fungoides-associated lncRNAs and novel transcripts
BLOOD
2012; 120 (16): 3288-3297
Abstract
Sézary syndrome (SS) is an aggressive cutaneous T-cell lymphoma (CTCL) of unknown etiology in which malignant cells circulate in the peripheral blood. To identify viral elements, gene fusions, and gene expression patterns associated with this lymphoma, flow cytometry was used to obtain matched pure populations of malignant Sézary cells (SCs) versus nonmalignant CD4(+) T cells from 3 patients for whole transcriptome, paired-end sequencing with an average depth of 112 million reads per sample. Pathway analysis of differentially expressed genes identified mis-regulation of PI3K/Akt, TGFβ, and NF-κB pathways as well as T-cell receptor signaling. Bioinformatic analysis did not detect either nonhuman transcripts to support a viral etiology of SS or recurrently expressed gene fusions, but it did identify 21 SC-associated annotated long noncoding RNAs (lncRNAs). Transcriptome assembly by multiple algorithms identified 13 differentially expressed unannotated transcripts termed Sézary cell-associated transcripts (SeCATs) that include 12 predicted lncRNAs and a novel transcript with coding potential. High-throughput sequencing targeting the 3' end of polyadenylated transcripts in archived tumors from 24 additional patients with tumor-stage CTCL confirmed the differential expression of SC-associated lncRNAs and SeCATs in CTCL. Our findings characterize the SS transcriptome and support recent reports that implicate lncRNA dysregulation in human malignancies.
View details for DOI 10.1182/blood-2012-04-423061
View details for PubMedID 22936659
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Rapid identification of non-human sequences in high-throughput sequencing datasets
BIOINFORMATICS
2012; 28 (8): 1174-1175
Abstract
Rapid identification of non-human sequences (RINS) is an intersection-based pathogen detection workflow that utilizes a user-provided custom reference genome set for identification of non-human sequences in deep sequencing datasets. In <2 h, RINS correctly identified the known virus in the dataset SRR73726 and is compatible with any computer capable of running the prerequisite alignment and assembly programs. RINS accurately identifies sequencing reads from intact or mutated non-human genomes in a dataset and robustly generates contigs with these non-human sequences (Supplementary Material).RINS is available for free download at http://khavarilab.stanford.edu/resources.html.
View details for DOI 10.1093/bioinformatics/bts100
View details for Web of Science ID 000302806900022
View details for PubMedID 22377895
View details for PubMedCentralID PMC3324519
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Suppression of progenitor differentiation requires the long noncoding RNA ANCR
GENES & DEVELOPMENT
2012; 26 (4): 338-343
Abstract
Long noncoding RNAs (lncRNAs) regulate diverse processes, yet a potential role for lncRNAs in maintaining the undifferentiated state in somatic tissue progenitor cells remains uncharacterized. We used transcriptome sequencing and tiling arrays to compare lncRNA expression in epidermal progenitor populations versus differentiating cells. We identified ANCR (anti-differentiation ncRNA) as an 855-base-pair lncRNA down-regulated during differentiation. Depleting ANCR in progenitor-containing populations, without any other stimuli, led to rapid differentiation gene induction. In epidermis, ANCR loss abolished the normal exclusion of differentiation from the progenitor-containing compartment. The ANCR lncRNA is thus required to enforce the undifferentiated cell state within epidermis.
View details for DOI 10.1101/gad.182121.111
View details for Web of Science ID 000300626800004
View details for PubMedID 22302877
View details for PubMedCentralID PMC3289881
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Adoption of Western Culture by Californian Asian Americans Attitudes and Practices Promoting Sun Exposure
International Investigative Dermatology Meeting
AMER MEDICAL ASSOC. 2009: 552–56
Abstract
To investigate whether the adoption of Western culture is associated with attitudes and practices promoting sun exposure among Asian Americans.Survey conducted from November 28, 2007, to January 28, 2008.Primarily northern California community groups via online survey.Adult volunteers who self-identified as Asian American.Results based on 546 questionnaires returned.The overall response rate was 74.4%. Multivariate regression analysis controlling for age and skin type showed that westernization (as determined by generation in the United States, location raised, or self-rated acculturation) was associated with attitudes and behaviors promoting sun exposure (including the belief that having a tan is attractive, negative attitudes toward use of sunscreen and sun protective clothing, and increased weekend sun exposure, lying out to get a tan, and tanning bed use) at a level of P < .05.Our data suggest that adoption of Western culture may be associated with attitudes and behaviors promoting sun exposure among Asian Americans. This group should be targeted by dermatologists for increased education regarding sun protection, solar damage, and skin cancer prevention and detection.
View details for Web of Science ID 000266207400006
View details for PubMedID 19451499
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Expression of cyclooxygenase-2 and peroxisome proliferator-activated receptor gamma during malignant melanoma progression
JOURNAL OF CUTANEOUS PATHOLOGY
2008; 35 (11): 989-994
Abstract
Cancer chemoprevention using nonsteroidal anti-inflammatory drugs is frequently attributed to cyclooxygenase-2 (COX-2) inhibition, although recent studies suggest that peroxisome proliferator-activated receptor gamma (PPARgamma) may also be involved. While surgical excision remains the treatment mainstay for localized malignant melanoma, certain high-risk patients may benefit from adjunctive chemotherapy. In this study, we compared COX-2 and PPARgamma immunohistological staining in benign nevi, primary melanomas and metastatic melanomas to help predict the effectiveness of compounds targeting these markers.COX-2 and PPARgamma immunohistological staining was performed and reviewed in 99 melanocytic lesions, including 38 benign nevi, 32 primary melanomas and 29 metastatic melanomas.There was a significant increase in both COX-2 and PPARgamma immunostaining in melanomas compared with benign nevi. Metastatic melanomas were more likely to have a higher number of PPARgamma-immunopositive cells. They were also more likely to express COX-2 than primary melanomas. Neither COX-2 nor PPARgamma expression was associated with a specific pathologic subtype.COX-2 and PPARgamma may help modulate the progression of melanocytic precursor lesions to disseminated malignant melanoma. As such, they may serve as candidate substrates for targeted cancer therapies and may be particularly useful as adjuncts to surgery.
View details for DOI 10.1111/j.1600-0560.2007.00939.x
View details for Web of Science ID 000259955200002
View details for PubMedID 18537861