{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T23:53:34Z","timestamp":1790898814304,"version":"4.1.0"},"reference-count":79,"publisher":"Oxford University Press (OUP)","issue":"5","funder":[{"DOI":"10.13039\/100018576","name":"Harrington Discovery Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100018576","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000048","name":"American Cancer Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000048","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,10,17]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Cutaneous squamous cell carcinomas (cSCCs) 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To define the transcriptome landscape at different stages in the progression of normal skin to cSCC via a meta-analysis of publicly available RNA-Seq samples.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Whole-transcriptome data from 73 clinically normal skin samples, 46 actinic keratoses (AK) samples, 16 in situ SCC samples, 13 keratoacanthoma (KA) samples and 147 cSCC samples [including 30 samples from immunocompromised patients and 8 from individuals with recessive dystrophic epidermolysis bullosa (RDEB)] were uniformly processed to harmonize gene expression. Differential expression, fusion detection and cell-type deconvolution analyses were performed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Individual RNA-Seq studies of cSCC 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 cSCC development, and used single-cell RNA-Seq data to demonstrate that DEGs are often \u2013 but not always \u2013 expressed by tumour-specific keratinocytes (TSKs). Analysis of the cellular composition of cSCC, KA and RDEB-cSCC identified an increase in differentiated keratinocytes in KA, while RDEB-cSCC contained the most TSKs. Compared with cSCC arising in immunocompetent individuals, cSCC samples from immunosuppressed patients demonstrated fewer memory B cells and CD8+ T cells. A comprehensive and unbiased search for fusion transcripts in cSCC and intermediate disease stages identified few candidates that recurred in &amp;gt;1% of all specimens, suggesting that most cSCC are not driven by oncogenic gene fusions. Finally, using Genotype-Tissue Expression (GTEx) data, we distilled a novel 300-gene signature of chronic sun exposure that affirms greater cumulative ultraviolet (UV) exposure in later stages of cSCC development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results define the gene expression landscape of cSCC progression, characterize cell subpopulation heterogeneity in cSCC subtypes that contribute to their distinct clinical phenotypes, demonstrate that gene fusions are not a common cause of cSCC and identify UV-responsive genes associated with cSCC development.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/bjd\/ljae249","type":"journal-article","created":{"date-parts":[[2024,6,12]],"date-time":"2024-06-12T03:50:37Z","timestamp":1718164237000},"page":"760-774","source":"Crossref","is-referenced-by-count":18,"title":["Gene expression landscape of cutaneous squamous cell carcinoma progression"],"prefix":"10.1093","volume":"191","author":[{"given":"Tomas","family":"Bencomo","sequence":"first","affiliation":[{"name":"Stanford Program in Epithelial Biology, Stanford University , Stanford, CA ,","place":["USA"]},{"name":"Medical Scientist Training Program, University of Washington , Seattle, WA ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carolyn S","family":"Lee","sequence":"additional","affiliation":[{"name":"Stanford Program in Epithelial Biology, Stanford University , Stanford, CA ,","place":["USA"]},{"name":"Veterans Affairs Palo Alto Healthcare System , Palo Alto, CA ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,6,13]]},"reference":[{"key":"2024102112263662200_ljae249-B1","doi-asserted-by":"crossref","first-page":"1081","DOI":"10.1001\/jamadermatol.2015.1187","article-title":"Incidence estimate of 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