{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T21:25:37Z","timestamp":1789593937714,"version":"build-2803163510"},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,4,17]],"date-time":"2017-04-17T00:00:00Z","timestamp":1492387200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Danish-American Fulbright Commission"},{"name":"Aage Bangs Foundation"},{"name":"Bispebjerg Hospital"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Photoderm Photoimm Photomed"],"published-print":{"date-parts":[[2017,5]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Photochemotherapy with psoralen and ultraviolet A (PUVA), with or without adjuvant interferon\u2010\u03b1 (IFN\u2010\u03b1), is a first\u2010line therapy for early\u2010stage mycosis fungoides and other forms of cutaneous T\u2010cell lymphoma (CTCL). However, the mechanism by which PUVA with IFN\u2010\u03b1 work in CTCL is poorly understood.<\/jats:p><\/jats:sec><jats:sec><jats:title>Purpose<\/jats:title><jats:p>To develop a model to investigate the mechanisms of PUVA and PUVA with IFN\u2010\u03b1 in CTCL cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>An <jats:italic>in\u00a0vitro<\/jats:italic> model to study the molecular mechanisms of PUVA was created using two different CTCL cell lines, MyLa, which has functional p53, and HuT\u201078, in which p53 is inactivated due to a homozygous nonsense mutation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>PUVA caused G2\/M cell cycle block and apoptosis of MyLa and HuT\u201078 accompanied by increase in the expression of the mitochondrial pro\u2010apoptotic genes Bax, BAK, and PUMA and a downregulation in anti\u2010apoptotic Bcl\u20102. p53 was induced and c\u2010Myc was repressed by PUVA, but neither were essential for PUVA\u2010induced apoptosis. IFN\u2010\u03b1 augmented PUVA\u2010induced apoptosis via the JAK1 pathway, and this activity could be inhibited by ruxolitinib.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>PUVA induces p53\u2010independent apoptosis in CTCL cell lines, and this process is augmented by type I interferons via the JAK1 pathway.<\/jats:p><\/jats:sec>","DOI":"10.1111\/phpp.12302","type":"journal-article","created":{"date-parts":[[2017,2,14]],"date-time":"2017-02-14T20:32:45Z","timestamp":1487104365000},"page":"164-171","source":"Crossref","is-referenced-by-count":21,"title":["Psoralen with ultraviolet A\u2010induced apoptosis of cutaneous lymphoma cell lines is augmented by type I interferons via the JAK1\u2013STAT1 pathway"],"prefix":"10.1111","volume":"33","author":[{"given":"Walter","family":"Liszewski","sequence":"first","affiliation":[{"name":"Department of Dermatology Bispebjerg Hospital Copenhagen 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