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Nevertheless, approximately 20\u201330% of cases progress to tumors or erythroderma, resulting in poor outcome. At present, factors contributing to this switch from indolent to aggressive disease are only insufficiently understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In patients with advanced-stage MF, we compared patches with longstanding history to newly developed plaques and tumors by using single-cell RNA sequencing, and compared results with early-stage MF as well as nonlesional MF and healthy control skin.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Despite considerable inter-individual variability, lesion progression was uniformly associated with downregulation of the tissue residency markers\n                      <jats:italic>CXCR4<\/jats:italic>\n                      and\n                      <jats:italic>CD69<\/jats:italic>\n                      , the heat shock protein\n                      <jats:italic>HSPA1A<\/jats:italic>\n                      , the tumor suppressors and immunoregulatory mediators\n                      <jats:italic>ZFP36<\/jats:italic>\n                      and\n                      <jats:italic>TXNIP<\/jats:italic>\n                      , and the interleukin 7 receptor (\n                      <jats:italic>IL7R)<\/jats:italic>\n                      within the malignant clone, but not in benign T cells. This phenomenon was not only found in conventional TCR-\u03b1\u03b2 MF, but also in a case of TCR-\u03b3\u03b4 MF, suggesting a common mechanism across MF subtypes. Conversely, malignant cells in clinically unaffected skin from MF patients showed upregulation of these markers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our data reveal a specific panel of biomarkers that might be used for monitoring MF disease progression. Altered expression of these genes may underlie the switch in clinical phenotype observed in advanced-stage MF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12943-021-01419-2","type":"journal-article","created":{"date-parts":[[2021,9,28]],"date-time":"2021-09-28T03:17:13Z","timestamp":1632799033000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":82,"title":["Single-cell RNA sequencing reveals markers of disease progression in primary cutaneous T-cell lymphoma"],"prefix":"10.1186","volume":"20","author":[{"given":"Katharina","family":"Rindler","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Constanze","family":"Jonak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalia","family":"Alkon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix M.","family":"Thaler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald","family":"Kurz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa E.","family":"Shaw","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Georg","family":"Stingl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang","family":"Weninger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Halbritter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang M.","family":"Bauer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Farlik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3488-3345","authenticated-orcid":false,"given":"Patrick M.","family":"Brunner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,9,28]]},"reference":[{"key":"1419_CR1","doi-asserted-by":"crossref","unstructured":"Brunner PM, Jonak C, Knobler R. 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CJ is an investigator for Eli Lilly and Company, LEO Pharma, Novartis, and 4SC (grant paid to her institution). GS received personal fees from Boehringer Ingelheim, Sanofi-Genzyme, Almirall, and Novartis. WW is an employee of the Medical University of Vienna and has received personal fees from LEO Pharma, Pfizer, Sanofi Genzyme, Eli Lilly, Novartis, Boehringer Ingelheim, AbbVie, and Janssen. WMB is an employee of the Medical University of Vienna and has received personal fees from Takeda, Abbvie, GSK\/ViiV and Gilead. PMB is an employee of the Medical University of Vienna, and has received personal fees from LEO Pharma, Pfizer, Sanofi Genzyme, Eli Lilly, Novartis, Celgene, UCB Pharma, Biotest, Boehringer Ingelheim, AbbVie, Amgen, Arena Pharmaceuticals, GSK and Regeneron independently from this work. PMB is an investigator for Novartis (grant paid to his institution). The rest of the authors declare that they have no relevant conflicts of interest.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"124"}}