{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T17:38:35Z","timestamp":1793122715431,"version":"4.5.0"},"reference-count":134,"publisher":"MDPI AG","issue":"17","license":[{"start":{"date-parts":[[2022,8,26]],"date-time":"2022-08-26T00:00:00Z","timestamp":1661472000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancers"],"abstract":"<jats:p>Plasmacytoid Dendritic Cells (pDC) are type I interferon (IFN)-producing cells that play a key role in immune responses. Two major types of neoplastic counterparts for pDC are now discriminated: Blastic pDC Neoplasm (BPDCN) and Mature pDC Proliferation (MPDCP), associated with myeloid neoplasm. Two types of MPDCP are now better described: Chronic MyeloMonocytic Leukemia with pDC expansion (pDC-CMML) and Acute Myeloid Leukemia with pDC expansion (pDC-AML). Differential diagnosis between pDC-AML and BPDCN is particularly challenging, and genomic features can help for diagnosis. Here, we systematically review the cytogenetic, molecular, and transcriptional characteristics of BPDCN and pDC-AML. BPDCN are characterized by frequent complex karyotypes with recurrent MYB\/MYC rearrangements as well as recurrent deletions involving ETV6, IKZF1, RB1, and TP53 loci. Epigenetic and splicing pathways are also particularly mutated, while original processes are dysregulated, such as NF-kB, TCF4, BCL2, and IFN pathways; neutrophil-specific receptors; and cholinergic signaling. In contrast, cytogenetic abnormalities are limited in pDC-AML and are quite similar to other AML. Interestingly, RUNX1 is the most frequently mutated gene (70% of cases). These typical genomic features are of potential interest for diagnosis, and also from a prognostic or therapeutic perspective.<\/jats:p>","DOI":"10.3390\/cancers14174132","type":"journal-article","created":{"date-parts":[[2022,8,28]],"date-time":"2022-08-28T21:22:56Z","timestamp":1661721776000},"page":"4132","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Genetics and Epigenetics in Neoplasms with Plasmacytoid Dendritic Cells"],"prefix":"10.3390","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6149-0547","authenticated-orcid":false,"given":"Florian","family":"Renosi","sequence":"first","affiliation":[{"name":"INSERM, EFS BFC, UMR1098 RIGHT, University of Bourgogne Franche-Comt\u00e9, F-25000 Besancon, France"},{"name":"Laboratoire d\u2019H\u00e9matologie et d\u2019Immunologie R\u00e9gional, Etablissement Fran\u00e7ais du Sang Bourgogne Franche-Comt\u00e9, F-25000 Besancon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary","family":"Callanan","sequence":"additional","affiliation":[{"name":"INSERM 1231 and 1209, University of Bourgogne-Franche Comt\u00e9, F-21000 Dijon, France"},{"name":"Service d\u2019Oncologie G\u00e9n\u00e9tique, CHU Dijon Bourgogne, F-21000 Dijon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine","family":"Lefebvre","sequence":"additional","affiliation":[{"name":"INSERM 1209 and CNRS UMR 5309, Universit\u00e9 Grenoble-Alpes, F-38000 Grenoble, France"},{"name":"Laboratoire de G\u00e9n\u00e9tique des h\u00e9mopathies, Institut de Biologie et de Pathologie, CHU Grenoble Alpes, F-38000 Grenoble, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,8,26]]},"reference":[{"key":"ref_1","unstructured":"Swerdlow, S.H., Campo, E., Harris, N.L., Jaffe, E.S., Pileri, S.A., Stein, H., Thiele, J., Arber, D.A., Hasserjian, R., and Le Beau, M.M. 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