{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T16:35:01Z","timestamp":1793205301005,"version":"4.5.0"},"reference-count":84,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T00:00:00Z","timestamp":1781568000000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T00:00:00Z","timestamp":1780272000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["HemaSphere"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    ERCC6L2 disease (ED) is a rare bone marrow failure syndrome caused by biallelic germline mutations in\n                    <jats:italic>ERCC6L2<\/jats:italic>\n                    . ED leads to the accumulation of somatic\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations, myelodysplastic syndrome, and acute myeloid leukemia (AML) with erythroid predominance and poor prognosis. While ERCC6L2 is implicated in DNA replication and repair, the transcriptomic events underlying delayed erythropoiesis and leukemic progression remain largely undefined. To delineate these processes, we leverage bulk and single\u2010cell transcriptomics of patient fibroblasts, bone marrow, and peripheral blood across disease stages, including single\u2010cell\n                    <jats:italic>TP53<\/jats:italic>\n                    genotyping. We identify disease\u2010associated erythroid dysregulation and ferroptotic stress emerging prior to\n                    <jats:italic>TP53<\/jats:italic>\n                    mutation, highlighting an early vulnerability in ED leukemogenesis. We compare ED to Shwachman\u2013Diamond syndrome (SDS) to reveal shared and disease\u2010specific transcriptional programs.\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations in ED and SDS arise in hematopoietic stem and progenitor cells but do not independently drive changes in cell cycle or stress pathways during erythropoiesis, despite harboring distinct germline defects. Both diseases converge in late erythropoiesis into a stress state characterized by ferroptotic signaling, G1 arrest, and\n                    <jats:italic>BCL2L1<\/jats:italic>\n                    upregulation. As a disease\u2010specific pattern, ED shows aberrant erythroid priming with\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010driven differentiation arrest shaping progression toward erythroid leukemia. Thereby, we establish the first patient\u2010level single\u2010cell map of ED and provide a curated resource for future work on ED, SDS, and\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010driven leukemogenesis. Overall, our findings in pre\u2010malignant ED offer a window into early alterations leading to high\u2010risk leukemia.\n                  <\/jats:p>","DOI":"10.1002\/hem3.70374","type":"journal-article","created":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T10:22:43Z","timestamp":1781605363000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Distinct stem cell identities converge into shared erythroid stress in ERCC6L2 disease and Shwachman\u2013Diamond syndrome"],"prefix":"10.1002","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0493-5551","authenticated-orcid":false,"given":"Laura","family":"Langohr","sequence":"first","affiliation":[{"name":"Applied Tumor Genomics Research Program, Research Programs Unit, Faculty of Medicine University of Helsinki Helsinki Finland"},{"name":"Institute for Molecular Medicine Finland (FIMM), HiLIFE University of Helsinki Helsinki Finland"},{"name":"Department of Medical and Clinical Genetics, Medicum University of Helsinki Helsinki Finland"},{"name":"iCAN Digital Precision Cancer Medicine Flagship Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-0415-8679","authenticated-orcid":false,"given":"Ilse","family":"Kaaja","sequence":"additional","affiliation":[{"name":"Applied Tumor Genomics Research Program, Research Programs Unit, Faculty of Medicine University of Helsinki Helsinki Finland"},{"name":"Department of Medical and Clinical Genetics, Medicum University of Helsinki Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4412-688X","authenticated-orcid":false,"given":"Suvi P. 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