{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T18:57:48Z","timestamp":1780081068482,"version":"3.54.0"},"reference-count":31,"publisher":"The Company of Biologists","license":[{"start":{"date-parts":[[2012,12,15]],"date-time":"2012-12-15T00:00:00Z","timestamp":1355529600000},"content-version":"vor","delay-in-days":349,"URL":"http:\/\/www.biologists.com\/user-licence-1-1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>Cell fusion plays a well-recognized, physiologic role during development. Bone marrow-derived hematopoietic cells have been shown to fuse with non-hematopoietic cells in a wide variety of tissues. Some organs appear to resolve the changes in ploidy status, generating functional and mitotically-competent events. However, cell fusion exclusively involving hematopoietic cells has not been reported. Indeed, genomic copy number variation (CNV) in highly replicative hematopoietic cells is widely considered a hallmark of malignant transformation. Here we show that cell fusion occurs between cells of the hematopoietic system under injury as well as non-injury conditions. Experiments reveal the acquisition of genetic markers in fusion products, their tractable maintenance during hematopoietic differentiation and long-term persistence after serial transplantation. Fusion events were identified in clonogenic progenitors as well as differentiated myeloid and lymphoid cells. These observations provide a new experimental model for the study of non-pathogenic somatic diversity in the hematopoietic system.<\/jats:p>","DOI":"10.1242\/jcs.100123","type":"journal-article","created":{"date-parts":[[2012,3,6]],"date-time":"2012-03-06T05:07:03Z","timestamp":1331010423000},"source":"Crossref","is-referenced-by-count":15,"title":["Intra-hematopoietic cell fusion as a source of somatic variation in the hematopoietic system"],"prefix":"10.1242","author":[{"given":"Amy M.","family":"Skinner","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Grompe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Kurre","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2012,1,1]]},"reference":[{"key":"2021042521502116500_b1","doi-asserted-by":"publisher","first-page":"356","DOI":"10.1038\/nature09650","article-title":"Genetic variegation of clonal architecture and propagating cells in leukaemia.","volume":"469","author":"Anderson","year":"2011","journal-title":"Nature"},{"key":"2021042521502116500_b2","doi-asserted-by":"publisher","first-page":"13156","DOI":"10.1073\/pnas.0604203103","article-title":"Myeloid lineage progenitors give rise to vascular endothelium.","volume":"103","author":"Bailey","year":"2006","journal-title":"Proc. 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