{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["119(37)"],"submitter":["Hermange G"],"pubmed_abstract":["The developmental history of blood cancer begins with mutation acquisition and the resulting malignant clone expansion. The two most prevalent driver mutations found in myeloproliferative neoplasms-<i>JAK2<sup>V617F</sup></i> and <i>CALR<sup>m</sup></i>-occur in hematopoietic stem cells, which are highly complex to observe in vivo. To circumvent this difficulty, we propose a method relying on mathematical modeling and statistical inference to determine disease initiation and dynamics. Our findings suggest that <i>CALR<sup>m</sup></i> mutations tend to occur later in life than <i>JAK2<sup>V617F</sup></i>. Our results confirm the higher proliferative advantage of the <i>CALR<sup>m</sup></i> malignant clone compared to <i>JAK2<sup>V617F</sup></i>. Furthermore, we illustrate how mathematical m"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pagination":["e2120374119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9478641"],"repository":["biostudies-literature"],"pubmed_title":["Inferring the initiation and development of myeloproliferative neoplasms."],"pmcid":["PMC9478641"],"pubmed_authors":["Tisserand A","Girodon F","Cournede PH","Rakotonirainy A","Hermange G","Bentriou M","Marzac C","Plo I","El-Khoury M","Vainchenker W"],"additional_accession":[]},"is_claimable":false,"name":"Inferring the initiation and development of myeloproliferative neoplasms.","description":"The developmental history of blood cancer begins with mutation acquisition and the resulting malignant clone expansion. The two most prevalent driver mutations found in myeloproliferative neoplasms-<i>JAK2<sup>V617F</sup></i> and <i>CALR<sup>m</sup></i>-occur in hematopoietic stem cells, which are highly complex to observe in vivo. To circumvent this difficulty, we propose a method relying on mathematical modeling and statistical inference to determine disease initiation and dynamics. Our findings suggest that <i>CALR<sup>m</sup></i> mutations tend to occur later in life than <i>JAK2<sup>V617F</sup></i>. Our results confirm the higher proliferative advantage of the <i>CALR<sup>m</sup></i> malignant clone compared to <i>JAK2<sup>V617F</sup></i>. Furthermore, we illustrate how mathematical m","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2025-04-04T13:02:47.775Z","creation":"2025-04-04T13:02:47.775Z"},"accession":"S-EPMC9478641","cross_references":{"pubmed":["36083966"],"doi":["10.1073/pnas.2120374119"]}}