<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Clarke M</submitter><funding>Austrian Science Fund FWF</funding><funding>Medical Research Council</funding><funding>Wellcome Trust</funding><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>661-70</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3593183</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(3)</volume><pubmed_abstract>The haematopoietic system is prone to age-related disorders ranging from deficits in functional blood cells to the development of neoplastic states. Such neoplasms often involve recurrent cytogenetic abnormalities, among which a deletion in the long arm of chromosome 20 (del20q) is common in myeloid malignancies. The del20q minimum deleted region contains nine genes, including MYBL2, which encodes a key protein involved in the maintenance of genome integrity. Here, we show that mice expressing half the normal levels of Mybl2 (Mybl2(+/Δ)) develop a variety of myeloid disorders upon ageing. These include myeloproliferative neoplasms, myelodysplasia (MDS) and myeloid leukaemia, mirroring the human conditions associated with del20q. Moreover, analysis of gene expression profiles from patients </pubmed_abstract><journal>Leukemia</journal><pubmed_title>MYBL2 haploinsufficiency increases susceptibility to age-related haematopoietic neoplasia.</pubmed_title><pmcid>PMC3593183</pmcid><funding_grant_id>G9818340B</funding_grant_id><funding_grant_id>P 23257</funding_grant_id><funding_grant_id>MR/K01076X/1</funding_grant_id><funding_grant_id>BB/E001459/1</funding_grant_id><funding_grant_id>1092244</funding_grant_id><pubmed_authors>Jager R</pubmed_authors><pubmed_authors>Dawood B</pubmed_authors><pubmed_authors>Kralovics R</pubmed_authors><pubmed_authors>Frampton J</pubmed_authors><pubmed_authors>Freeman S</pubmed_authors><pubmed_authors>Lorvellec M</pubmed_authors><pubmed_authors>Dumon S</pubmed_authors><pubmed_authors>Sheriff L</pubmed_authors><pubmed_authors>Ward C</pubmed_authors><pubmed_authors>Clarke M</pubmed_authors><pubmed_authors>Garcia P</pubmed_authors></additional><is_claimable>false</is_claimable><name>MYBL2 haploinsufficiency increases susceptibility to age-related haematopoietic neoplasia.</name><description>The haematopoietic system is prone to age-related disorders ranging from deficits in functional blood cells to the development of neoplastic states. Such neoplasms often involve recurrent cytogenetic abnormalities, among which a deletion in the long arm of chromosome 20 (del20q) is common in myeloid malignancies. The del20q minimum deleted region contains nine genes, including MYBL2, which encodes a key protein involved in the maintenance of genome integrity. Here, we show that mice expressing half the normal levels of Mybl2 (Mybl2(+/Δ)) develop a variety of myeloid disorders upon ageing. These include myeloproliferative neoplasms, myelodysplasia (MDS) and myeloid leukaemia, mirroring the human conditions associated with del20q. Moreover, analysis of gene expression profiles from patients </description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Mar</publication><modification>2026-04-29T08:13:43.497Z</modification><creation>2019-03-27T01:05:51Z</creation></dates><accession>S-EPMC3593183</accession><cross_references><pubmed>22910183</pubmed><doi>10.1038/leu.2012.241</doi></cross_references></HashMap>