<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nilsson T</submitter><funding>Vetenskapsrådet</funding><funding>Västra Götalandsregionen</funding><funding>Barncancerfonden</funding><funding>Cancerfonden</funding><pagination>770-782</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9545334</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>151(5)</volume><pubmed_abstract>Acute myeloid leukemia (AML) results from aberrant hematopoietic processes and these changes are frequently initiated by chromosomal translocations. One particular subtype, AML with translocation t(7;12)(q36;p13), is found in children diagnosed before 2 years of age. The mechanisms for leukemogenesis induced by t(7;12) is not understood, in part because of the lack of efficient methods to reconstruct the leukemia-associated genetic aberration with correct genomic architecture and regulatory elements. We therefore created induced pluripotent stem cell (iPSC) lines that carry the translocation t(7;12) using CRISPR/Cas9. These t(7;12) iPSC showed propensity to differentiate into all three germ layers, confirming retained stem cell properties. The potential for differentiation into hematopoiet</pubmed_abstract><journal>International journal of cancer</journal><pubmed_title>An induced pluripotent stem cell t(7;12)(q36;p13) acute myeloid leukemia model shows high expression of MNX1 and a block in differentiation of the erythroid and megakaryocytic lineages.</pubmed_title><pmcid>PMC9545334</pmcid><funding_grant_id>ALFGBG‐431881</funding_grant_id><funding_grant_id>2018‐05973</funding_grant_id><funding_grant_id>PR2014‐0125</funding_grant_id><funding_grant_id>PR2019‐0013</funding_grant_id><funding_grant_id>TJ2019‐0053</funding_grant_id><funding_grant_id>CAN2017/461</funding_grant_id><pubmed_authors>Abrahamsson J</pubmed_authors><pubmed_authors>Asp J</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Fogelstrand L</pubmed_authors><pubmed_authors>Ostlund A</pubmed_authors><pubmed_authors>Nilsson T</pubmed_authors><pubmed_authors>Palmqvist L</pubmed_authors><pubmed_authors>Waraky A</pubmed_authors><pubmed_authors>Staffas A</pubmed_authors></additional><is_claimable>false</is_claimable><name>An induced pluripotent stem cell t(7;12)(q36;p13) acute myeloid leukemia model shows high expression of MNX1 and a block in differentiation of the erythroid and megakaryocytic lineages.</name><description>Acute myeloid leukemia (AML) results from aberrant hematopoietic processes and these changes are frequently initiated by chromosomal translocations. One particular subtype, AML with translocation t(7;12)(q36;p13), is found in children diagnosed before 2 years of age. The mechanisms for leukemogenesis induced by t(7;12) is not understood, in part because of the lack of efficient methods to reconstruct the leukemia-associated genetic aberration with correct genomic architecture and regulatory elements. We therefore created induced pluripotent stem cell (iPSC) lines that carry the translocation t(7;12) using CRISPR/Cas9. These t(7;12) iPSC showed propensity to differentiate into all three germ layers, confirming retained stem cell properties. The potential for differentiation into hematopoiet</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2026-04-08T11:50:11.245Z</modification><creation>2025-02-19T01:02:58.144Z</creation></dates><accession>S-EPMC9545334</accession><cross_references><pubmed>35583991</pubmed><doi>10.1002/ijc.34122</doi></cross_references></HashMap>