{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Stetka J"],"funding":["Grantová Agentura České Republiky","Internal Grant Agency of Palacky University","OP VaVpI","Danish Cancer Society","Swedish Research Council","Novo Nordisk Fonden","Ministry of Education, Youth, and Sports and European Regional Development Fund (ERDF)"],"pagination":["E903"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7226398"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(4)"],"pubmed_abstract":["Inflammatory and oncogenic signaling, both known to challenge genome stability, are key drivers of <i>BCR-ABL</i>-positive chronic myeloid leukemia (CML) and <i>JAK2</i> V617F-positive chronic myeloproliferative neoplasms (MPNs). Despite similarities in chronic inflammation and oncogene signaling, major differences in disease course exist. Although BCR-ABL has robust transformation potential, <i>JAK2</i> V617F-positive polycythemia vera (PV) is characterized by a long and stable latent phase. These differences reflect increased genomic instability of <i>BCR-ABL</i>-positive CML, compared to genome-stable PV with rare cytogenetic abnormalities. Recent studies have implicated BCR-ABL in the development of a \"mutator\" phenotype fueled by high oxidative damage, deficiencies of DNA repair, and "],"journal":["Cancers"],"pubmed_title":["Role of DNA Damage Response in Suppressing Malignant Progression of Chronic Myeloid Leukemia and Polycythemia Vera: Impact of Different Oncogenes."],"pmcid":["PMC7226398"],"funding_grant_id":["IGA_LF_2019_006","17-05988S","LM2018126","NNF15OC0016584","CZ.1.05/2.1.00/19.0395 and CZ.1.05/1.1.00/02.0109","-"],"pubmed_authors":["Stetka J","Linan Velasquez J","Bartek J","Mojzikova R","Divoky V","Gursky J","Vyhlidalova P","Vrablova L"],"additional_accession":[]},"is_claimable":false,"name":"Role of DNA Damage Response in Suppressing Malignant Progression of Chronic Myeloid Leukemia and Polycythemia Vera: Impact of Different Oncogenes.","description":"Inflammatory and oncogenic signaling, both known to challenge genome stability, are key drivers of <i>BCR-ABL</i>-positive chronic myeloid leukemia (CML) and <i>JAK2</i> V617F-positive chronic myeloproliferative neoplasms (MPNs). Despite similarities in chronic inflammation and oncogene signaling, major differences in disease course exist. Although BCR-ABL has robust transformation potential, <i>JAK2</i> V617F-positive polycythemia vera (PV) is characterized by a long and stable latent phase. These differences reflect increased genomic instability of <i>BCR-ABL</i>-positive CML, compared to genome-stable PV with rare cytogenetic abnormalities. Recent studies have implicated BCR-ABL in the development of a \"mutator\" phenotype fueled by high oxidative damage, deficiencies of DNA repair, and ","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Apr","modification":"2026-04-07T14:54:43.407Z","creation":"2020-05-23T07:09:04Z"},"accession":"S-EPMC7226398","cross_references":{"pubmed":["32272770"],"doi":["10.3390/cancers12040903"]}}