biostudies-literatureStetka JGrantová Agentura České RepublikyInternal Grant Agency of Palacky UniversityOP VaVpIDanish Cancer SocietySwedish Research CouncilNovo Nordisk FondenMinistry of Education, Youth, and Sports and European Regional Development Fund (ERDF)E903https://www.ebi.ac.uk/biostudies/studies/S-EPMC7226398biostudies-literatureUnknown12(4)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 CancersRole of DNA Damage Response in Suppressing Malignant Progression of Chronic Myeloid Leukemia and Polycythemia Vera: Impact of Different Oncogenes.PMC7226398IGA_LF_2019_00617-05988SLM2018126NNF15OC0016584CZ.1.05/2.1.00/19.0395 and CZ.1.05/1.1.00/02.0109-Stetka JLinan Velasquez JBartek JMojzikova RDivoky VGursky JVyhlidalova PVrablova LfalseRole of DNA Damage Response in Suppressing Malignant Progression of Chronic Myeloid Leukemia and Polycythemia Vera: Impact of Different Oncogenes.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 2020-01-01T00:00:00Z2020 Apr2026-04-07T14:54:43.407Z2020-05-23T07:09:04ZS-EPMC72263983227277010.3390/cancers12040903