{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T11:01:24Z","timestamp":1780916484910,"version":"3.54.1"},"reference-count":55,"publisher":"Harborside Press, LLC","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,2]]},"abstract":"<jats:p>Chronic myeloid leukemia (CML) is a model of genomically based diagnosis and management where <jats:italic>BCR<\/jats:italic>::<jats:italic>ABL1<\/jats:italic> is successfully targeted by tyrosine kinase inhibitor (TKI) therapy in most patients. The dynamics of <jats:italic>BCR<\/jats:italic>::<jats:italic>ABL1<\/jats:italic> transcript decline during therapy is a dependable biomarker of response, relapse, and drug resistance. Missense mutations acquired within the <jats:italic>BCR<\/jats:italic>::<jats:italic>ABL1<\/jats:italic> kinase domain that disrupt TKI binding can evolve during therapy and are frequently detected in patients for whom TKI treatment fails. Importantly, specific <jats:italic>BCR<\/jats:italic>::<jats:italic>ABL1<\/jats:italic> missense mutations are targetable alterations and direct therapeutic decisions based on the individual mutant TKI sensitivity profile. Nevertheless, <jats:italic>BCR<\/jats:italic>::<jats:italic>ABL1<\/jats:italic> mutations are only implicated in approximately half of the cases of acquired resistance. Furthermore, not all patients with a single <jats:italic>BCR<\/jats:italic>::<jats:italic>ABL1<\/jats:italic> mutation that is predicted to be sensitive to a specific TKI will experience a response when switched to that TKI. Progression to blast phase heralds independence from <jats:italic>BCR<\/jats:italic>::<jats:italic>ABL1<\/jats:italic>, and this phase of the disease is notoriously difficult to treat. The independent drivers of resistance and disease progression have long been investigated to both predict progression and to find targets for therapeutic intervention. Recent data reaffirm that drug resistance and disease progression is a mutation-driven process in CML, and somatic variants in genes that are known to drive acute myeloid and lymphoid leukemia have been detected in patients in the advanced phases of CML. Genomic testing over the last few decades for patients with blood cancer has revealed of variety of genomic aberrations that drive disease. Consequently, incorporation of genomic factors into patient management for a range of blood cancers has led to the implementation of high-throughput gene testing to detect clinically actionable variants. Is it time to integrate broader genomic screening into clinical management strategies for patients with CML?<\/jats:p>","DOI":"10.6004\/jnccn.2023.7335","type":"journal-article","created":{"date-parts":[[2024,2,23]],"date-time":"2024-02-23T20:29:42Z","timestamp":1708720182000},"source":"Crossref","is-referenced-by-count":12,"title":["Beyond BCR::ABL1\u2014The Role of Genomic Analyses in the Management of CML"],"prefix":"10.6004","volume":"22","author":[{"given":"Susan","family":"Branford","sequence":"first","affiliation":[{"name":"Department of Genetics and Molecular Pathology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia"},{"name":"Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia"},{"name":"School of Medicine, The University of Adelaide, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adelina","family":"Fernandes","sequence":"additional","affiliation":[{"name":"Department of Genetics and Molecular Pathology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia"},{"name":"School of Medicine, The University of Adelaide, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"NurHezrin","family":"Shahrin","sequence":"additional","affiliation":[{"name":"Department of Genetics and Molecular Pathology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Muneeza","family":"Maqsood","sequence":"additional","affiliation":[{"name":"Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naranie","family":"Shanmuganathan","sequence":"additional","affiliation":[{"name":"Department of Genetics and Molecular Pathology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia"},{"name":"Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia"},{"name":"School of Medicine, The University of Adelaide, Adelaide, Australia"},{"name":"Department of Haematology, Royal Adelaide Hospital and SA Pathology, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carol","family":"Wadham","sequence":"additional","affiliation":[{"name":"Department of Genetics and Molecular Pathology, Centre for Cancer Biology, SA Pathology, Adelaide, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"4047","reference":[{"key":"B1","article-title":"NCCN Clinical Practice Guidelines in Oncology: Chronic Myeloid Leukemia","author":"Shah NP","unstructured":"Shah NP, Bhatia R, Altman JK,  NCCN Clinical Practice Guidelines in Oncology: Chronic Myeloid Leukemia. 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