Cytogenetics-based risk prediction of blastic transformation of chronic myeloid leukemia in the era of TKI therapy

Gong, Zimu; Medeiros, L. Jeffrey; Cortes, Jorge; Chen, Zi; Zheng, Lan; Li, Yan; Bai, Shuxiong; Lin, Pei; Miranda, Roberto N.; Jorgensen, Jeffrey L.; McDonnell, Timothy J.; Wang, Wei; Kantarjian, Hagop M.; Hu, Shimin

doi:10.1182/bloodadvances.2017011858

Cited by 35 publications

(43 citation statements)

References 46 publications

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“…Not all ACA indicate progression equally. A cytogenetic risk classification has therefore been proposed to allow risk-based treatment adaptation [17,86].…”

Section: Treatment Options For Resistant Bcr-abl1 Mutationsmentioning

confidence: 99%

European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia

et al. 2020

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The therapeutic landscape of chronic myeloid leukemia (CML) has profoundly changed over the past 7 years. Most patients with chronic phase (CP) now have a normal life expectancy. Another goal is achieving a stable deep molecular response (DMR) and discontinuing medication for treatment-free remission (TFR). The European LeukemiaNet convened an expert panel to critically evaluate and update the evidence to achieve these goals since its previous recommendations. First-line treatment is a tyrosine kinase inhibitor (TKI; imatinib brand or generic, dasatinib, nilotinib, and bosutinib are available firstline). Generic imatinib is the cost-effective initial treatment in CP. Various contraindications and side-effects of all TKIs should be considered. Patient risk status at diagnosis should be assessed with the new EUTOS long-term survival (ELTS)score. Monitoring of response should be done by quantitative polymerase chain reaction whenever possible. A change of treatment is recommended when intolerance cannot be ameliorated or when molecular milestones are not reached. Greater than 10% BCR-ABL1 at 3 months indicates treatment failure when confirmed. Allogeneic transplantation continues to be a therapeutic option particularly for advanced phase CML. TKI treatment should be withheld during pregnancy. Treatment discontinuation may be considered in patients with durable DMR with the goal of achieving TFR.

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“…Not all ACA indicate progression equally. A cytogenetic risk classification has therefore been proposed to allow risk-based treatment adaptation [17,86].…”

Section: Treatment Options For Resistant Bcr-abl1 Mutationsmentioning

confidence: 99%

European LeukemiaNet 2020 recommendations for treating chronic myeloid leukemia

et al. 2020

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“…A cytogenetic risk classification has been proposed to allow risk-based treatment adaptation. 47 , 48 , 78 …”

Section: Imatinib Resistance Second Generation Tki and Second-line mentioning

confidence: 99%

“… 141 Also, somatic mutations have been detected in BC and are associated with poor risk disease when detected at diagnosis. 78 , 79 Blast increase in blood or marrow represents the end stage of progression.…”

Section: End Phase CML and Blast Crisismentioning

confidence: 99%

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Chronic Myeloid Leukemia in 2020

Hehlmann

2020

HemaSphere

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New insights have emerged from maturing long-term academic and commercial clinical trials regarding optimum management of chronic myeloid leukemia (CML). Velocity of response has unexpectedly proved less important than hitherto thought, does not predict survival, and is of unclear relevance for treatment-free remission (TFR). Serious and cumulative toxicity has been observed with tyrosine kinase inhibitors that had been expected to replace imatinib. Generic imatinib has become cost-effective first-line treatment in chronic phase despite chronic low-grade side-effects in many patients. Earlier recognition of end-phase by genetic assessment might improve prospects for blast crisis (BC). TFR has become an important new treatment goal of CML. To reflect this new situation ELN has recently revised and updated its recommendations for treating CML. After a brief review of 175 years of CML history this review will focus on recent developments and on current evidence for treating CML in 2020.

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“…In a recent study, we investigated the impact of different type of ACAs on the disease progression of CML and found a significant difference in the latency from the emergence of ACAs to blastic transformation among different ACAs (Interval 2) [ 6 ]. Based on the difference, we establish a four-tier risk stratification model: the high-risk group includes patients with 3q26.2 rearrangement, -7/7q- or i(17q), either as an isolated single ACA or as a component of a complex karyotype.…”

mentioning

confidence: 99%