Myelodysplastic Syndrome with Ph Negative Monosomy 7 Chromosome following Transient Bone Marrow Dysplasia during Imatinib Treatment for Chronic Myeloid Leukemia

Karimata, Kaori; Masuko, Masayoshi; Ushiki, Takashi; Kozakai, Takashi; Shibasaki, Yasuhiko; Yano, Toshio; Abe, Takashi; Matsushima, Masato; Toba, Kenji; Furukawa, Tatsuo; Aizawa, Yoshifusa

doi:10.2169/internalmedicine.50.4481

Cited by 11 publications

(7 citation statements)

References 23 publications

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“…Risk of development of MDS or AML has been reported in the literature among patients with these abnormalities. 14,15,28,29 In our present series, 2 of 4 patients with monosomy 7 developed AML or MDS, confirming the risk of this occurrence.…”

Section: Discussionsupporting

confidence: 86%

Clonal chromosomal abnormalities appearing in Philadelphia chromosome–negative metaphases during CML treatment

Issa¹,

Kantarjian²,

González

et al. 2017

Blood

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Clonal chromosomal abnormalities in Philadelphia chromosome-negative (CCA/Ph) metaphases emerge as patients with chronic phase chronic myeloid leukemia (CP-CML) are treated with tyrosine kinase inhibitors (TKIs). We assessed the characteristics and prognostic impact of 598 patients with CP-CML treated on clinical trials with various TKIs. CCA/Ph occurred in 58 patients (10%); the most common were -Y in 25 (43%) and trisomy 8 in 7 patients (12%). Response to TKI therapy was similar for patients with CCA/Ph and those without additional chromosomal abnormalities (ACAs). We further categorized CCA/Ph into those in which -Y was the only clonal abnormality, and all others. We found that patients with non -Y CCA/Ph had worse failure-free survival (FFS), event-free survival (EFS), transformation-free survival (TFS), and overall survival (OS) compared with those without ACAs with the following 5-year rates: FFS (52% vs 70%, = .02), EFS (68% vs 86%, = .02), TFS (76% vs 94%, < .01), and OS (79% vs 94%, = .03). In a multivariate analysis, non -Y CCA/Ph increased the risk of transformation or death when baseline characteristics were considered with a hazard ratio of 2.81 (95% confidence interval, 1.15-6.89; = .02). However, this prognostic impact was not statistically significant when achieving <10% at 3 months was included in the analysis. In conclusion, non -Y CCA/Ph are associated with decreased survival when emerging in patients with chronic-phase CML across various TKIs. This trial was registered at www.clinicaltrials.gov as #NCT00048672, #NCT00038649, and #NCT00050531 (imatinib); #NCT00254423 (dasatinib); #NCT00129740 (nilotinib); and NCT01570868 (ponatinib).

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Section: Discussionsupporting

confidence: 86%

Clonal chromosomal abnormalities appearing in Philadelphia chromosome–negative metaphases during CML treatment

Issa¹,

Kantarjian²,

González

et al. 2017

Blood

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“…58 Progression to myelodysplastic syndromes and acute myeloid leukemia have been reported in patients with monosomy 7 (del 7q). [59][60][61]…”

Section: Clonal Cytogenetic Evolutionmentioning

confidence: 99%

Chronic Myeloid Leukemia, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology

Deininger

Shah

Altman³

et al. 2020

Journal of the National Comprehensive Cancer Network

193

210

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Chronic myeloid leukemia (CML) is defined by the presence of Philadelphia chromosome (Ph) which results from a reciprocal translocation between chromosomes 9 and 22 [t(9;22] that gives rise to a BCR-ABL1 fusion gene. CML occurs in 3 different phases (chronic, accelerated, and blast phase) and is usually diagnosed in the chronic phase. Tyrosine kinase inhibitor therapy is a highly effective first-line treatment option for all patients with newly diagnosed chronic phase CML. This manuscript discusses the recommendations outlined in the NCCN Guidelines for the diagnosis and management of patients with chronic phase CML.

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“…The pathogenesis of MDS/AML development during TKI treatment remains unclear. According to a previous report, inhibition of signaling of molecules other than BCR/ABL in normal hematopoietic stem cells can cause MDS/AML during imatinib treatment ( 15 ). Other previous reports have suggested the possibility of TKI-induced clonal cytogenetic changes in normal ABL protein ( 16 , 17 ).…”

Section: Discussionmentioning

confidence: 99%

Clinical Features of Clonal Cytogenetic Abnormalities in Philadelphia-negative Cells Developed During Tyrosine Kinase Inhibitor Treatment

et al. 2024

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Most clonal cytogenetic abnormalities of Philadelphia-negative cells (CCA/Ph-) occurring during tyrosine kinase inhibitor (TKI) treatment are transient, and the development of secondary myelodysplastic syndrome (MDS)/acute myeloid leukemia (AML) is rare, but the frequency and clinical significance in Japanese patients are still unknown. We herein report four patients who developed CCA/Ph- during TKI therapy and were diagnosed with secondary MDS/AML. The duration from TKI therapy initiation to MDS/AML onset ranged from 3 to 48 months, and the survival ranged from 5 to 84 months. The occurrence of CCA/Ph- with MDS/AML may be associated with a poor prognosis, and careful follow-up is recommended for patients who receive TKI therapy.

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Myelodysplastic Syndrome with Ph Negative Monosomy 7 Chromosome following Transient Bone Marrow Dysplasia during Imatinib Treatment for Chronic Myeloid Leukemia

Cited by 11 publications

References 23 publications

Clonal chromosomal abnormalities appearing in Philadelphia chromosome–negative metaphases during CML treatment

Clonal chromosomal abnormalities appearing in Philadelphia chromosome–negative metaphases during CML treatment

Chronic Myeloid Leukemia, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology

Clinical Features of Clonal Cytogenetic Abnormalities in Philadelphia-negative Cells Developed During Tyrosine Kinase Inhibitor Treatment

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