Molecular monitoring of patients with <i>ETV6‐PDGFRB</i> rearrangement: Implications for therapeutic adaptation

Bidet, Audrey; Chollet, Claudine; Gardembas, Martine; Nicolini, Franck E.; Genet, Philippe; Delmer, Alain; Caillot, Denis; Dulucq, Stéphanie; Mahon, François‐Xavier; Lippert, Éric

doi:10.1111/bjh.14748

Cited by 6 publications

(2 citation statements)

References 10 publications

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“…RT-PCR and RT-qPCR are more sensitive for the detection of complex and/or cryptic cases not evident by conventional cytogenetics and are well suited to monitor response to treatment. 41,50 However, the use of RT-PCR is limited by the large number of partner fusion genes. RNA sequencing may also be considered in cases with complex/cryptic fusions.…”

Section: Cytogenetic and Molecular Testingmentioning

confidence: 99%

Myeloid/Lymphoid Neoplasms with Eosinophilia and TK Fusion Genes, Version 3.2021, NCCN Clinical Practice Guidelines in Oncology

Gerds

Gotlib

Bose

et al. 2020

Journal of the National Comprehensive Cancer Network

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Eosinophilic disorders and related syndromes represent a heterogeneous group of neoplastic and nonneoplastic conditions, characterized by more eosinophils in the peripheral blood, and may involve eosinophil-induced organ damage. In the WHO classification of myeloid and lymphoid neoplasms, eosinophilic disorders characterized by dysregulated tyrosine kinase (TK) fusion genes are recognized as a new category termed, myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA, PDGFRB or FGFR1 or with PCM1-JAK2. In addition to these aforementioned TK fusion genes, rearrangements involving FLT3 and ABL1 genes have also been described. These new NCCN Guidelines include recommendations for the diagnosis, staging, and treatment of any one of the myeloid/lymphoid neoplasms with eosinophilia (MLN-Eo) and a TK fusion gene included in the 2017 WHO Classification, as well as MLN-Eo and a FLT3 or ABL1 rearrangement.

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Section: Cytogenetic and Molecular Testingmentioning

confidence: 99%

Myeloid/Lymphoid Neoplasms with Eosinophilia and TK Fusion Genes, Version 3.2021, NCCN Clinical Practice Guidelines in Oncology

Gerds

Gotlib

Bose

et al. 2020

Journal of the National Comprehensive Cancer Network

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“…4 Moreover, studies using patient–derived xenograft (PDX) models have shown sensitivity after in vivo or ex vivo exposure to imatinib or dasatinib for ABL1 -, ABL2 -, PDGFRB -, and CSF1R -fused ALL. 4 , 20 , 21 , 22 Based on these preclinical studies and several case studies, 4 , 5 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 current ALL treatment protocols include either imatinib (EsPhALL2017/COG AALL1631/ALLTogether-1) or dasatinib (COG AALL1131/DFCI ALL 16-001/Total Therapy XVII) as first-line treatment for pediatric patients with ABL-class ALL given the approval of these TKIs for patients with BCR :: ABL1 -positive ALL. 51 …”

Section: Introductionmentioning

confidence: 99%

Tyrosine kinase inhibitor response of ABL-class acute lymphoblastic leukemia: the role of kinase type and SH3 domain

van Outersterp,

Tasian,

Reichert

et al. 2024

Blood

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Acute lymphoblastic leukemia (ALL) with fusions of ABL-class tyrosine kinase genes other than BCR::ABL1 occurs in approximately 3% of children with ALL. The tyrosine kinase genes involved in this BCR::ABL1-like (Ph-like) subtype include ABL1, PDGFRB, ABL2, and CSF1R, which each have up to ten described partner genes. ABL-class ALL resembles BCR::ABL1-positive ALL by a similar gene expression profile, a poor response to chemotherapy, and sensitivity to tyrosine kinase inhibitors (TKIs). There is a lack of comprehensive data regarding TKI sensitivity for the heterogeneous group of ABL-class ALL. We observed variability in TKI sensitivity both within and amongst each ABL-class tyrosine kinase gene subgroup. We showed that ALL samples with fusions of any of the four tyrosine kinase genes were relatively sensitive to imatinib. In contrast, PDGFRB-fused ALL samples were less sensitive to dasatinib and bosutinib. Variation in ex vivo TKI response within the subset of samples with the same ABL-class tyrosine kinase gene was not associated with ALL immunophenotype, 5' fusion partner, the presence or absence of the Src-homology-2/3 domains, or deletions of IKZF1, PAX5, or CDKN2A/B. In conclusion, the tyrosine kinase gene involved in ABL-class ALL is the main determinant for TKI sensitivity and is relevant for specific TKI selection.

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Cytogenetics in the management of myeloproliferative neoplasms, mastocytosis and myelodysplastic/myeloproliferative neoplasms: Guidelines from the Group Francophone de Cytogénétique Hématologique (GFCH)

Decamp,

Klein,

Godon

et al. 2023

Current Research in Translational Medicine

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Molecular monitoring of patients with ETV6‐PDGFRB rearrangement: Implications for therapeutic adaptation

Cited by 6 publications

References 10 publications

Myeloid/Lymphoid Neoplasms with Eosinophilia and TK Fusion Genes, Version 3.2021, NCCN Clinical Practice Guidelines in Oncology

Myeloid/Lymphoid Neoplasms with Eosinophilia and TK Fusion Genes, Version 3.2021, NCCN Clinical Practice Guidelines in Oncology

Tyrosine kinase inhibitor response of ABL-class acute lymphoblastic leukemia: the role of kinase type and SH3 domain

Cytogenetics in the management of myeloproliferative neoplasms, mastocytosis and myelodysplastic/myeloproliferative neoplasms: Guidelines from the Group Francophone de Cytogénétique Hématologique (GFCH)

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