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Article: Integrating copy number data of 64 iAMP21 BCP-ALL patients narrows the common region of amplification to 1.57 Mb.

Hormann, Femke M / Hoogkamer, Alex Q / Boeree, Aurélie / Sonneveld, Edwin / Escherich, Gabriele / den Boer, Monique L / Boer, Judith M

Frontiers in oncology

2023 Volume 13, Page(s) 1128560

Abstract: Background and purpose: Intrachromosomal amplification of chromosome 21 (iAMP21) is a rare subtype of B-cell precursor acute lymphoblastic leukaemia (BCP-ALL). It is unknown how iAMP21 contributes to leukaemia. The currently known commonly amplified ... ...

Abstract	Background and purpose: Intrachromosomal amplification of chromosome 21 (iAMP21) is a rare subtype of B-cell precursor acute lymphoblastic leukaemia (BCP-ALL). It is unknown how iAMP21 contributes to leukaemia. The currently known commonly amplified region is 5.1 Mb. Methods: We aimed to narrow down the common region of amplification by using high resolution techniques. Array comparative genomic hybridization (aCGH) was used to determine copy number aberrations, Affymetrix U133 Plus2 expression arrays were used to determine gene expression. Genome-wide expression correlations were evaluated using Globaltest. Results: We narrowed down the common region of amplification by combining copy number data from 12 iAMP21 cases with 52 cases from literature. The combined common region of amplification was 1.57 Mb, located from 36.07 to 37.64 Mb (GRCh38). This region is located telomeric from, but not including, Discussion: The more precise definition of the common region of amplification could be beneficial in the diagnosis of iAMP21 based on copy number analysis from DNA sequencing or arrays as well as stimulate functional research into the role of the included genes in iAMP21 biology.
Language	English
Publishing date	2023-02-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1128560
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Article ; Online: Tyrosine kinase inhibitor response of ABL-class acute lymphoblastic leukemia: The role of kinase type and SH3 domain.

van Outersterp, Inge / Tasian, Sarah K / Reichert, Caitlin Ej / Boeree, Aurélie / de Groot-Kruseman, Hester A / Escherich, Gabriele / Boer, Judith M / den Boer, Monique L

Blood

2024

Abstract: 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, ... ...

Abstract	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.
Language	English
Publishing date	2024-02-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2023023120
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Article ; Online: Tyrosine kinase inhibitor resistance in de novo BCR::ABL1-positive BCP-ALL beyond kinase domain mutations.

van Outersterp, Inge / Boer, Judith M / van de Ven, Cesca / Reichert, Caitlin E J / Boeree, Aurelie / Kruisinga, Brian / de Groot-Kruseman, Hester A / Escherich, Gabriele / Sijs-Szabo, Aniko / Rijneveld, Anita W / den Boer, Monique L

Blood advances

2024 Volume 8, Issue 8, Page(s) 1835–1845

Abstract: Abstract: A better understanding of ABL1 kinase domain mutation-independent causes of tyrosine kinase inhibitor (TKI) resistance is needed for BCR::ABL1-positive B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Although TKIs have dramatically ... ...

Abstract	Abstract: A better understanding of ABL1 kinase domain mutation-independent causes of tyrosine kinase inhibitor (TKI) resistance is needed for BCR::ABL1-positive B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Although TKIs have dramatically improved outcomes, a subset of patients still experiences relapsed or refractory disease. We aimed to identify potential biomarkers of intrinsic TKI resistance at diagnosis in samples from 32 pediatric and 19 adult patients with BCR::ABL1-positive BCP-ALL. Reduced ex vivo imatinib sensitivity was observed in cells derived from newly diagnosed patients who relapsed after combined TKI and chemotherapy treatment compared with cells derived from patients who remained in continuous complete remission. We observed that ex vivo imatinib resistance was inversely correlated with the amount of (phosphorylated) BCR::ABL1/ABL1 protein present in samples that were taken at diagnosis without prior TKI exposure. This suggests an intrinsic cause of TKI resistance that is independent of functional BCR::ABL1 signaling. Simultaneous deletions of IKZF1 and CDKN2A/B and/or PAX5 (IKZF1plus), as well as deletions of PAX5 alone, were related to ex vivo imatinib resistance. In addition, somatic lesions involving ZEB2, SETD2, SH2B3, and CRLF2 were associated with reduced ex vivo imatinib sensitivity. Our data suggest that the poor prognostic value of IKZF1(plus) deletions is linked to intrinsic mechanisms of TKI resistance other than ABL1 kinase domain mutations in newly diagnosed pediatric and adult BCR::ABL1-positive BCP-ALL.
MeSH term(s)	Adult ; Humans ; Child ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/therapeutic use ; Fusion Proteins, bcr-abl/metabolism ; Tyrosine Kinase Inhibitors ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Mutation ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/diagnosis ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics
Chemical Substances	Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Tyrosine Kinase Inhibitors ; Protein Kinase Inhibitors
Language	English
Publishing date	2024-02-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023012162
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Article: Ibrutinib is not an effective drug in primografts of TCF3-PBX1.

van de Ven, Cesca / Boeree, Aurélie / Stalpers, Femke / Zwaan, C Michel / Den Boer, Monique L

Translational oncology

2020 Volume 13, Issue 10, Page(s) 100817

Abstract: Aim: The Bruton's tyrosine kinase (BTK) inhibitor Ibrutinib (PCI-32765) is effective in patients with multiple myeloma, non-Hodgkin lymphoma and chronic lymphoblastic leukemia. We previously showed that primary cells of children with TCF3-PBX1 positive ... ...

Abstract	Aim: The Bruton's tyrosine kinase (BTK) inhibitor Ibrutinib (PCI-32765) is effective in patients with multiple myeloma, non-Hodgkin lymphoma and chronic lymphoblastic leukemia. We previously showed that primary cells of children with TCF3-PBX1 positive B-cell precursor acute lymphoblastic leukemia (BCP-ALL) express BTK and are sensitive to ibrutinib in vitro. However, preclinical studies in mice are lacking that justify clinical implementation. Methods: Immunocompromised NSG mice were engrafted with a luciferase-positive TCF3-PBX1 leukemic cell line or primary leukemic cells and treated with ibrutinib or placebo. Additionally, primary cells were exposed in vitro to 4 main induction drugs as monotherapy and in combination with ibrutinib. Results: Treatment with ibrutinib of mice engrafted with a TCF3-PBX1 cell line, TCF3-PBX1 positive or TCF3-PBX1 negative primary leukemic cells did not result in prolonged life span compared to placebo treated mice. In vitro sensitivity to ibrutinib was unaltered in leukemic cells obtained from engrafted mice compared to the original material. However, ibrutinib treatment did not affect leukemic cell viability and tumor outgrowth, nor could lymphocytosis be detected. Ibrutinib was biologically active, since hCD19 Conclusions: We conclude that ibrutinib is not the precision medicine of choice for TCF3-PBX1 positive BCP-ALL.
Language	English
Publishing date	2020-06-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233 ; 1936-5233 ; 1944-7124
ISSN (online)	1936-5233
ISSN	1936-5233 ; 1944-7124
DOI	10.1016/j.tranon.2020.100817
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Article ; Online: Characterization of a novel

Van Outersterp, Inge / Hormann, Femke M / Hoogkamer, Alex Q / Boeree, Aurélie / Van den Broek, Stijn A / Den Boer, Monique L / Boer, Judith M

Haematologica

2023 Volume 108, Issue 10, Page(s) 2859–2864

MeSH term(s)	Humans ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Transcription Factors ; Cell Line ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; MEF2 Transcription Factors/genetics ; MEF2 Transcription Factors/metabolism
Chemical Substances	Transcription Factors ; Oncogene Proteins, Fusion ; BCL9 protein, human ; MEF2D protein, human ; MEF2 Transcription Factors
Language	English
Publishing date	2023-10-01
Publishing country	Italy
Document type	Letter
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2022.281712
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Article ; Online: Copy number alterations in B-cell development genes, drug resistance, and clinical outcome in pediatric B-cell precursor acute lymphoblastic leukemia.

Steeghs, Elisabeth M P / Boer, Judith M / Hoogkamer, Alex Q / Boeree, Aurélie / de Haas, Valerie / de Groot-Kruseman, Hester A / Horstmann, Martin A / Escherich, Gabriele / Pieters, Rob / den Boer, Monique L

Scientific reports

2019 Volume 9, Issue 1, Page(s) 4634

Abstract: Pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is associated with a high frequency of copy number alterations (CNAs) in IKZF1, EBF1, PAX5, CDKN2A/B, RB1, BTG1, ETV6, and/or the PAR1 region (henceforth: B-cell development genes). We ... ...

Abstract	Pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is associated with a high frequency of copy number alterations (CNAs) in IKZF1, EBF1, PAX5, CDKN2A/B, RB1, BTG1, ETV6, and/or the PAR1 region (henceforth: B-cell development genes). We aimed to gain insight in the association between CNAs in these genes, clinical outcome parameters, and cellular drug resistance. 71% of newly diagnosed pediatric BCP-ALL cases harbored one or more CNAs in these B-cell development genes. The distribution and clinical relevance of these CNAs was highly subtype-dependent. In the DCOG-ALL10 cohort, only loss of IKZF1 associated as single marker with unfavorable outcome parameters and cellular drug resistance. Prednisolone resistance was observed in IKZF1-deleted primary high hyperdiploid cells (~1500-fold), while thiopurine resistance was detected in IKZF1-deleted primary BCR-ABL1-like and non-BCR-ABL1-like B-other cells (~2.7-fold). The previously described risk stratification classifiers, i.e. IKZF1
MeSH term(s)	Adolescent ; B-Lymphocytes/metabolism ; Child ; Child, Preschool ; Cohort Studies ; DNA Copy Number Variations/genetics ; Drug Resistance ; Female ; Gene Dosage ; Genes, p16/physiology ; Humans ; Ikaros Transcription Factor/genetics ; Male ; Neoplasm Proteins/genetics ; PAX5 Transcription Factor/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Prognosis ; Proto-Oncogene Proteins c-ets/genetics ; Repressor Proteins/genetics ; Retinoblastoma Binding Proteins/genetics ; Trans-Activators/genetics ; Ubiquitin-Protein Ligases/genetics ; ETS Translocation Variant 6 Protein
Chemical Substances	EBF1 protein, human ; IKZF1 protein, human ; Neoplasm Proteins ; PAX5 Transcription Factor ; PAX5 protein, human ; Proto-Oncogene Proteins c-ets ; RB1 protein, human ; Repressor Proteins ; Retinoblastoma Binding Proteins ; Trans-Activators ; BTG1 protein, human (146835-72-5) ; Ikaros Transcription Factor (148971-36-2) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2019-03-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-41078-4
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Article ; Online: NUTM1

Hormann, Femke M / Hoogkamer, Alex Q / Beverloo, H Berna / Boeree, Aurélie / Dingjan, Ilse / Wattel, Moniek M / Stam, Ronald W / Escherich, Gabriele / Pieters, Rob / den Boer, Monique L / Boer, Judith M

Haematologica

2019 Volume 104, Issue 10, Page(s) e455–e459

MeSH term(s)	Child ; Chromosome Banding ; Chromosomes, Human ; Female ; Gene Expression Regulation, Leukemic ; Humans ; Male ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Nuclear Proteins/biosynthesis ; Nuclear Proteins/genetics ; Oncogene Proteins, Fusion/biosynthesis ; Oncogene Proteins, Fusion/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology
Chemical Substances	NUTM1 protein, human ; Neoplasm Proteins ; Nuclear Proteins ; Oncogene Proteins, Fusion
Language	English
Publishing date	2019-03-14
Publishing country	Italy
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2018.206961
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Article ; Online: JAK2

Steeghs, Elisabeth M P / Jerchel, Isabel S / de Goffau-Nobel, Willemieke / Hoogkamer, Alex Q / Boer, Judith M / Boeree, Aurélie / van de Ven, Cesca / Koudijs, Marco J / Besselink, Nicolle J M / de Groot-Kruseman, Hester A / Zwaan, Christian Michel / Horstmann, Martin A / Pieters, Rob / den Boer, Monique L

Oncotarget

2017 Volume 8, Issue 52, Page(s) 89923–89938

Abstract: ... ...

Abstract	JAK2
Language	English
Publishing date	2017-10-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.21027
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Article ; Online: Tyrosine kinase fusion genes in pediatric BCR-ABL1-like acute lymphoblastic leukemia.

Boer, Judith M / Steeghs, Elisabeth M P / Marchante, João R M / Boeree, Aurélie / Beaudoin, James J / Beverloo, H Berna / Kuiper, Roland P / Escherich, Gabriele / van der Velden, Vincent H J / van der Schoot, C Ellen / de Groot-Kruseman, Hester A / Pieters, Rob / den Boer, Monique L

Oncotarget

2016 Volume 8, Issue 3, Page(s) 4618–4628

Abstract: Approximately 15% of pediatric B cell precursor acute lymphoblastic leukemia (BCP-ALL) is characterized by gene expression similar to that of BCR-ABL1-positive disease and unfavorable prognosis. This BCR-ABL1-like subtype shows a high frequency of B-cell ...

Abstract	Approximately 15% of pediatric B cell precursor acute lymphoblastic leukemia (BCP-ALL) is characterized by gene expression similar to that of BCR-ABL1-positive disease and unfavorable prognosis. This BCR-ABL1-like subtype shows a high frequency of B-cell development gene aberrations and tyrosine kinase-activating lesions. To evaluate the clinical significance of tyrosine kinase gene fusions in children with BCP-ALL, we studied the frequency of recently identified tyrosine kinase fusions, associated genetic features, and prognosis in a representative Dutch/German cohort. We identified 14 tyrosine kinase fusions among 77 BCR-ABL1-like cases (18%) and none among 76 non-BCR-ABL1-like B-other cases. Novel exon fusions were identified for RCSD1-ABL2 and TERF2-JAK2. JAK2 mutation was mutually exclusive with tyrosine kinase fusions and only occurred in cases with high CRLF2 expression. The non/late response rate and levels of minimal residual disease in the fusion-positive BCR-ABL1-like group were higher than in the non-BCR-ABL1-like B-others (p<0.01), and also higher, albeit not statistically significant, compared with the fusion-negative BCR-ABL1-like group. The 8-year cumulative incidence of relapse in the fusion-positive BCR-ABL1-like group (35%) was comparable with that in the fusion-negative BCR-ABL1-like group (35%), and worse than in the non-BCR-ABL1-like B-other group (17%, p=0.07). IKZF1 deletions, predominantly other than the dominant-negative isoform and full deletion, co-occurred with tyrosine kinase fusions. This study shows that tyrosine kinase fusion-positive cases are a high-risk subtype of BCP-ALL, which warrants further studies with specific kinase inhibitors to improve outcome.
MeSH term(s)	Adolescent ; Cohort Studies ; Female ; Fusion Proteins, bcr-abl/genetics ; Gene Deletion ; Germany ; Humans ; Ikaros Transcription Factor/genetics ; Intracellular Signaling Peptides and Proteins/genetics ; Janus Kinase 2/genetics ; Male ; Mutation ; Netherlands ; Oligonucleotide Array Sequence Analysis ; Oncogene Proteins, Fusion/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Protein-Tyrosine Kinases/genetics ; Telomeric Repeat Binding Protein 2/genetics ; Young Adult
Chemical Substances	BCR-ABL1 fusion protein, human ; IKZF1 protein, human ; Intracellular Signaling Peptides and Proteins ; Oncogene Proteins, Fusion ; RCSD1 protein, human ; TERF2 protein, human ; Telomeric Repeat Binding Protein 2 ; Ikaros Transcription Factor (148971-36-2) ; ARG tyrosine kinase (EC 2.7.1.-) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; JAK2 protein, human (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2)
Language	English
Publishing date	2016-11-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.13492
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