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  1. AU="Den Boer, Monique L"
  2. AU="Potts, T."
  3. AU="Cifuentes-Diaz, Carmen"
  4. AU="Alvim, Ricardo G"
  5. AU="Barron II, Joseph C"
  6. AU="Godin, Shea-Lee"
  7. AU="Leng, Chengcai"
  8. AU="Hyslop, Brian W"
  9. AU="Suzanne Fischer"
  10. AU="Aboelata, Noha"
  11. AU="Chiang, Sarah N"
  12. AU="Wessel, Kristin M"
  13. AU="Wilson, Jenna M"
  14. AU="Goines, Paula"
  15. AU=Ippolito Mariachiara AU=Ippolito Mariachiara
  16. AU="Jose Chauca"
  17. AU="Asih, Puji B S"
  18. AU="Dsane-Selby, Lydia"
  19. AU="Tolossa, Tadesse"
  20. AU="Erdal Bedir"

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  1. Artikel: 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  Band 13, Seite(n) 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.
    Sprache Englisch
    Erscheinungsdatum 2023-02-23
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2023.1128560
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: The impact of an additional copy of chromosome 21 in B-cell precursor acute lymphoblastic leukemia.

    Hormann, Femke M / Mooij, Eva J / van de Mheen, Marieke / Beverloo, H Berna / den Boer, Monique L / Boer, Judith M

    Genes, chromosomes & cancer

    2023  Band 63, Heft 1, Seite(n) e23217

    Abstract: A common finding in pediatric B-cell precursor acute lymphoblastic leukemia (BCPALL) is that chromosome 21 is never lost and an extra chromosome 21 is often gained. This implies an important role for chromosome 21 in the pathobiology of BCPALL, ... ...

    Abstract A common finding in pediatric B-cell precursor acute lymphoblastic leukemia (BCPALL) is that chromosome 21 is never lost and an extra chromosome 21 is often gained. This implies an important role for chromosome 21 in the pathobiology of BCPALL, emphasized by the increased risk of BCPALL in children with Down syndrome. However, model systems of chromosome 21 gain are lacking. We therefore developed a BCPALL cell line (Nalm-6, DUX4-rearranged) with an additional chromosome 21 by means of microcell-mediated chromosome transfer. FISH, PCR, multiplex ligation-dependent probe amplification, and whole exome sequencing showed that an additional chromosome 21 was successfully transferred to the recipient cells. Transcription of some but not all genes on chromosome 21 was increased, indicating tight transcriptional regulation. Nalm-6 cells with an additional chromosome 21 proliferated slightly slower compared with parental Nalm-6 and sensitivity to induction chemotherapeutics was mildly increased. The extra copy of chromosome 21 did not confer sensitivity to targeted signaling inhibitors. In conclusion, a BCPALL cell line with an additional human chromosome 21 was developed, validated, and subjected to functional studies, which showed a minor but potentially relevant effect in vitro. This cell line offers the possibility to study further the role of chromosome 21 in ALL.
    Mesh-Begriff(e) Humans ; Child ; Chromosomes, Human, Pair 21/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Polymerase Chain Reaction ; Burkitt Lymphoma
    Sprache Englisch
    Erscheinungsdatum 2023-12-12
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1018988-9
    ISSN 1098-2264 ; 1045-2257
    ISSN (online) 1098-2264
    ISSN 1045-2257
    DOI 10.1002/gcc.23217
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: B-cell precursor acute lymphoblastic leukemia elicits an interferon-α/β response in bone marrow-derived mesenchymal stroma.

    Smeets, Mandy W E / Steeghs, Elisabeth M P / Orsel, Jan / Stalpers, Femke / Vermeeren, Myrthe M P / Veltman, Christina H J / Slenders, Lotte / Nierkens, Stefan / Van de Ven, Cesca / Den Boer, Monique L

    Haematologica

    2024  

    Abstract: B-cell precursor acute lymphoblastic leukemia (BCP-ALL) can hijack the normal bone marrow microenvironment to create a leukemic niche which facilitates blast cell survival and promotes drug resistance. Bone marrow-derived mesenchymal stromal cells (MSCs) ...

    Abstract B-cell precursor acute lymphoblastic leukemia (BCP-ALL) can hijack the normal bone marrow microenvironment to create a leukemic niche which facilitates blast cell survival and promotes drug resistance. Bone marrow-derived mesenchymal stromal cells (MSCs) mimic this protective environment in ex vivo co-cultures with leukemic cells obtained from children with newly diagnosed BCP-ALL. We examined the potential mechanisms of this protection by RNA sequencing of flowsorted MSCs after co-culture with BCP-ALL cells. Leukemic cells induced an interferon (IFN)-related gene signature in MSCs, which was partially dependent on direct cell-cell signaling. The signature was selectively induced by BCP-ALL cells, most profoundly by ETV6-RUNX1 positive ALL cells, as coculture of MSCs with healthy immune cells did not provoke a similar IFN signature. Leukemic cells and MSCs both secreted IFNα and IFNβ, but no IFNγ. In line, the IFN-gene signature was sensitive to blockade of IFNα/β signaling, but less to that of IFNγ. The viability of leukemic cells and level of resistance to three chemotherapeutic agents was not affected by interference with IFN signaling using selective IFNα/β inhibitors or silencing of IFN-related genes. Taken together, our data suggest that the leukemia-induced expression of IFNα/β-related genes by MSCs does not support survival of BCPALL cells but may serve a different role in the pathobiology of BCP-ALL.
    Sprache Englisch
    Erscheinungsdatum 2024-02-29
    Erscheinungsland Italy
    Dokumenttyp Journal Article
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2023.283494
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; 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  Band 8, Heft 8, Seite(n) 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-Begriff(e) 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
    Chemische Substanzen Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Tyrosine Kinase Inhibitors ; Protein Kinase Inhibitors
    Sprache Englisch
    Erscheinungsdatum 2024-02-21
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2023012162
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; 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 E J / Boeree, Aurélie / de Groot-Kruseman, Hester A / Escherich, Gabriele / Boer, Judith M / den Boer, Monique L

    Blood

    2024  Band 143, Heft 21, Seite(n) 2178–2189

    Abstract: Abstract: Acute lymphoblastic leukemia (ALL) with fusions of ABL-class tyrosine kinase genes other than BCR::ABL1 occurs in ∼3% of children with ALL. The tyrosine kinase genes involved in this BCR::ABL1-like (Ph-like) subtype include ABL1, PDGFRB, ABL2, ...

    Abstract Abstract: Acute lymphoblastic leukemia (ALL) with fusions of ABL-class tyrosine kinase genes other than BCR::ABL1 occurs in ∼3% of children with ALL. The tyrosine kinase genes involved in this BCR::ABL1-like (Ph-like) subtype include ABL1, PDGFRB, ABL2, and CSF1R, each of which has up to 10 described partner genes. ABL-class ALL resembles BCR::ABL1-positive ALL with a similar gene expression profile, poor response to chemotherapy, and sensitivity to tyrosine kinase inhibitors (TKIs). There is a lack of comprehensive data regarding TKI sensitivity in the heterogeneous group of ABL-class ALL. We observed variability in TKI sensitivity within and among each ABL-class tyrosine kinase gene subgroup. We showed that ALL samples with fusions for any of the 4 tyrosine kinase genes were relatively sensitive to imatinib. In contrast, the 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 the ALL immunophenotype, 5' fusion partner, presence or absence of 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 of TKI sensitivity and relevant for specific TKI selection.
    Mesh-Begriff(e) Humans ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Protein Kinase Inhibitors/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Child ; Proto-Oncogene Proteins c-abl/genetics ; Proto-Oncogene Proteins c-abl/metabolism ; src Homology Domains ; Adolescent ; Child, Preschool ; Female ; Male ; Imatinib Mesylate/therapeutic use ; Imatinib Mesylate/pharmacology ; Receptor, Platelet-Derived Growth Factor beta/genetics ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Dasatinib/therapeutic use ; Dasatinib/pharmacology ; Oncogene Proteins, Fusion/genetics ; Tyrosine Kinase Inhibitors
    Chemische Substanzen Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-abl (EC 2.7.10.2) ; ABL1 protein, human (EC 2.7.10.2) ; Imatinib Mesylate (8A1O1M485B) ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.10.1) ; Dasatinib (RBZ1571X5H) ; Oncogene Proteins, Fusion ; Tyrosine Kinase Inhibitors
    Sprache Englisch
    Erscheinungsdatum 2024-02-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2023023120
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: 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  Band 13, Heft 10, Seite(n) 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.
    Sprache Englisch
    Erscheinungsdatum 2020-06-18
    Erscheinungsland United States
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: ABL-class Genomic Breakpoint Q-PCR: A Patient-specific Approach for MRD Monitoring in Acute Lymphoblastic Leukemia.

    van Outersterp, Inge / van der Velden, Vincent H J / Hoogeveen, Patricia G / Vaitkevičienė, Goda E / Sonneveld, Edwin / van Haaften, Gijs / Kuiper, Roland P / Zur Stadt, Udo / Escherich, Gabriele / Boer, Judith M / den Boer, Monique L

    HemaSphere

    2023  Band 7, Heft 10, Seite(n) e967

    Sprache Englisch
    Erscheinungsdatum 2023-09-19
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2572-9241
    ISSN (online) 2572-9241
    DOI 10.1097/HS9.0000000000000967
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  8. Artikel ; 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  Band 108, Heft 10, Seite(n) 2859–2864

    Mesh-Begriff(e) 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
    Chemische Substanzen Transcription Factors ; Oncogene Proteins, Fusion ; BCL9 protein, human ; MEF2D protein, human ; MEF2 Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2023-10-01
    Erscheinungsland Italy
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: BCR-ABL1-like acute lymphoblastic leukaemia: From bench to bedside.

    Boer, Judith M / den Boer, Monique L

    European journal of cancer (Oxford, England : 1990)

    2017  Band 82, Seite(n) 203–218

    Abstract: Acute lymphoblastic leukaemia (ALL) occurs in approximately 1:1500 children and is less frequently found in adults. The most common immunophenotype of ALL is the B cell lineage and within B cell precursor ALL, specific genetic aberrations define subtypes ...

    Abstract Acute lymphoblastic leukaemia (ALL) occurs in approximately 1:1500 children and is less frequently found in adults. The most common immunophenotype of ALL is the B cell lineage and within B cell precursor ALL, specific genetic aberrations define subtypes with distinct biological and clinical characteristics. With more advanced genetic analysis methods such as whole genome and transcriptome sequencing, novel genetic subtypes have recently been discovered. One novel class of genetic aberrations comprises tyrosine kinase-activating lesions, including translocations and rearrangements of tyrosine kinase and cytokine receptor genes. These newly discovered genetic aberrations are harder to detect by standard diagnostic methods such as karyotyping, fluorescent in situ hybridisation (FISH) or polymerase chain reaction (PCR) because they are diverse and often cryptic. These lesions involve one of several tyrosine kinase genes (among others, v-abl Abelson murine leukaemia viral oncogene homologue 1 (ABL1), v-abl Abelson murine leukaemia viral oncogene homologue 2 (ABL2), platelet-derived growth factor receptor beta polypeptide (PDGFRB)), each of which can be fused to up to 15 partner genes. Together, they compose 2-3% of B cell precursor ALL (BCP-ALL), which is similar in size to the well-known fusion gene BCR-ABL1 subtype. These so-called BCR-ABL1-like fusions are mutually exclusive with the sentinel translocations in BCP-ALL (BCR-ABL1, ETV6-RUNX1, TCF3-PBX1, and KMT2A (MLL) rearrangements) and have the promising prospect to be sensitive to tyrosine kinase inhibitors similar to BCR-ABL1. In this review, we discuss the types of tyrosine kinase-activating lesions discovered, and the preclinical and clinical evidence for the use of tyrosine kinase inhibitors in the treatment of this novel subtype of ALL.
    Mesh-Begriff(e) Antineoplastic Agents ; Fusion Proteins, bcr-abl/genetics ; Humans ; Molecular Targeted Therapy/methods ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Protein Kinase Inhibitors/therapeutic use ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Protein-Tyrosine Kinases/metabolism ; Receptors, Cytokine/metabolism
    Chemische Substanzen Antineoplastic Agents ; Protein Kinase Inhibitors ; Receptors, Cytokine ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
    Sprache Englisch
    Erscheinungsdatum 2017-09
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 82061-1
    ISSN 1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
    ISSN (online) 1879-0852
    ISSN 0277-5379 ; 0959-8049 ; 0964-1947
    DOI 10.1016/j.ejca.2017.06.012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: BEHAV3D: a 3D live imaging platform for comprehensive analysis of engineered T cell behavior and tumor response.

    Alieva, Maria / Barrera Román, Mario / de Blank, Sam / Petcu, Diana / Zeeman, Amber L / Dautzenberg, Noël M M / Cornel, Annelisa M / van de Ven, Cesca / Pieters, Rob / den Boer, Monique L / Nierkens, Stefan / Calkoen, Friso G J / Clevers, Hans / Kuball, Jürgen / Sebestyén, Zsolt / Wehrens, Ellen J / Dekkers, Johanna F / Rios, Anne C

    Nature protocols

    2024  

    Abstract: Modeling immuno-oncology by using patient-derived material and immune cell co-cultures can advance our understanding of immune cell tumor targeting in a patient-specific manner, offering leads to improve cellular immunotherapy. However, fully exploiting ... ...

    Abstract Modeling immuno-oncology by using patient-derived material and immune cell co-cultures can advance our understanding of immune cell tumor targeting in a patient-specific manner, offering leads to improve cellular immunotherapy. However, fully exploiting these living cultures requires analysis of the dynamic cellular features modeled, for which protocols are currently limited. Here, we describe the application of BEHAV3D, a platform that implements multi-color live 3D imaging and computational tools for: (i) analyzing tumor death dynamics at both single-organoid or cell and population levels, (ii) classifying T cell behavior and (iii) producing data-informed 3D images and videos for visual inspection and further insight into obtained results. Together, this enables a refined assessment of how solid and liquid tumors respond to cellular immunotherapy, critically capturing both inter- and intratumoral heterogeneity in treatment response. In addition, BEHAV3D uncovers T cell behavior involved in tumor targeting, offering insight into their mode of action. Our pipeline thereby has strong implications for comparing, prioritizing and improving immunotherapy products by highlighting the behavioral differences between individual tumor donors, distinct T cell therapy concepts or subpopulations. The protocol describes critical wet lab steps, including co-culture preparations and fast 3D imaging with live cell dyes, a segmentation-based image processing tool to track individual organoids, tumor and immune cells and an analytical pipeline for behavioral profiling. This 1-week protocol, accessible to users with basic cell culture, imaging and programming expertise, can easily be adapted to any type of co-culture to visualize and exploit cell behavior, having far-reaching implications for the immuno-oncology field and beyond.
    Sprache Englisch
    Erscheinungsdatum 2024-03-19
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2244966-8
    ISSN 1750-2799 ; 1754-2189
    ISSN (online) 1750-2799
    ISSN 1754-2189
    DOI 10.1038/s41596-024-00972-6
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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