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BIOMARKER:

CBFB-MYH11 fusion

i
Other names: CBFB, Core-Binding Factor Subunit Beta 2, SL3/AKV Core-Binding Factor Beta Subunit, SL3-3 Enhancer Factor 1 Subunit Beta, Core-Binding Factor Beta Subunit, PEBP2-Beta, PEA2-Beta, CBF-Beta, PEBP2B, Polyomavirus Enhancer Binding Protein 2, Beta Subunit, Polyomavirus Enhancer-Binding Protein 2 Beta Subunit, SL3-3 Enhancer Factor 1 Beta Subunit, Core-Binding Factor, Beta Subunit, CBFB, MYH11, Myosin Heavy Chain 11, SMMHC, Myosin, Heavy Polypeptide 11, Smooth Muscle, Myosin Heavy Chain, Smooth Muscle
Entrez ID:
Related biomarkers:
1d
Three samples in which CD11b increased in response to ATRA had an inversion of chromosome 16 as well as the CBFB-MYH11 fusion gene, and the fourth sample was from a patient with KMT2A-rearranged, therapy-related AML. In conclusion, we identified a subgroup of non-APL AML patients with inv(16) and CBFB-MYH11 as the most sensitive to ATRA-mediated differentiation in vitro, and our results can help identify patients who may benefit from ATRA treatment.
Journal
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KMT2A (Lysine Methyltransferase 2A) • ITGAM (Integrin, alpha M)
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MLL rearrangement • CBFB-MYH11 fusion
1d
Additionally, we provide insights into the transcriptional landscapes that differentiate these distinct CBFB-MYH11 AML subtypes. Children's Oncology Group trials include CCG-2961 (registered at www.clinicaltrials.gov as NCT00002798), AAML03P1 (NCT00070174), AAML0531 (NCT00372593), and AAML1031 (NCT01371981).
Journal
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KIT (KIT proto-oncogene, receptor tyrosine kinase)
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KIT mutation • CBFB-MYH11 fusion • KIT exon 17 mutation
2ms
We demonstrate that RUNX1 directly interacts with DNMT3A and that CBFB-MYH11 fusion protein sequesters RUNX1 in the cytoplasm, thereby preventing RUNX1 from interacting with and recruiting DNMT3A to its target genes. Our results identify a novel regulation of DNA methylation and provide a molecular basis how CBFB-MYH11 fusion contributes to leukemogenesis.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1) • RUNX1 (RUNX Family Transcription Factor 1) • CBFB (Core-Binding Factor Subunit Beta 2) • MYH11 (Myosin Heavy Chain 11)
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DNMT3A mutation • CBFB-MYH11 fusion
2ms
In subgroup analysis, pretransplant MRD status significantly affected relapse and LFS only in patients with t(8;21) undergoing allogeneic HCT during CR2. In conclusion, our data demonstrate the different prognostic values of pretransplant MRD for CBF-AML, highlighting the need to develop effective therapeutic strategies for such MRD-positive patients.
Clinical • Journal
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RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
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CBFB-MYH11 fusion
5ms
P3, N=203, Active, not recruiting, University of Ulm | Recruiting --> Active, not recruiting | Trial primary completion date: Feb 2021 --> Feb 2024
Clinical • Enrollment closed • Trial primary completion date
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RUNX1 (RUNX Family Transcription Factor 1) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
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RUNX1-RUNX1T1 fusion • CBFB-MYH11 fusion
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dasatinib • daunorubicin • idarubicin hydrochloride
7ms
Although most chronic phase CML patients can be successfully treated with ABL1 tyrosine kinase inhibitors (TKIs), such as imatinib, up to one third of CML patients require alternative treatment...Our findings suggest that secondary fusions, some of which are cytogenetically cryptic, beyond BCR-ABL1 are present in a subset of patients with BCR-ABL1 kinase-independent resistance and demonstrate decreased sensitivity to TKI treatment in vitro. Further characterization of the molecular mechanisms associated with these fusions in the context of BCR-ABL1 open opportunities for identifying new combination treatment strategies to overcome this type of resistance and improve outcomes for these patients.
ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • RUNX1 (RUNX Family Transcription Factor 1) • MECOM (MDS1 And EVI1 Complex Locus)
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BCR-ABL1 fusion • BCR-ABL1 mutation • CBFB-MYH11 fusion
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imatinib
11ms
Characterized a first comprehensive genomic landscape of Chinese pediatric AML, our results reveal a distinct mutation profile as compared to the Western cohort, in terms of both mutation frequency and patterns of mutation co-occurrence. These findings further reveal the complexity of pediatric AML and highlight the importance of tailored risk stratification for Chinese patients in clinical management.
Clinical
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KRAS (KRAS proto-oncogene GTPase) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • NPM1 (Nucleophosmin 1) • JAK2 (Janus kinase 2) • NF1 (Neurofibromin 1) • RUNX1 (RUNX Family Transcription Factor 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • IKZF1 (IKAROS Family Zinc Finger 1) • KMT2C (Lysine Methyltransferase 2C) • PTPN11 (Protein Tyrosine Phosphatase Non-Receptor Type 11) • CBL (Cbl proto-oncogene) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • CSF3R (Colony Stimulating Factor 3 Receptor) • KDM6A (Lysine Demethylase 6A) • GATA2 (GATA Binding Protein 2) • NUP214 (Nucleoporin 214) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
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KRAS mutation • FLT3 mutation • NPM1 mutation • KIT mutation • NF1 mutation • MLL rearrangement • CEBPA mutation • CBFB-MYH11 fusion
11ms
Even in biological subgroups of AML expected to have sensitive disease, induction failure is not rare. Fortunately, the CBM could identify causes of failure and suggest alternative therapies based on co-occurring genomic abnormalities to mitigate the ineffectiveness of standard induction regimens in patients with resistant disease despite their favorable biology. The identification of patient-specific resistance mechanisms characterizes a new therapeutic imperative founded on deep molecular diagnosis that promises to enhance disease outcomes, inform treatment planning, avoid adverse events from ineffective therapies, and reduce costs.
Clinical
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DNMT3A (DNA methyltransferase 1) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • RUNX1 (RUNX Family Transcription Factor 1) • HOXA9 (Homeobox A9) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1)
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DNMT3A mutation • EZH2 mutation • RUNX1-RUNX1T1 fusion • CBFB-MYH11 fusion
1year
In addition, with chromatin immunocleavage sequencing (ChIC-seq) assay, we observed a significant enrichment of RUNX1/CBFβ-SMMHC target genes in Runx1f/fMx1-CreCbfb+/56M cells, especially among down-regulated genes, suggesting that RUNX1 and CBFβ-SMMHC mainly function together as activators of gene expression through direct target gene binding. These data indicate that Runx1 is indispensable for Cbfb-MYH11 induced leukemogenesis by working together with CBFβ-SMMHC to regulate critical genes associated with the generation of a functional AMP population.
Journal
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RUNX1 (RUNX Family Transcription Factor 1)
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CBFB-MYH11 fusion
1year
We provide proof of principle for immunologically targeting AML-initiating fusions and demonstrate that targeting neoantigens has clinical relevance even in low-mutational frequency cancers like fusion-driven AML. This work also represents a first critical step toward the development of TCR T cell immunotherapy targeting fusion gene-driven AML.
Journal
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CD8 (cluster of differentiation 8)
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CBFB-MYH11 fusion