|
Acute myelomonocytic leukemia
|
0.550 |
GeneticVariation
|
disease |
BEFREE |
Initial results of bone marrow, chromosome, and flow cytometric analyses were not in accordance with the diagnosis of acute myelomonocytic leukemia with eosinophilia (AML-M4Eo) or AML with a CBFB/MYH11 rearrangement.
|
19215788 |
2009 |
|
Acute myelomonocytic leukemia
|
0.550 |
FusionGene
|
disease |
ORPHANET |
The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes.
|
19357394 |
2009 |
|
Acute myelomonocytic leukemia
|
0.550 |
Biomarker
|
disease |
BEFREE |
Banding and molecular cytogenetic studies detected a CBFB-MYH11 fusion gene that appeared as abnormal chromosomes 1 and 16 in a baby with acute myeloid leukemia FAB M4-Eo.
|
18328953 |
2008 |
|
Acute myelomonocytic leukemia
|
0.550 |
AlteredExpression
|
disease |
LHGDN |
Comparative analysis of genes regulated in acute myelomonocytic leukemia with and without inv(16)(p13q22) using microarray techniques, real-time PCR, immunohistochemistry, and flow cytometry immunophenotyping.
|
17571080 |
2007 |
|
Acute myelomonocytic leukemia
|
0.550 |
GeneticVariation
|
disease |
BEFREE |
Deletion of CBFB in a patient with acute myelomonocytic leukemia (AML M4Eo) and inversion 16.
|
15381374 |
2004 |
|
Acute myelomonocytic leukemia
|
0.550 |
Biomarker
|
disease |
BEFREE |
This hypothesis was confirmed by the detection of deletions of the 3' regions of the CBFB and the MLL genes in AML M4 patients with inv(16) and in patients with ALL and AML associated with MLL gene translocations, respectively.
|
11369654 |
2001 |
|
Acute myelomonocytic leukemia
|
0.550 |
Biomarker
|
disease |
CTD_human |
A unique structural abnormality of chromosome 16 resulting in a CBF beta-MYH11 fusion transcript in a patient with acute myeloid leukemia, FAB M4.
|
10958941 |
2000 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Inversion of chromosome 16 (inv(16)) generates a fusion gene CBFB-MYH11, which is a driver mutation for acute myeloid leukemia (AML).
|
31624376 |
2020 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
We here describe a unique case of de novo AML-M1, with inv(16)(p13q22), leading to an unusual CBFB-MYH11 fusion transcript, and der(7)t(7;11)(q31;q21).
|
31353165 |
2020 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
AML with CBFB-MYH11, RUNX1-RUNX1T1, mutated NPM1, and FLT3-ITD were excluded and accrued to genotype-specific trials.
|
30728457 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The inv(16) acute myeloid leukemia-associated CBFβ-MYH11 fusion is proposed to block normal myeloid differentiation, but whether this subtype of leukemia cells is poised for a unique cell lineage remains unclear.
|
30850577 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
BEFREE |
Ninety acute myeloid leukemia (AML) patients with inv(16) were monitored CBFβ/MYH11 transcript around allogeneic hematopoietic stem cell transplantation (allo-HSCT).
|
30159599 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
A common mutation in AML is the inversion of chromosome 16 [inv (16)], which generates a fusion between the genes for core binding factor beta (<i>CBFB)</i> and smooth muscle myosin heavy chain gene (<i>MYH11</i>), forming the oncogene <i>CBFB-MYH11</i>.
|
30814129 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
BEFREE |
Clinical Relevance of RUNX1 and CBFB Alterations in Acute Myeloid Leukemia and Other Hematological Disorders.
|
28299658 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
BEFREE |
At univariate analysis for CR achievement, age < 60 years (P < .001), World Health Organization classification (P = .045), low-risk karyotype (P < .001), no high-risk karyotype (P = .006), positivity for AML-ETO (P = .004)/CBFβ-MYH11 (P = .003)/CD15 (P = .006)/CD11b (P = .013), negativity for FLT3-ITD (P = .001), Hb > 8 g/dL (P = .020), and white blood cell < 50 × 10<sup>9</sup> /L (P = .034) had a favorable impact.
|
27400753 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
BEFREE |
Molecular Basis and Targeted Inhibition of CBFβ-SMMHC Acute Myeloid Leukemia.
|
28299661 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
BEFREE |
This general method can also be applied to other AML-associated fusion transcripts such as CBFB-MYH11 and RUNX1-RUNX1T1.
|
28735486 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Myeloid neoplasms with isolated del(16q) with deletion of the CBFB but lacking CBFB-MYH11 rearrangement should not be considered a variant of the AML-defining inv(16).
|
28375434 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
CBFB rearrangement, particularly CBFB-MYH11 fusion resulting from inv(16)(p13.1q22) or t(16;16)(p13.1;q22), is an acute myeloid leukemia (AML)-defining alteration that is associated with a favorable outcome.
|
28253536 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
BEFREE |
Targeting binding partners of the CBFβ-SMMHC fusion protein for the treatment of inversion 16 acute myeloid leukemia.
|
27542261 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
CTD_human |
Outside of signaling alterations, RUNX1-RUNX1T1 and CBFB-MYH11 AMLs demonstrated remarkably different spectra of cooperating mutations, as RUNX1-RUNX1T1 cases harbored recurrent mutations in DHX15 and ZBTB7A, as well as an enrichment of mutations in epigenetic regulators, including ASXL2 and the cohesin complex.
|
27798625 |
2016 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Here, we show that p53 activity is inhibited in inv(16)(+) AML LSCs via interactions with the CBFβ-SMMHC (CM) fusion protein and histone deacetylase 8 (HDAC8).
|
26387755 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Eighty-six adult patients with inv(16) acute myeloid leukemia (AML) in first complete remission (CR1) were serially monitored for CBFB-MYH11 transcript levels during the early courses of chemotherapy.
|
25804769 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
Biomarker
|
disease |
BEFREE |
Here, we report a novel hypomethylation pattern, specific to CBFB-MYH11 fusion resulting from inv(16) rearrangement that is associated with genes previously described as upregulated in inv(16) AML.
|
25266220 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
We confirmed this finding in Mll-Af9 knock-in mice and human M4/M5 acute myeloid leukemia (AML) cell lines, with or without MLL translocations, showing that MLL translocations cause a hypomorph phenotype of RUNX1/CBFβ.
|
24449215 |
2014 |