Results 1 to 10 of about 31,800 (109)

Outcome and prognostic factors of CBF pediatric AML patients with t(8;21) differ from patients with inv(16) [PDF]

open access: yesBMC Cancer, 2023
Purpose To explore the outcome and prognostic factors between inv(16) and t(8;21) disrupt core binding factor (CBF) in acute myeloid leukemia (AML). Methods The clinical characteristic, probability of achieving complete remission (CR), overall survival ...
Kun-yin Qiu   +6 more
doaj   +2 more sources

Targeting miR-126 in inv(16) acute myeloid leukemia inhibits leukemia development and leukemia stem cell maintenance [PDF]

open access: yesNature Communications, 2021
miR-126 is highly expressed in inv(16) Acute myeloid leukemia (AML) but its role is unclear. Here, the authors show that the aberrant expression of miR-126 in inv(16) AML is directly due to the CBFB-MYH11 fusion gene and that it can promote AML ...
Lianjun Zhang   +24 more
doaj   +2 more sources

Acute myeloid leukemia with inv(16)(p13.1q22) and deletion of the 5’MYH11/3’CBFB gene fusion: a report of two cases and literature review [PDF]

open access: yesMolecular Cytogenetics, 2020
Background Abnormalities of chromosome 16 are found in about 5–8% of acute myeloid leukemia (AML). The AML with inv(16)(p13.1q22) or t (16;16)(p13.1;q22) is associated with a high rate of complete remission (CR) and favorable overall survival (OS) when ...
Lili Lv, Jingwei Yu, Zhongxia Qi
doaj   +2 more sources

Faggot cells in therapy‐related acute myeloid leukemia with inv(16) [PDF]

open access: yesClinical Case Reports, 2021
Faggot cells are an uncommon finding in nonacute promyelocytic leukemia, even rarer when observed in mature granulocytic cells. Inv(16) should be dismissed when pre‐eosinophilic granulation and faggot neutrophils are observed.
Ana Vega González de Viñaspre   +5 more
doaj   +2 more sources

Preleukemia and Leukemia-Initiating Cell Activity in inv(16) Acute Myeloid Leukemia [PDF]

open access: yesFrontiers in Oncology, 2018
Acute myeloid leukemia (AML) is a collection of hematologic malignancies with specific driver mutations that direct the pathology of the disease. The understanding of the origin and function of these mutations at early stages of transformation is ...
John Anto Pulikkan   +1 more
doaj   +2 more sources

Disrupting the CBFβ-SMMHC-RUNX1 oncogenic protein–protein interaction in inv(16) AML: from fusion biology to targeted therapy [PDF]

open access: yesDiscover Oncology
Core-binding factor (CBF) leukemias, including inv(16) AML, involve RUNX1/CBFβ chromosomal rearrangements that generate oncogenic fusion proteins. In inv(16) AML, the CBFβ–SMMHC fusion (CBFB–MYH11) dominantly perturbs RUNX1 by sequestering it in aberrant,
Emadeldin M. Kamel   +6 more
doaj   +2 more sources

Rare type I CBFβ/MYH11 fusion transcript in primary acute myeloid leukemia with inv(16)(p13.1q22): a case report [PDF]

open access: yesBrazilian Journal of Medical and Biological Research, 2021
Inv(16)(p13.1q22) in acute myeloid leukemia (AML) is a common chromosomal abnormality. It leads to the core-binding factor ß-subunit (CBFβ)/smooth muscle myosin heavy chain 11 (MYH11) fusion gene.
Wenyi Zhang   +5 more
doaj   +2 more sources

Genome-wide binding of transcription factors in inv(16) acute myeloid leukemia [PDF]

open access: yesGenomics Data, 2014
The inv(16) translocation is associated with 5% of AML cases and gives rise to expression of the oncofusion protein CBFβ-MYH11. Although different molecular mechanisms for the oncogenic activity of this fusion protein have been proposed these were mostly
A. Mandoli, K. Prange, J.H.A. Martens
doaj   +2 more sources

Constitutional pericentric inversion of chromosome 16, inv(16)(p13.1q22), mimicking acute myeloid leukemia [PDF]

open access: yeseJHaem, 2022
Shuji Ozaki   +6 more
doaj   +2 more sources

PB1836: LOSS OF HETEROZYGOSITY IN AML PATIENTS WITH INV(16) [PDF]

open access: yesHemaSphere, 2023
Dmitry Bessmertniy   +4 more
doaj   +2 more sources

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