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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Ets variant gene 6

Top mentioned proteins: AML1, TEL, p13, HAD, trkC
Papers on ETV6
High-resolution antibody array analysis of childhood acute leukemia cells.
Kalina et al., Praha, Czech Republic. In Mol Cell Proteomics, Feb 2016
In addition, OPAL1 overexpression corresponded to ETV6-RUNX1 chromosomal translocation.
Concurrent detection of targeted copy number variants and mutations using a myeloid malignancy next generation sequencing panel allows comprehensive genetic analysis using a single testing strategy.
Kelley et al., Salt Lake City, United States. In Br J Haematol, Feb 2016
The most frequent CNVs were 7q deletion including LUC7L2 and EZH2, TP53 deletion, ETV6 deletion, gain of RAD21 on 8q, and 5q deletion, including NSD1 and NPM1.
Myelodysplastic syndromes: Contemporary review and how we treat.
Tefferi et al., Rochester, United States. In Am J Hematol, Jan 2016
With the advent of next generation sequencing, recurrent somatic mutations in genes involved in epigenetic regulation (TET2, ASXL1, EZH2, DNMT3A, IDH1/2), RNA splicing (SF3B1, SRSF2, U2AF1, ZRSR2), DNA damage response (TP53), transcriptional regulation (RUNX1, BCOR, ETV6) and signal transduction (CBL, NRAS, JAK2) have been identified in MDS.
[Detection of copy number variations in pediatric ETV6/RUNX1-positive acute lymphoblastic leukemia with multiplex ligation-dependent probe amplification].
Zhu et al., Tianjin, China. In Zhongguo Dang Dai Er Ke Za Zhi, Jan 2016
OBJECTIVE: To investigate the application of multiplex ligation-dependent probe amplification (MLPA) in the detection of copy number variations (CNVs) in pediatric ETV6/RUNX1-positive acute lymphoblastic leukemia (ALL), to compare this method with conventional karyotype analysis and fluorescence in situ hybridization (FISH), and to evaluate the value of MLPA.
Determination of ETV6-RUNX1 genomic breakpoint by next-generation sequencing.
Chai et al., China. In Cancer Med, Jan 2016
UNASSIGNED: The t(12;21)(p13;q22) ETV6-RUNX1 gene fusion is one of the most common chromosomal translocation in childhood acute lymphoblastic leukemia (ALL).
Genetic predisposition to myelodysplastic syndrome and acute myeloid leukemia in children and young adults.
Olson et al., Philadelphia, United States. In Leuk Lymphoma, Jan 2016
Here, we provide a practical algorithm for approaching a patient with a suspected MDS/AML predisposition, and provide an in-depth review of the established and emerging familial MDS/AML syndromes caused by mutations in the ANKRD26, CEBPA, DDX41, ETV6, GATA2, RUNX1, SRP72 genes.
Germline genetic variation in ETV6 and risk of childhood acute lymphoblastic leukaemia: a systematic genetic study.
Yang et al., Memphis, United States. In Lancet Oncol, Dec 2015
Recent reports of germline ETV6 variations associated with substantial familial clustering of haematological malignancies indicated that this gene is a potentially important genetic determinant for ALL susceptibility.
Mediator kinase inhibition further activates super-enhancer-associated genes in AML.
Shair et al., Cambridge, United States. In Nature, Nov 2015
In AML cells, CA upregulated SE-associated genes with tumour suppressor and lineage-controlling functions, including the transcription factors CEBPA, IRF8, IRF1 and ETV6 (refs 6-8).
Prognostification of ALL by Cytogenetics.
Lone et al., Sr─źnagar, India. In Indian J Hematol Blood Transfus, Sep 2015
Some chromosomal abnormalities are associated with more favorable outcomes, such as high hyperdiploidy (51-65 chromosomes) and the ETV6-RUNX1 fusion.
Molecular signature of salivary gland tumors: potential use as diagnostic and prognostic marker.
Vargas et al., Piracicaba, Brazil. In J Oral Pathol Med, Jun 2015
Finally, the identification of ETV6-NTRK3 in cases previously diagnosed as uncommon acinic cell carcinomas, cystadenocarcinomas, and adenocarcinomas not otherwise specified led to the characterization of a completely new and now widely accepted entity, including, therefore, mammary analogue secretory carcinoma in the list of well-recognized salivary gland carcinomas.
Germline mutations in ETV6 are associated with thrombocytopenia, red cell macrocytosis and predisposition to lymphoblastic leukemia.
Di Paola et al., Aurora, United States. In Nat Genet, May 2015
Whole-exome sequencing identified a heterozygous single-nucleotide change in ETV6 (ets variant 6), c.641C>T, encoding a p.Pro214Leu substitution in the central domain, segregating with thrombocytopenia and elevated MCV.
The utility of next-generation sequencing in diagnosis and monitoring of acute myeloid leukemia and myelodysplastic syndromes.
Tandon et al., Saint Louis, United States. In Int J Lab Hematol, May 2015
DNA-level mutations in several of these genes including NPM1, FLT3, and CEBPA in AML and ASXL1, ETV6, EZH2, RUNX1, and TP53 in MDS are associated with changes in patient outcomes and are now tested for in clinical laboratories.
Germline ETV6 mutations in familial thrombocytopenia and hematologic malignancy.
Shimamura et al., Seattle, United States. In Nat Genet, Feb 2015
We report germline missense mutations in ETV6 segregating with the dominant transmission of thrombocytopenia and hematologic malignancy in three unrelated kindreds, defining a new hereditary syndrome featuring thrombocytopenia with susceptibility to diverse hematologic neoplasms.
Secretory breast carcinoma in a 41-year-old man with long-term follow-up: a special report.
Yang et al., Haikou, China. In Future Oncol, 2014
ETV6-NTRK3 fusion gene is a specific genetic alteration in SBC.
Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia.
Mullighan et al., Memphis, United States. In N Engl J Med, 2014
Cell lines and human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to crizotinib.
Control of endothelial sprouting by a Tel-CtBP complex.
Baker et al., Leiden, Netherlands. In Nat Cell Biol, 2010
the transcriptional repressor Tel plays an evolutionarily conserved role in angiogenesis: it is indispensable for the sprouting of human endothelial cells and for normal development of the Danio rerio blood circulatory system
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