ArticlePloS one2010
Identification of two critically deleted regions within chromosome segment 7q35-q36 in EVI1 deregulated myeloid leukemia cell lines.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- The Tumor-suppressive role of CNTNAP2 in glioma: Dual regulation of the NDN-ERK axis and M2 macrophage polarization.Cancer gene therapy · 2026Article
- Review
- Revertant somatic mosaicism as a cause of cancer.Cancer science · 2021Review
- EVI1 dysregulation: impact on biology and therapy of myeloid malignancies.Blood cancer journal · 2021Review
- Article
- Newly emerged isolated Del(7q) in patients with prior cytotoxic therapies may not always be associated with therapy-related myeloid neoplasms.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- -7/7q- syndrome in myeloid-lineage hematopoietic malignancies: attempts to understand this complex disease entity.Oncogene · 2015Review
- Genomic aberrations of the CACNA2D1 gene in three patients with epilepsy and intellectual disability.European journal of human genetics : EJHG · 2015Article
- Clinical relevance of breast cancer-related genes as potential biomarkers for oral squamous cell carcinoma.BMC cancer · 2014Article
- Mate pair sequencing for the detection of chromosomal aberrations in patients with intellectual disability and congenital malformations.European journal of human genetics : EJHG · 2014Article
- Genetic risk prediction for normal-karyotype acute myeloid leukemia using whole-exome sequencing.Genomics & informatics · 2013Article
- Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomal rearrangements involving the EVI1 proto-oncogene are a recurrent finding in myeloid leukemias and are indicative of a poor prognosis. Rearrangements of the EVI1 locus are often associated with monosomy 7 or cytogenetic detectable deletions of part of 7q. As EVI1 overexpression alone is not sufficient to induce leukemia, loss of a 7q tumour suppressor gene might be a required cooperating event. To test this hypothesis, we performed high-resolution array comparative genomic hybridization analysis of twelve EVI1 overexpressing patients and three EVI1 deregulated cell lines to search for 7q submicroscopic deletions. This analysis lead to the delineation of two critical regions, one of 0.39 Mb on 7q35 containing the CNTNAP2 gene and one of 1.33 Mb on chromosome bands 7q35-q36 comprising nine genes in EVI1 deregulated cell lines. These findings open the way to further studies aimed at identifying the culprit EVI1 implicated tumour suppressor genes on 7q.
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