ArticlePloS one2013
ERG transcriptional networks in primary acute leukemia cells implicate a role for ERG in deregulated kinase signaling.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Transcriptome Analysis in Mexican Adults with Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- Article
- Deletion of 3p13 is a late event linked to progression ofCancer management and research · 2018Article
- The oncogenic transcription factor ERG represses the transcription of the tumour suppressor geneOncology letters · 2017Article
- Article
- Article
- Articular cartilage endurance and resistance to osteoarthritic changes require transcription factor Erg.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- ERG induces a mesenchymal-like state associated with chemoresistance in leukemia cells.Oncotarget · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High expression of the E26 transforming sequence related gene (ERG) is associated with poor prognosis in a subgroup of leukemia patients with acute myeloid (AML) and acute T-lymphoblastic leukemia (T-ALL). In a previous study we proposed that ERG overexpression may deregulate several signaling cascades in acute leukemia. Herein, we further expand those studies by identifying a consensus of biological targets in primary blasts of newly diagnosed acute leukemia patients. Our findings of chromatin immunoprecipitation-on-chip of primary samples revealed 48 significantly enriched single genes including DAAM1 and NUMB. Significantly enriched signaling pathways included WNT/β-catenin, p53, and PI3K/AKT with ERG overexpression inducing dephosphorylation of AKT(Ser473) relative to non ERG expressing K562 cells. Cell based ERG overexpression studies also revealed drug resistance to multi-kinase inhibitor, BAY 43-9006 (Sorafenib) and to the tyrosine kinase inhibitor TKI258. Thus in primary leukemic cells, ERG may contribute to the dysregulation of kinase signaling, which results in resistance to kinase inhibitors.
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Registered trials
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