ArticleBlood2006
The ETS factor TEL2 is a hematopoietic oncoprotein.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- ETV7 promotes 5-FU resistance and malignant progression through CXCL1-induced NETs formation in colorectal cancer.Communications biology · 2026Article
- Enhancing the potency of CAR-T cells against solid tumors through transcription factor engineering.JCI insight · 2025Review
- ETS-1 in tumor immunology: implications for novel anti-cancer strategies.Frontiers in immunology · 2025Review
- Assembly of mTORC3 Involves Binding of ETV7 to Two Separate Sequences in the mTOR Kinase Domain.International journal of molecular sciences · 2024Article
- Mitigation of Breast Cancer Cells' Invasiveness via Down Regulation of ETV7, Hippo, and PI3K/mTOR Pathways by Vitamin D3 Gold-Nanoparticles.International journal of molecular sciences · 2024Article
- ETV7 promotes colorectal cancer progression through upregulation of IFIT3.Functional & integrative genomics · 2024Article
- Mapping interindividual dynamics of innate immune response at single-cell resolution.Nature genetics · 2023Article
- ETV7 reduces inflammatory responses in breast cancer cells by repressing the TNFR1/NF-κB axis.Cell death & disease · 2023Article
- Article
- ETV7 regulates breast cancer stem-like cell features by repressing IFN-response genes.Cell death & disease · 2021Article
- Observational
- Integrated Analysis of the ETS Family in Melanoma Reveals a Regulatory Role of ETV7 in the Immune Microenvironment.Frontiers in immunology · 2020Article
- Mechanistic Modeling of Gene Regulation and Metabolism Identifies Potential Targets for Hepatocellular Carcinoma.Frontiers in genetics · 2020Article
- Article
- Establishment of a transgenic mouse to model ETV7 expressing human tumors.Transgenic research · 2019Article
- Snail promotes metastasis of nasopharyngeal carcinoma partly by down-regulating TEL2.Cancer communications (London, England) · 2018Article
- ETV7 is an essential component of a rapamycin-insensitive mTOR complex in cancer.Science advances · 2018Article
- ETV7-Mediated DNAJC15 Repression Leads to Doxorubicin Resistance in Breast Cancer Cells.Neoplasia (New York, N.Y.) · 2018Article
- The ETS family of oncogenic transcription factors in solid tumours.Nature reviews. Cancer · 2017Review
- TEL2 suppresses metastasis by down-regulating SERPINE1 in nasopharyngeal carcinoma.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
TEL2/ETV7 is highly homologous to the ETS transcription factor TEL/ETV6, a frequent target of chromosome translocation in human leukemia. Although both proteins are transcriptional inhibitors binding similar DNA recognition sequences, they have opposite biologic effects: TEL inhibits proliferation while TEL2 promotes it. In addition, forced expression of TEL2 but not TEL blocks vitamin D3-induced differentiation of U937 and HL60 myeloid cells. TEL2 is expressed in the hematopoietic system, and its expression is up-regulated in bone marrow samples of some patients with leukemia, suggesting a role in oncogenesis. Recently we also showed that TEL2 cooperates with Myc in B lymphomagenesis in mice. Here we show that forced expression of TEL2 alone in mouse bone marrow causes a myeloproliferative disease with a long latency period but with high penetrance. This suggested that secondary mutations are necessary for disease development. Treating mice receiving transplants with TEL2-expressing bone marrow with the chemical carcinogen N-ethyl-N-nitrosourea (ENU) resulted in significantly accelerated disease onset. Although the mice developed a GFP-positive myeloid disease with 30% of the mice showing elevated white blood counts, they all died of T-cell lymphoma, which was GFP negative. Together our data identify TEL2 as a bona fide oncogene, but leukemic transformation is dependent on secondary mutations.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.