ArticleLeukemia2011
Revealing the role of TEL/AML1 for leukemic cell survival by RNAi-mediated silencing.
Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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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
8 citing papers in PubMed, 15 citations in OpenAlex.
- RNA binding protein IGF2BP1 synergizes with ETV6-RUNX1 to drive oncogenic signaling in B-cell Acute Lymphoblastic Leukemia.Journal of experimental & clinical cancer research : CR · 2023Article
- Article
- Dysregulation of BCL-2 family proteins by leukemia fusion genes.The Journal of biological chemistry · 2017Review
- Pathogenesis of ETV6/RUNX1-positive childhood acute lymphoblastic leukemia and mechanisms underlying its relapse.Oncotarget · 2017Review
- Effects of p38α/β inhibition on acute lymphoblastic leukemia proliferation and survival in vivo.Leukemia · 2015Article
- Article
- Targeting the PI3K/Akt/mTOR signaling pathway in B-precursor acute lymphoblastic leukemia and its therapeutic potential.Leukemia · 2014Article
- Silencing of ETV6/RUNX1 abrogates PI3K/AKT/mTOR signaling and impairs reconstitution of leukemia in xenografts.Leukemia · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Translocation (12;21), the most frequent chromosomal aberration in childhood acute lymphoblastic leukemia, creates TEL/AML1 fusion gene. Resulting hybrid protein was shown to have a role in pre-leukemia establishment. To address its role for leukemic cell survival, we applied RNA interference to silence TEL/AML1 in leukemic cells. We designed and tested 11 different oligonucleotides targeting the TEL/AML1 fusion site. Using most efficient siRNAs, we achieved an average of 74-86% TEL/AML1 protein knockdown in REH and UOC-B6 leukemic cells, respectively. TEL/AML1 silencing neither decreased cell viability, nor induced apoptosis. On the contrary, it resulted in the modest but significant increase in the S phase fraction and in higher proliferation rate. Opposite effects on cell cycle distribution and proliferation were induced by AML1 silencing, thus, supporting our hypothesis that TEL/AML1 may block AML1-mediated promotion of G1/S progression through the cell cycle. In line with the lack of major effect on phenotype, we found no significant changes in clonogenic potential and global gene expression pattern upon TEL/AML1 depletion. Our data suggest that though TEL/AML1 is important for the (pre)leukemic clone development, it may be dispensable for leukemic cell survival and would not be a suitable target for gene-specific therapy.
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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.