ArticleJournal of oncology2012
Modulation of telomeres in alternative lengthening of telomeres type I like human cells by the expression of werner protein and telomerase.
Article in Journal of oncology, 2012. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
8 citing papers in PubMed, 9 citations in OpenAlex.
- Genome-nanosurface interaction of titania nanotube arrays: evaluation of telomere, telomerase and NF-κB activities on an epithelial cell model.RSC advances · 2022Article
- Telomere Length Maintenance in Cancer: At the Crossroad between Telomerase and Alternative Lengthening of Telomeres (ALT).International journal of molecular sciences · 2018Review
- Co-targeting ALK and EGFR parallel signaling in oral squamous cell carcinoma.Oral oncology · 2016Article
- Telomere profiles and tumor-associated macrophages with different immune signatures affect prognosis in glioblastoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- The DNA structure and sequence preferences of WRN underlie its function in telomeric recombination events.Nature communications · 2015Article
- The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair.DNA repair · 2014Review
- WRN loss induces switching of telomerase-independent mechanisms of telomere elongation.PloS one · 2014Article
- The roles of WRN and BLM RecQ helicases in the Alternative Lengthening of Telomeres.Nucleic acids research · 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
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The alternative lengthening of telomeres (ALT) is a recombination-based mechanism of telomere maintenance activated in 5-20% of human cancers. In Saccharomyces cerevisiae, survivors that arise after inactivation of telomerase can be classified as type I or type II ALT. In type I, telomeres have a tandem array structure, with each subunit consisting of a subtelomeric Y' element and short telomere sequence. Telomeres in type II have only long telomere repeats and require Sgs1, the S. cerevisiae RecQ family helicase. We previously described the first human ALT cell line, AG11395, that has a telomere structure similar to type I ALT yeast cells. This cell line lacks the activity of the Werner syndrome protein, a human RecQ helicase. The telomeres in this cell line consist of tandem repeats containing SV40 DNA, including the origin of replication, and telomere sequence. We investigated the role of the SV40 origin of replication and the effects of Werner protein and telomerase on telomere structure and maintenance in AG11395 cells. We report that the expression of Werner protein facilitates the transition in human cells of ALT type I like telomeres to type II like telomeres in some aspects. These findings have implications for the diagnosis and treatment of cancer.
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.