ArticleInternational journal of cancer2009
Telomere homolog oligonucleotides induce apoptosis in malignant but not in normal lymphoid cells: mechanism and therapeutic potential.
Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Review
- Quantitative Biology of Human Shelterin and Telomerase: Searching for the Weakest Point.International journal of molecular sciences · 2019Review
- Effect of therapies-mediated modulation of telomere and/or telomerase on cancer cells radiosensitivity.Oncotarget · 2018Review
- Oligonucleotides Targeting Telomeres and Telomerase in Cancer.Molecules (Basel, Switzerland) · 2018Review
- Treating Cancer by Targeting Telomeres and Telomerase.Antioxidants (Basel, Switzerland) · 2017Review
- Site specific replacements of a single loop nucleoside with a dibenzyl linker may switch the activity of TBA from anticoagulant to antiproliferative.Nucleic acids research · 2015Article
- Star-shaped tetraspermine enhances cellular uptake and cytotoxicity of T-oligo in prostate cancer cells.Pharmaceutical research · 2015Article
- Article
- T-oligo as an anticancer agent in colorectal cancer.Biochemical and biophysical research communications · 2014Article
- Epstein-Barr virus and telomerase: from cell immortalization to therapy.Infectious agents and cancer · 2014Article
- Histone acetyltransferase-deficient p300 mutants in diffuse large B cell lymphoma have altered transcriptional regulatory activities and are required for optimal cell growth.Molecular cancer · 2014Article
- Non-small cell lung cancer is susceptible to induction of DNA damage responses and inhibition of angiogenesis by telomere overhang oligonucleotides.Cancer letters · 2014Article
- Beyond Telomerase: Telomere Instability as a Novel Target for Cancer Therapy.Journal of molecular and genetic medicine : an international journal of biomedical research · 2013Article
- Enhanced cytotoxicity from deoxyguanosine-enriched T-oligo in prostate cancer cells.Nucleic acid therapeutics · 2013Article
- Clinical implications of antitelomeric drugs with respect to the nontelomeric functions of telomerase in cancer.OncoTargets and therapy · 2013Review
- Telomere-homologous G-rich oligonucleotides sensitize human ovarian cancer cells to TRAIL-induced growth inhibition and apoptosis.Nucleic acid therapeutics · 2013Article
- Mechanism of DNA damage responses induced by exposure to an oligonucleotide homologous to the telomere overhang in melanoma.Oncotarget · 2013Article
- Suppressive oligodeoxynucleotides synergistically enhance antiproliferative effects of anticancer drugs in A549 human lung cancer cells.International journal of oncology · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Human B- or T-cell lymphoma lines and primary murine lymphomas were treated with DNA oligonucleotides homologous to the telomere (TTAGGG repeat; "T-oligo"), either alone or in combination with standard, widely-used anticancer chemotherapeutic agents. T-oligo induces cell cycle arrest and apoptosis in cultured human or murine B or T-lymphoma cell lines and primary tumor cells, but exerts no detectable toxicity on normal human or murine primary lymphocytes. Exposure to T-oligo is hypothesized to mimic exposure of the 3' telomere repeat sequence, activating the ataxia telangiectasia mutated kinase, which phosphorylates downstream effectors such as p53, but effects are not dependent solely on functional p53. T-oligo causes early S-phase arrest and cooperates well with G(2)- or M-phase-specific anticancer agents; when combined at 1/10th of the conventional dose, vincristine and T-oligo produce greater-than-additive killing of human or murine lymphoma cells (78% of cells undergoing apoptosis after 6 hr vs. 5% of control cells). In mice, 1/10th of the conventional dose of a standard combination of cyclophosphamide, adriamycin, vincristine and prednisone is twice as effective when used in combination with low dose T-oligo. Thus, T-oligo sensitizes tumors to traditional anticancer agents and represents a potentially important new addition to the therapeutic arsenal for aggressive lymphomas.
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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.