Evidence map›Paper›PMID 17257427›Full record

ArticleBreast cancer research : BCR2007

Telomeric DNA induces apoptosis and senescence of human breast carcinoma cells.

Mina Yaar, Mark S Eller, Izabela Panova, John Kubera, Lee Hng Wee, Kenneth H Cowan, Barbara A Gilchrest

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 15% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. The Role of Telomerase in Breast Cancer's Response to Therapy.International journal of molecular sciences · 2022
    Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Telomerase and drug resistance in cancer.Cellular and molecular life sciences : CMLS · 2017
    Review
  8. Treating Cancer by Targeting Telomeres and Telomerase.Antioxidants (Basel, Switzerland) · 2017
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. T-oligo as an anticancer agent in colorectal cancer.Biochemical and biophysical research communications · 2014
    Article
  14. Article
  15. Article
  16. Beyond Telomerase: Telomere Instability as a Novel Target for Cancer Therapy.Journal of molecular and genetic medicine : an international journal of biomedical research · 2013
    Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Mina YaarDepartment of Dermatology, Boston University School of Medicine, Albany Street, Boston, MA 02118-2394, USA.
Mark S Eller
Izabela Panova
John Kubera
Lee Hng Wee
Kenneth H Cowan
Barbara A Gilchrest
Boston University · USUniversity of Nebraska Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCancer is a leading cause of death in Americans. We have identified an inducible cancer avoidance mechanism in cells that reduces mutation rate, reduces and delays carcinogenesis after carcinogen exposure, and induces apoptosis and/or senescence of already transformed cells by simultaneously activating multiple overlapping and redundant DNA damage response pathways.

methodsThe human breast carcinoma cell line MCF-7, the adriamycin-resistant MCF-7 (Adr/MCF-7) cell line, as well as normal human mammary epithelial (NME) cells were treated with DNA oligonucleotides homologous to the telomere 3' overhang (T-oligos). SCID mice received intravenous injections of MCF-7 cells followed by intravenous administration of T-oligos.

resultsActing through ataxia telangiectasia mutated (ATM) and its downstream effectors, T-oligos induced apoptosis and senescence of MCF-7 cells but not NME cells, in which these signaling pathways were induced to a far lesser extent. In MCF-7 cells, experimental telomere loop disruption caused identical responses, consistent with the hypothesis that T-oligos act by mimicking telomere overhang exposure. In vivo, T-oligos greatly prolonged survival of SCID mice following intravenous injection of human breast carcinoma cells.

conclusionBy inducing DNA damage-like responses in MCF-7 cells, T-oligos provide insight into innate cancer avoidance mechanisms and may offer a novel approach to treatment of breast cancer and other malignancies.

Indexed as

ApoptosisCellular SenescenceDNA DamageBreast NeoplasmsFemaleHumansOligonucleotidesTelomereTumor Cells, CulturedOligonucleotides

Identifiers

PMID17257427
PMCPMC1851376
OpenAlexW1540774389

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.