Evidence map›Paper›PMID 15557801›Full record

ReviewJournal of mammary gland biology and neoplasia2004

Telomere shortening occurs early during breast tumorigenesis: a cause of chromosome destabilization underlying malignant transformation?

Alan K Meeker, Pedram Argani

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 100 citations in OpenAlex.

  1. Abnormal mRNA Expression Levels of Telomere-Binding Proteins Represent Biomarkers in Myelodysplastic Syndromes: A Case-Control Study.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2017
    Trial
  2. Trial
  3. Review
  4. Review
  5. Expression and clinical significance ofInternational journal of clinical and experimental pathology · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Cancer telomeres and white crows.American journal of clinical and experimental urology · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
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  19. Article
  20. Telomere instability in papillary bladder urothelial carcinomas: Comparison with grading and risk of recurrence.Indian journal of urology : IJU : journal of the Urological Society of India · 2014
    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

2 authors at 1 institution in 1 country.

Alan K MeekerDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ameeker@mail.jhmi.edu
Pedram Argani
Johns Hopkins Medicine · US

Funding

TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
VACCINES--A NEW PARADIGM FOR BREAST CANCERP50CA088843 · NCI · JOHNS HOPKINS UNIVERSITY · PI DAVIDSON, NANCY ELLEN · 2000 to 2010
$27.8M
Urology Research Training GrantT32DK007552 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI COFFEY, DONALD STRALEY · 1987 to 2012
$2.9M
NCI NIH HHS CA58236NCI NIH HHS CA88843NIDDK NIH HHS T32DK07552
6 · The paper itself

Abstract

Chromosomal instability appears early during breast carcinogenesis and is considered a major driving force in malignant transformation. While current evidence suggests that centrosomal and mitotic checkpoint defects may, in large part, account for numerical chromosomal abnormalities, the mechanisms underlying structural chromosomal abnormalities remain largely unknown. Telomeres stabilize and protect chromosomal termini, but shorten due to cell division and oxidative damage. Moderate telomere shortening signals a tumor suppressive growth arrest in normal cells. Critically short telomeres, in the setting of abrogated DNA damage checkpoints, cause chromosomal instability due to end-to-end chromosomal fusions, subsequent breakage, and rearrangement, resulting in an increased cancer incidence in animal models. Recent results from high resolution in situ telomere length assessment in human breast tissues indicate that significant telomere shortening is prevalent in preinvasive breast lesions (DCIS), as well as focal areas of histologically normal epithelium from which breast carcinoma is thought to arise. Telomere shortening is therefore a strong candidate for the cause of structural chromosome defects that contribute to breast cancer development.

Indexed as

Chromosomal InstabilityBreast NeoplasmsCarcinoma, Intraductal, NoninfiltratingCell Transformation, NeoplasticDNA DamageEpithelial CellsHumansTelomeraseTelomereTelomerase

Identifiers

PMID15557801
OpenAlexW2037803457

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.