Evidence map›Paper›PMID 12204535›Full record

ArticleCancer cell2002

Telomere dysfunction provokes regional amplification and deletion in cancer genomes.

Rónán C O'Hagan, Sandy Chang, Richard S Maser, Ramya Mohan, Steven E Artandi, Lynda Chin, Ronald A DePinho

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cancer cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 2% 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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.

  1. Pooled it
  2. Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026
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35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Rónán C O'HaganDepartment of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Sandy Chang
Richard S Maser
Ramya Mohan
Steven E Artandi
Lynda Chin
Ronald A DePinho
Harvard University · USBrigham and Women's Hospital · USStanford University · US

Funding

GENOMIC INSTABILITY IN TELOMERASE AND AGING MOUSE MODELSK08AG001019 · NIA · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI CHANG, SANDY S · 2001 to 2003
$373k
NIA NIH HHS 1KO8AG01019-01NIA NIH HHS K08 AG001019
6 · The paper itself

Abstract

Telomere dysfunction and associated fusion-breakage in the mouse encourages epithelial carcinogenesis and a more humanized genomic profile that includes nonreciprocal translocations (NRTs). Here, array comparative genomic hybridization was used to determine the pathogenic significance of NRTs and to determine whether telomere dysfunction also drives amplifications and deletions of cancer-relevant loci. Compared to tumors arising in mice with intact telomeres, tumors with telomere dysfunction possessed higher levels of genomic instability and showed numerous amplifications and deletions in regions syntenic to human cancer hotspots. These observations suggest that telomere-based crisis provides a mechanism of chromosomal instability, including regional amplifications and deletions, that drives carcinogenesis. This model provides a platform for discovery of genes responsible for the major cancers affecting aged humans.

Indexed as

Gene AmplificationGene DeletionAnimalsChromosome AberrationsChromosomes, MammalianDNA, NeoplasmGenes, p53GenomeHumansMiceNeoplasmsRNASyntenyTelomeraseTelomereDNA, NeoplasmRNATelomerasetelomerase RNA

Identifiers

PMID12204535
OpenAlexW1969649126

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.