Evidence map›Paper›PMID 11867754›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Genetic instability favoring transversions associated with ErbB2-induced mammary tumorigenesis.

Shiquan Liu, Wenjing Liu, John L Jakubczak, Gregory L Erexson, Kenneth R Tindall, Richard Chan, William J Muller, Sankar Adhya, Susan Garges, Glenn Merlino

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Cytogenetic analysis of a malignant triton tumour by comparative genomic hybridization (CGH) and review of the literature.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2011
    Review
  7. Article
  8. Article
  9. Modeling variation in tumors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  10. Article
  11. A new mutator phenotype in breast cancer?Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Shiquan LiuLaboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892-4264, USA.
Wenjing Liu
John L Jakubczak
Gregory L Erexson
Kenneth R Tindall
Richard Chan
William J Muller
Sankar Adhya
Susan Garges
Glenn Merlino
National Cancer Institute · USNational Institute of Environmental Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been argued that genetic instability is required to generate the myriad mutations that fuel tumor initiation and progression and, in fact, patients with heritable cancer susceptibility syndromes harbor defects in specific genes that normally maintain DNA integrity. However, the vast majority of human cancers arise sporadically, in the absence of deficiencies in known "mutator" genes. We used a cII-based mutation detection assay to show that the mean frequency of forward mutations in primary mammary adenocarcinomas arising in mouse mammary tumor virus-c-erbB2 transgenic mice harboring multiple copies of the lambda bacteriophage genome was significantly higher than in aged-matched, wild-type mammary tissue. Analysis of the cII mutational spectrum within the mammary tumor genomic DNA demonstrated a >6-fold elevation in transversion mutation frequency, resulting in a highly unusual inversion of the transition/transversion ratio characteristic of normal epithelium; frameshift mutation frequencies were unaltered. Arising oncogenic point mutations within the c-erbB2 transgene of such tumors were predominantly transversions as well. Data from this model system support the notion that elaboration of a mutator phenotype is a consequential event in breast cancer and suggest that a novel DNA replication/repair gene is a relatively early mutational target in c-erbB2-induced mammary tumorigenesis.

Indexed as

AdenocarcinomaAgingAmino Acid SequenceAnimalsBacteriophage lambdaCell Transformation, NeoplasticDNA DamageDNA Mutational AnalysisErb-b2 Receptor Tyrosine KinasesFemaleFibroblastsGene FrequencyKineticsMaleMammary Glands, AnimalMammary Neoplasms, AnimalErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID11867754
PMCPMC122599
OpenAlexW2013299815

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.