Evidence map›Paper›PMID 11840334›Full record

ArticleOncogene2002

Centrosome abnormalities, recurring deletions of chromosome 4, and genomic amplification of HER2/neu define mouse mammary gland adenocarcinomas induced by mutant HER2/neu.

Cristina Montagna, Eran R Andrechek, Hesed Padilla-Nash, William J Muller, Thomas Ried

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
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  4. Tools used to assay genomic instability in cancers and cancer meiomitosis.Journal of cell communication and signaling · 2022
    Review
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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

5 authors at 2 institutions in 2 countries.

Cristina MontagnaGenetics Branch, Center for Cancer Research, National Cancer Institute/NIH, Bldg. 9, Rm. 1N105, 9 Memorial Drive, Bethesda, MD 20892, USA.
Eran R Andrechek
Hesed Padilla-Nash
William J Muller
Thomas Ried
National Institutes of Health · USMcMaster University · CA

Funding

Mechanisms of breast cancer progressionU01CA105490 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CHODOSH, LEWIS A · 2004 to 2013
$6.7M
NCI NIH HHS U01 CA105490
6 · The paper itself

Abstract

The conditional expression of activated HER2/neu gene under its endogenous promoter in the mammary epithelium of the mouse results in accelerated lobular development and focal mammary tumors. Carcinogenesis, however, requires amplification and considerably increased expression levels of oncogenic neu. Deducing from the multiple genetic aberrations required for human breast cancer to develop, we hypothesized that in addition to the over-expression of an activated HER2/neu, secondary aberrations would occur. We have therefore conducted a genomic screen for chromosomal imbalances and translocations using comparative genomic hybridization and spectral karyotyping. The results reveal a moderate degree of chromosomal instability and micronuclei formation in short-term cultures established from primary tumors. Genomic instability appears to be linked to the amplification of functional centrosomes, a phenomenon that we frequently observed in other tumor types. Seventy per cent of the tumors revealed genomic amplification of HER2/neu, often in the form of double minute chromosomes, which correlated with recurring loss of mouse chromosome 4D-E, a region that is orthologous to distal human chromosome 1p. It is likely that this region contains putative tumor suppressor genes whose inactivation is required for tumor formation in this model of human breast cancer.

Indexed as

Chromosome AberrationsChromosome DeletionGene AmplificationGenes, erbB-2Genes, Tumor SuppressorAdenocarcinomaAnimalsCell Transformation, NeoplasticCentrosomeChromosome MappingErb-b2 Receptor Tyrosine KinasesFemaleFlow CytometryGene SilencingIn Situ Hybridization, FluorescenceKaryotypingErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID11840334
OpenAlexW2139578605

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.