Evidence map›Paper›PMID 21311097›Full record

ArticleOncotarget2010

A molecular signature of normal breast epithelial and stromal cells from Li-Fraumeni syndrome mutation carriers.

Brittney-Shea Herbert, Rebecca A Chanoux, Yunlong Liu, Peter H Baenziger, Chirayu P Goswami, Jeanette N McClintick, Howard J Edenberg, Robert E Pennington, Steven M Lipkin, Levy Kopelovich

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Rewired mNature communications · 2023
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  5. Prostaglandin EThe Journal of biological chemistry · 2019
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  14. Heritable one-hit events defining cancer prevention?Cell cycle (Georgetown, Tex.) · 2013
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Brittney-Shea HerbertDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Rebecca A ChanouxDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Yunlong LiuDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Peter H BaenzigerCenter for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN, USA.
Chirayu P GoswamiCenter for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN, USA.
Jeanette N McClintickCenter for Medical Genomics, Indiana University School of Medicine, Indianapolis, IN, USA.
Howard J EdenbergDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Robert E PenningtonDepartment of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
Steven M LipkinDepartments of Medicine and Genetic Medicine, Weill Cornell Medical College, New York, NY, USA.
Levy KopelovichDivision of Cancer Prevention, National Cancer Institute, Bethesda, MD, USA.
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineCornell University · USNational Cancer Institute · US

Funding

NCI NIH HHS N01 CN043300
6 · The paper itself

Abstract

Specific changes in gene expression during cancer initiation should enable discovery of biomarkers for risk assessment, early detection and targets for chemoprevention. It has been previously demonstrated that altered mRNA and proteome signatures of morphologically normal cells bearing a single inherited "hit" in a tumor suppressor gene parallel many changes observed in the corresponding sporadic cancer. Here, we report on the global gene expression profile of morphologically normal, cultured primary breast epithelial and stromal cells from Li-Fraumeni syndrome (LFS) TP53 mutation carriers. Our analyses identified multiple changes in gene expression in both morphologically normal breast epithelial and stromal cells associated with TP53 haploinsufficiency, as well as interlocking pathways. Notably, a dysregulated p53 signaling pathway was readily detectable. Pharmacological intervention with the p53 rescue compounds CP-31398 and PRIMA-1 provided further evidence in support of the central role of p53 in affecting these changes in LFS cells and treatment for this cancer. Because loss of signaling mediated by TP53 is associated with the development and survival of many human tumors, identification of gene expression profiles in morphologically normal cells that carry "one-hit" p53 mutations may reveal novel biomarkers, enabling the discovery of potential targets for chemoprevention of sporadic tumors as well.

Indexed as

Gene Expression Regulation, NeoplasticAdolescentAdultAza CompoundsBiomarkers, TumorBreast NeoplasmsBridged Bicyclo Compounds, HeterocyclicCarcinoma, Ductal, BreastCells, CulturedEpithelial CellsFemaleGene Expression ProfilingGenetic Predisposition to DiseaseGerm-Line MutationHaploinsufficiencyHumans2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-oneAza CompoundsBiomarkers, TumorBridged Bicyclo Compounds, HeterocyclicCP 31398Neoplasm ProteinsPyrimidinesRNA, MessengerTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID21311097
PMCPMC3039408
OpenAlexW1827153018

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.