Evidence map›Paper›PMID 20407015›Full record

Trial reportMolecular cancer research : MCR2010

Altered-function p53 missense mutations identified in breast cancers can have subtle effects on transactivation.

Jennifer J Jordan, Alberto Inga, Kathleen Conway, Sharon Edmiston, Lisa A Carey, Lin Wu, Michael A Resnick

Open access · bronzeAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Molecular cancer research : MCR, 2010. 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
2.3field-weighted citation impact, top 12% 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, 78 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Jennifer J JordanLaboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709, USA.
Alberto Inga
Kathleen Conway
Sharon Edmiston
Lisa A Carey
Lin Wu
Michael A Resnick
University of Trento · ITMaterials Systems (United States) · US

Funding

Tissue Procurement & PathologyP50CA058223 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KATHERINE A. HOADLEY · 1992 to 2026
$59.3M
Zonisamide in Patients with Neuropathic Pain Associated with Diabetic NeuropathyM01RR000046 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JOY, MELANIE S · 1985 to 2008
$38.5M
Human Genes Affecting Chromosome Metabolism and Stress ResponseZIAES065079 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MENENDEZ RENDON, DANIEL · 2009 to 2021
$12.5M
ISOLATION &CHARACTERIZATION OF GENES AFFECTING YEAST CHROMOSOME METABOLISMZ01ES065079 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RESNICK, MICHAEL A · 1994 to 2008
$1.8M
Intramural NIH HHS Z01 ES065079NCI NIH HHS CA58223NCI NIH HHS P50 CA058223NCRR NIH HHS M01 RR000046NCRR NIH HHS M01RR00046
6 · The paper itself

Abstract

Mutations of the sequence-specific master regulator p53 that alter transactivation function from promoter response elements (RE) could result in changes in the strength of gene activation or spectra of genes regulated. Such mutations in this tumor suppressor might lead to dramatic phenotypic changes and diversification of cell responses to stress. We have determined "functional fingerprints" of sporadic breast cancer-related p53 mutants, many of which are also associated with familial cancer proneness such as the Li-Fraumeni syndrome and germline BRCA1/2 mutant-associated cancers. The ability of p53, wild-type and mutants, to transactivate from 11 human target REs has been assessed at variable expression levels using a cellular, isogenomic yeast model system that allows for the rapid analysis of p53 function using a qualitative and a quantitative reporter. Among 50 missense mutants, 29 were classified as loss of function. The remaining 21 retained transactivation toward at least one RE. At high levels of galactose-induced p53 expression, 12 of 21 mutants that retain transactivation seemed similar to wild-type. When the level of galactose was reduced, transactivation defects could be revealed, suggesting that some breast cancer-related mutants can have subtle changes in transcription. These findings have been compared with clinical data from an ongoing neoadjuvant chemotherapy treatment trial for locally advanced breast tumors. The functional and nonfunctional missense mutations may distinguish tumors in terms of demographics, appearance, and relapse, implying that heterogeneity in the functionality of specific p53 mutations could affect clinical behavior and outcome.

Indexed as

Breast NeoplasmsCarcinomaFemaleGalactoseGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansMutagenesis, Site-DirectedMutation, MissensePromoter Regions, GeneticResponse ElementsTranscriptional ActivationTranscription, GeneticTumor Suppressor Protein p53GalactoseTumor Suppressor Protein p53

Identifiers

PMID20407015
PMCPMC2873663
OpenAlexW2158224935

What OpenQuestion holds

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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.