Evidence map›Paper›PMID 20658316›Full record

ArticleBreast cancer research and treatment2011

Polymorphic variants in TSC1 and TSC2 and their association with breast cancer phenotypes.

Madhura S Mehta, Alexei Vazquez, Diptee A Kulkarni, John E Kerrigan, Gurinder Atwal, Shoichi Metsugi, Deborah L Toppmeyer, Arnold J Levine, Kim M Hirshfield

Open access · greenAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  12. Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021
    Review
  13. Pharmacogenomics and personalized medicine · 2021
    Article
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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

9 authors at 4 institutions in 1 country.

Madhura S MehtaDepartment of Medicine, Division of Medical Oncology, The Cancer Institute of New Jersey, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA.
Alexei Vazquez
Diptee A Kulkarni
John E Kerrigan
Gurinder Atwal
Shoichi Metsugi
Deborah L Toppmeyer
Arnold J Levine
Kim M Hirshfield
Rutgers, The State University of New Jersey · USRutgers Cancer Institute of New JerseyCenter for Systems Biology · USCold Spring Harbor Laboratory · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
NCI NIH HHS P30 CA072720
6 · The paper itself

Abstract

TSC1 acts coordinately with TSC2 in a complex to inhibit mTOR, an emerging therapeutic target and known promoter of cell growth and cell cycle progression. Perturbation of the mTOR pathway, through abnormal expression or function of pathway genes, could lead to tumorigenesis. TSC1 and TSC2 expression is reduced in invasive breast cancer as compared with normal mammary epithelium. Because single nucleotide polymorphisms (SNPs) in regulatory genes have been implicated in risk and age at diagnosis of breast cancers, systematic SNP association studies were performed on TSC1 and TSC2 SNPs for their associations with clinical features of breast cancer. TSC1 and TSC2 haplotypes were constructed from genotyping of multiple loci in both genes in healthy volunteers. SNPs were selected for further study using a bioinformatics approach based on SNP associations with drug response in NCI-60 cell lines and evidence of selection bias based on haplotype frequencies. Genotyping for five TSC1 and one TSC2 loci were performed on genomic DNA from 1,137 women with breast cancer. This study found that for TSC1 rs7874234, TT variant carriers had a 9-year later age at diagnosis of estrogen receptor positive (ER+), but not ER-, ductal carcinomas (P = 0.0049). No other SNP locus showed an association with age at diagnosis, nor any other breast cancer phenotype. TSC1 rs7874234 is hypothesized to be functional in ER+ breast cancer because the T allele, but not the C allele, may create an estrogen receptor element (ERE) site, resulting in increased TSC1 transcription and subsequent inhibition of mTOR.

Indexed as

Gene Expression Regulation, NeoplasticPolymorphism, GeneticAllelesBreast NeoplasmsCarcinoma, DuctalComputational BiologyEstrogen Receptor alphaFemaleGenotypeHaplotypesHumansPhenotypeTime FactorsTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsEstrogen Receptor alphaTSC1 protein, humanTSC2 protein, humanTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID20658316
PMCPMC3876413
OpenAlexW2124527681

What OpenQuestion holds

Textmetadata
LicenceTDM
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.