Evidence map›Paper›PMID 21397008›Full record

ArticleFree radical biology & medicine2011

Differential gene expression in normal and transformed human mammary epithelial cells in response to oxidative stress.

Diego F Cortes, Wei Sha, Valerie Hower, Greg Blekherman, Reinhard Laubenbacher, Steven Akman, Suzy V Torti, Vladimir Shulaev

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. NAF-1 and mitoNEET are central to human breast cancer proliferation by maintaining mitochondrial homeostasis and promoting tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2013 · on this map
    Article
  8. Matrix metalloproteinase gene expressions might be oxidative stress targets in gastric cancer cell lines.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013
    Article
  9. Iron and cancer: more ore to be mined.Nature reviews. Cancer · 2013
    Review
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

8 authors.

Diego F CortesVirginia Bioinformatics Institute, Blacksburg, VA 24061, USA.
Wei Sha
Valerie Hower
Greg Blekherman
Reinhard Laubenbacher
Steven Akman
Suzy V Torti
Vladimir Shulaev

Funding

Training Program in Cancer BiologyT32CA079448 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI KRIDEL, STEVEN J. · 2000 to 2014
$6.5M
Molecular Fingerprinting of Breast Cancer DevelopmentR01CA120170 · NCI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SHULAEV, VLADIMIR · 2007 to 2009
$1.0M
NCI NIH HHS R01 CA120170NCI NIH HHS R01CA120170NCI NIH HHS T32 CA079448
6 · The paper itself

Abstract

Oxidative stress plays a key role in breast carcinogenesis. To investigate whether normal and malignant breast epithelial cells differ in their responses to oxidative stress, we examined the global gene expression profiles of three cell types, representing cancer progression from a normal to a malignant stage, under oxidative stress. Normal human mammary epithelial cells (HMECs), an immortalized cell line (HMLER-1), and a tumorigenic cell line (HMLER-5) were exposed to increased levels of reactive oxygen species (ROS) by treatment with glucose oxidase. Functional analysis of the metabolic pathways enriched with differentially expressed genes demonstrated that normal and malignant breast epithelial cells diverge substantially in their response to oxidative stress. Whereas normal cells exhibit the up-regulation of antioxidant mechanisms, cancer cells are unresponsive to the ROS insult. However, the gene expression response of normal HMECs under oxidative stress is comparable to that of the malignant cells under normal conditions, indicating that altered redox status is persistent in breast cancer cells, which makes them resistant to increased generation of ROS. We discuss some of the possible adaptation mechanisms of breast cancer cells under persistent oxidative stress that differentiate them from normal mammary epithelial cells as regards the response to acute oxidative stress.

Indexed as

Cell Transformation, NeoplasticOxidative StressBreast NeoplasmsCarcinomaCell Line, TransformedFemaleGene Expression ProfilingGlucose OxidaseHumansMammary Glands, HumanMicroarray AnalysisReactive Oxygen SpeciesGlucose OxidaseReactive Oxygen Species

Identifiers

PMID21397008
PMCPMC3119600

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Registered trials

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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.