Evidence map›Paper›PMID 21893353›Full record

ReviewTrends in pharmacological sciences2011

Nitric oxide and protein phosphatase 2A provide novel therapeutic opportunities in ER-negative breast cancer.

Christopher H Switzer, Sharon A Glynn, Lisa A Ridnour, Robert Y-S Cheng, Michael P Vitek, Stefan Ambs, David A Wink

Open access · greenAbstract readReview
In one paragraph

Review in Trends in pharmacological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. NO-PDT and chemotherapy: spatiotemporal control to achieve therapeutic synergy.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. The tumor-nerve circuit in breast cancer.Cancer metastasis reviews · 2023
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Nitric Oxide and S-Nitrosylation in Cancers: Emphasis on Breast Cancer.Breast cancer : basic and clinical research · 2020
    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

7 authors at 3 institutions in 2 countries.

Christopher H SwitzerRadiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Sharon A Glynn
Lisa A Ridnour
Robert Y-S Cheng
Michael P Vitek
Stefan Ambs
David A Wink
National Cancer Institute · USNational Institutes of Health · USDuke Medical Center · US

Funding

Nitric Oxide as a Modifier of Oxidative StressZIASC007281 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.1M
Properties of redox modified NSAIDs in cancer prevention and treatmentZIABC010899 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$6.7M
Intramural NIH HHS Z99 CA999999NCI NIH HHS Y99 CA999999
6 · The paper itself

Abstract

Basal-like breast cancer is an aggressive disease with limited therapeutic options because these tumors frequently express the 'triple-negative' phenotype. We have recently reported that inducible nitric oxide synthase (NOS2) is a strong predictor of survival in patients with estrogen receptor negative [ER(-)] breast cancer, and that NOS2 expression is correlated with a basal-like phenotype. Recent reports also describe the pro-tumor effects of NO in breast and many other types of cancer. NO promotes cancer progression by activating several oncogenic signaling pathways such as extracellular signal-regulated kinases (ERK)-1/2, phosphoinositide 3-kinases (PI3K)/Akt, and c-Myc. Protein phosphatase 2A (PP2A) is a tumor suppressor that negatively regulates the same cancer-related signaling pathways that are activated by NO. PP2A activity is suppressed in tumor cells, but potential pharmacological agents have recently been described to increase PP2A activity in ER(-) breast cancer cells. We examine here the various functions of NO and PP2A in breast cancer and propose a novel mechanism by which activation of PP2A antagonizes NO signaling that promotes ER(-) breast cancer.

Indexed as

Breast NeoplasmsExtracellular Signal-Regulated MAP KinasesFemaleHumansMolecular Targeted TherapyNeoplasmsNitric OxideProtein Phosphatase 2Receptors, EstrogenSignal TransductionTumor Cells, CulturedExtracellular Signal-Regulated MAP KinasesNitric OxideProtein Phosphatase 2Receptors, Estrogen

Identifiers

PMID21893353
PMCPMC3380363
OpenAlexW2077004299

What OpenQuestion holds

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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.