Evidence map›Paper›PMID 27464521›Full record

ReviewAntioxidants & redox signaling2017

Nitric Oxide Synthase-2-Derived Nitric Oxide Drives Multiple Pathways of Breast Cancer Progression.

Debashree Basudhar, Veena Somasundaram, Graciele Almeida de Oliveira, Aparna Kesarwala, Julie L Heinecke, Robert Y Cheng, Sharon A Glynn, Stefan Ambs, David A Wink, Lisa A Ridnour

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
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  8. NO- and HNitric oxide : biology and chemistry · 2024
    Review
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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

10 authors at 3 institutions in 3 countries.

Debashree Basudhar1 Cancer and Inflammation Program, National Cancer Institute-Frederick , Frederick, Maryland.
Veena Somasundaram1 Cancer and Inflammation Program, National Cancer Institute-Frederick , Frederick, Maryland.
Graciele Almeida de Oliveira1 Cancer and Inflammation Program, National Cancer Institute-Frederick , Frederick, Maryland.
Aparna Kesarwala2 Radiation Oncology Branch, National Cancer Institute , Bethesda, Maryland.
Julie L Heinecke1 Cancer and Inflammation Program, National Cancer Institute-Frederick , Frederick, Maryland.
Robert Y Cheng1 Cancer and Inflammation Program, National Cancer Institute-Frederick , Frederick, Maryland.
Sharon A Glynn3 Pathology, Lambe Institute for Translational Research, School of Medicine, National University of Ireland , Galway, Ireland .
Stefan Ambs4 Laboratory of Human Carcinogenesis, National Cancer Institute , Bethesda, Maryland.
David A Wink1 Cancer and Inflammation Program, National Cancer Institute-Frederick , Frederick, Maryland.
Lisa A Ridnour1 Cancer and Inflammation Program, National Cancer Institute-Frederick , Frederick, Maryland.
Cancer Institute (WIA) · INNational Cancer Institute · USNational University of Ireland · IE

Funding

Novel Markers for Disease Outcome in Breast CancerZIABC010887 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBS, STEFAN · 2009 to 2025
$11.5M
6 · The paper itself

Abstract

significanceBreast cancer is the second leading cause of cancer-related deaths among women in the United States. Development and progression of malignancy are associated with diverse cell signaling pathways that control cell proliferation, survival, motility, invasion, and metastasis. Recent Advances: An increasing number of clinical studies have implicated a strong relationship between elevated tumor nitric oxide synthase-2 (NOS2) expression and poor patient survival. CRITICAL ISSUES: Herein, we review what we believe to be key mechanisms in the role(s) of NOS2-derived nitric oxide (NO) as a driver of breast cancer disease progression. High NO increases cyclooxygenase-2 activity, hypoxia inducible factor-1 alpha protein stabilization, and activation of important cell signaling pathways, including phosphoinositide 3-kinase/protein kinase B, mitogen-activated protein kinase, epidermal growth factor receptor, and Ras, through post-translational protein modifications. Moreover, dysregulated NO flux within the tumor microenvironment has other important roles, including the promotion of angiogenesis and modulation of matrix metalloproteinase/tissue inhibitor matrix metalloproteinase associated with tumor progression. FUTURE DIRECTIONS: The elucidation of these and other NO-driven pathways implicates NOS2 as a key driver of breast cancer disease progression and provides a new perspective in the identification of novel targets that may be therapeutically beneficial in the treatment of estrogen receptor-negative disease. Antioxid. Redox Signal. 26, 1044-1058.

Indexed as

AnimalsBreast NeoplasmsDisease ProgressionFemaleGene Expression RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitNitric OxideNitric Oxide Synthase Type IIProtein StabilitySignal TransductionTumor MicroenvironmentHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNitric OxideNitric Oxide Synthase Type IINOS2 protein, humanbiomarkercancer progressionmetastasisnitric oxideNOS2

Identifiers

PMID27464521
PMCPMC5488348
OpenAlexW2510876230

What Socratic holds

Textmetadata
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 Socratic graph.