Evidence map›Paper›PMID 30165401›Full record

ArticleThe Journal of clinical endocrinology and metabolism2018

Alterations in Sod2-Induced Oxidative Stress Affect Endocrine Cancer Progression.

Amruta Ashtekar, Danielle Huk, Alexa Magner, Krista M D La Perle, Laura Boucai, Lawrence S Kirschner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
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  7. Article
  8. TheFrontiers in nutrition · 2025
    Article
  9. Article
  10. The Scavenging Activity of Coenzyme QInternational journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. HAntioxidants (Basel, Switzerland) · 2019
    Review
  20. Article
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

6 authors at 2 institutions in 1 country.

Amruta AshtekarDepartment of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio.
Danielle HukDepartment of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio.
Alexa MagnerDepartment of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio.
Krista M D La PerleDepartment of Veterinary Biosciences, The Ohio State University, Columbus, Ohio.
Laura BoucaiDepartment of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York.
Lawrence S KirschnerDepartment of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio.
The Ohio State University · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Jennifer A. Woyach · 1985 to 2026
$132.3M
Selective Modulation of Thyroidal RadioiodineP01CA124570 · NCI · OHIO STATE UNIVERSITY · PI RINGEL, MATTHEW D · 2008 to 2017
$23.4M
NCI NIH HHS P01 CA124570NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA016058
6 · The paper itself

Abstract

Context: Although important advances have been made in understanding the genetics of endocrine tumors, cellular physiology is relatively understudied as a determinant of tumor behavior. Oxidative stress and reactive oxygen species are metabolic factors that may affect tumor behavior, and these are, in part, controlled by manganese-dependent superoxide dismutase (MnSod), the mitochondrial superoxide dismutase (encoded by SOD2). Objective: We sought to understand the role of MnSod in the prognosis of aggressive human endocrine cancers and directly assessed the effect of MnSod under- or overexpression on tumor behavior, using established mouse thyroid cancer models. Methods: We performed transcriptome analysis of human and mouse models of endocrine cancer. To address the role of Sod2 in endocrine tumors, we introduced a Sod2 null allele or a transgenic Sod2 overexpression allele into mouse models of benign thyroid follicular neoplasia or aggressive, metastatic follicular thyroid cancer (FTC) and monitored phenotypic changes in tumor initiation and progression. Results: In the thyroid, SOD2/Sod2 was downregulated in FTC but not papillary thyroid cancer. Reduced expression of SOD2 was correlated with poorer survival of patients with aggressive thyroid or adrenal cancers. In mice with benign thyroid tumors, Sod2 overexpression increased tumor burden. In contrast, in mice with aggressive FTC, overexpression of Sod2 reduced tumor proliferation and improved mortality rates, whereas its deficiency enhanced tumor growth. Conclusion: Overall, our results indicate that SOD2 has dichotomous roles in cancer progression and acts in a context-specific manner.

Indexed as

Adenocarcinoma, FollicularAdrenal Gland NeoplasmsAnimalsCell Transformation, NeoplasticDisease Models, AnimalDisease ProgressionDown-RegulationFemaleGene Expression ProfilingHumansMaleMiceMice, TransgenicOxidative StressReactive Oxygen SpeciesSuperoxide DismutaseReactive Oxygen SpeciesSuperoxide DismutaseSuperoxide Dismutase 2

Identifiers

PMID30165401
PMCPMC6194813
OpenAlexW2888690979

What OpenQuestion 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 OpenQuestion graph.