Evidence map›Paper›PMID 26569310›Full record

ArticleCancers2015

Differences in Redox Regulatory Systems in Human Lung and Liver Tumors Suggest Different Avenues for Therapy.

Ryuta Tobe, Bradley A Carlson, Petra A Tsuji, Byeong Jae Lee, Vadim N Gladyshev, Dolph L Hatfield

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  8. Article
  9. Mitochondrial ROS control of cancer.Seminars in cancer biology · 2017
    Review
  10. 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

6 authors at 5 institutions in 2 countries.

Ryuta TobeMolecular Biology of Selenium Section, Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. tober@fc.ritsumei.ac.jp.
Bradley A CarlsonMolecular Biology of Selenium Section, Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. carlsonb@mail.nih.gov.
Petra A TsujiDepartment of Biological Sciences, Towson University, Towson, MD 21252, USA. ptsuji@towson.edu.
Byeong Jae LeeSchool of Biological Sciences, Seoul National University, Seoul 151-742, Korea. imbglmg@snu.ac.kr.
Vadim N GladyshevDepartment of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115,USA. vgladyshev@rics.bwh.harvard.edu.
Dolph L HatfieldMolecular Biology of Selenium Section, Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. hatfield@mail.nih.gov.
Cancer Genetics (United States) · USBrigham and Women's Hospital · USNational Cancer Institute · USSeoul National University · KRTowson University · US

Funding

Selenoproteins as Targets for Cancer PreventionR01CA080946 · NCI · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2001 to 2018
$4.5M
IDENTITY OF TERMINATOR AND SELENOCYSTEINE UGA CODONSR01GM061603 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2000 to 2016
$4.0M
Functions of thioredoxin reductases and their targetsR37GM065204 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2011 to 2020
$4.0M
Functions of Mammalian Thioredoxin ReductasesR01GM065204 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2002 to 2009
$2.2M
Selenium in Health and its incorporation into Protein as SelenocysteineZIABC011620 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HATFIELD, DOLPH · 2015 to 2016
$587k
NCI NIH HHS R01 CA080946NIGMS NIH HHS R01 GM061603NIGMS NIH HHS R01 GM065204NIGMS NIH HHS R37 GM065204
6 · The paper itself

Abstract

A common characteristic of many cancer cells is that they suffer from oxidative stress. They, therefore, require effective redox regulatory systems to combat the higher levels of reactive oxygen species that accompany accelerated growth compared to the normal cells of origin. An elevated dependence on these systems in cancers suggests that targeting these systems may provide an avenue for retarding the malignancy process. Herein, we examined the redox regulatory systems in human liver and lung cancers by comparing human lung adenocarcinoma and liver carcinoma to their respective surrounding normal tissues. Significant differences were found in the two major redox systems, the thioredoxin and glutathione systems. Thioredoxin reductase 1 levels were elevated in both malignancies, but thioredoxin was highly upregulated in lung tumor and only slightly upregulated in liver tumor, while peroxiredoxin 1 was highly elevated in lung tumor, but downregulated in liver tumor. There were also major differences within the glutathione system between the malignancies and their normal tissues. The data suggest a greater dependence of liver on either the thioredoxin or glutathione system to drive the malignancy, while lung cancer appeared to depend primarily on the thioredoxin system.

Indexed as

antioxidant systemsglutathioneglutathione peroxidasethioredoxin 1thioredoxin reductase 1

Identifiers

PMID26569310
PMCPMC4695889
OpenAlexW2195158294

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.