Evidence map›Paper›PMID 25576159›Full record

ArticleCarcinogenesis2015

Testosterone regulates thyroid cancer progression by modifying tumor suppressor genes and tumor immunity.

Lisa J Zhang, Yin Xiong, Naris Nilubol, Mei He, Swaroop Bommareddi, Xuguang Zhu, Li Jia, Zhen Xiao, Jeong-Won Park, Xia Xu and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-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

26 citing papers in PubMed, 40 citations in OpenAlex.

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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

14 authors at 4 institutions in 1 country.

Lisa J ZhangEndocrine Oncology Branch, Laboratory of Molecular Biology and Bioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Yin XiongEndocrine Oncology Branch, Laboratory of Molecular Biology and Bioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Naris NilubolEndocrine Oncology Branch, Laboratory of Molecular Biology and Bioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Mei HeEndocrine Oncology Branch, Laboratory of Molecular Biology and Bioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Swaroop BommareddiEndocrine Oncology Branch, Laboratory of Molecular Biology and Bioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Xuguang ZhuLaboratory of Molecular Biology and.
Li JiaBioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and.
Zhen XiaoLaboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Jeong-Won ParkLaboratory of Molecular Biology and.
Xia XuLaboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Dhaval PatelEndocrine Oncology Branch, Laboratory of Molecular Biology and Bioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Mark C WillinghamLaboratory of Molecular Biology and.
Sheue-Yann ChengLaboratory of Molecular Biology and.
Electron KebebewEndocrine Oncology Branch, Laboratory of Molecular Biology and Bioinformatics Core Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA and Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA kebebewe@mail.nih.gov.
Endocrine Society · USFrederick National Laboratory for Cancer Research · USDiabetes & Endocrine Associates · USNational Institutes of Health · US

Funding

Preclinical Mouse Models of Thyroid CancerZIABC011191 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CHENG, SHEUE-YANN · 2009 to 2025
$13.8M
Genomic and genetic studies of endocrine cancersZIABC011275 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KEBEBEW, ELECTRON · 2010 to 2018
$8.2M
NCI NIH HHS ZIA BC011275-05
6 · The paper itself

Abstract

Cancer gender disparity has been observed for a variety of human malignancies. Thyroid cancer is one such cancer with a higher incidence in women, but more aggressive disease in men. There is scant evidence on the role of sex hormones on cancer initiation/progression. Using a transgenic mouse model of follicular thyroid cancer (FTC), we found castration led to lower rates of cancer in females and less advanced cancer in males. Mechanistically, less advanced cancer in castrated males was due to increased expression of tumor suppressor (Glipr1, Sfrp1) and immune-regulatory genes and higher tumor infiltration with M1 macrophages and CD8 cells. Functional study showed that GLIPR1 reduced cell growth and increased chemokine secretion (Ccl5) that activates immune cells. Our data demonstrate that testosterone regulates thyroid cancer progression by reducing tumor suppressor gene expression and tumor immunity.

Indexed as

Genes, Tumor SuppressorAdenocarcinoma, FollicularAnimalsCastrationCD8-Positive T-LymphocytesCell LineCell ProliferationChemokine CCL5Disease ProgressionFemaleGene Expression ProfilingHEK293 CellsHumansIntercellular Signaling Peptides and ProteinsMacrophagesMaleCCL5 protein, humanChemokine CCL5GLIPR1 protein, humanIntercellular Signaling Peptides and ProteinsMembrane ProteinsNeoplasm ProteinsNerve Tissue ProteinsRNA, Small InterferingSecreted Frizzled-Related ProteinsSFRP1 protein, humanTestosteroneThyroid Hormone Receptors beta

Identifiers

PMID25576159
PMCPMC4392603
OpenAlexW2323882919

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.