Evidence map›Paper›PMID 29249638›Full record

ArticleMolecular metabolism2018

Androgen receptor overexpression in prostate cancer in type 2 diabetes.

Stefan Zoltán Lutz, Jörg Hennenlotter, Marcus Oliver Scharpf, Corinna Sailer, Louise Fritsche, Vera Schmid, Konstantinos Kantartzis, Robert Wagner, Rainer Lehmann, Lucia Berti and 8 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  15. Antihormone treatment differentially regulates PSA secretion, PSMA expression andJournal of cancer research and clinical oncology · 2021
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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

18 authors at 4 institutions in 1 country.

Stefan Zoltán LutzDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Jörg HennenlotterDepartment of Urology, University of Tübingen, Germany.
Marcus Oliver ScharpfInstitute of Pathology, University of Tübingen, Germany.
Corinna SailerInstitute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Louise FritscheInstitute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Vera SchmidDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Konstantinos KantartzisDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Robert WagnerDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Rainer LehmannDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Lucia BertiInstitute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany; Institute of Experimental Genetics, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.
Andreas PeterDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Harald StaigerInstitute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany; Institute of Pharmaceutical Sciences, Department of Pharmacy and Biochemistry, University of Tübingen, Germany.
Andreas FritscheDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Falko FendInstitute of Pathology, University of Tübingen, Germany.
Tilman TodenhöferDepartment of Urology, University of Tübingen, Germany.
Arnulf StenzlDepartment of Urology, University of Tübingen, Germany.
Hans-Ulrich HäringDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany. Electronic address: hans-ulrich.haering@med.uni-tuebingen.de.
Martin HeniDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University of Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases (IDM), Helmholtz Center Munich, University of Tübingen, Germany; German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
University of Tübingen · DEGerman Center for Diabetes Research · DEHeinrich Heine University Düsseldorf · DEDeutsches Diabetes-Zentrum e.V. · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWhile prostate cancer does not occur more often in men with diabetes, survival is markedly reduced in this patient group. Androgen signaling is a known and major driver for prostate cancer progression. Therefore, we analyzed major components of the androgen signaling chain and cell proliferation in relation to type 2 diabetes.

methodsTumor content of 70 prostate tissue samples of men with type 2 diabetes and 59 samples of patients without diabetes was quantified by an experienced pathologist, and a subset of 51 samples was immunohistochemically stained for androgen receptor (AR). mRNA expression of AR, insulin receptor isoform A (IR-A) and B (IR-B), IGF-1 receptor (IGF1R), Cyp27A1 and Cyp7B1, PSA gene KLK3, PSMA gene FOLH1, Ki-67 gene MKI67, and estrogen receptor beta (ESR2) were analyzed by RT-qPCR.

resultsAR mRNA and protein expression were associated with the tumor content only in men with diabetes. AR expression also correlated with downstream targets PSA (KLK3) and PSMA (FOLH1) and increased cell proliferation. Only in diabetes, AR expression was correlated to higher IR-A/IR-B ratio and lower IR-B/IGF1R ratio, thus, in favor of the mitogenic isoforms. Reduced Cyp27A1 and increased Cyp7B1 expressions in tumor suggest lower levels of protective estrogen receptor ligands in diabetes.

conclusionsWe report elevated androgen receptor signaling and activity presumably due to altered insulin/IGF-1 receptors and decreased levels of protective estrogen receptor ligands in prostate cancer in men with diabetes. Our results reveal new insights why these patients have a worse prognosis. These findings provide the basis for future clinical trials to investigate treatment response in patients with prostate cancer and diabetes.

Indexed as

AdultAgedAged, 80 and overAntigens, SurfaceCholestanetriol 26-MonooxygenaseCytochrome P450 Family 7Diabetes Mellitus, Type 2Estrogen Receptor betaGlutamate Carboxypeptidase IIHumansKallikreinsKi-67 AntigenMaleMiddle AgedProstateProstate-Specific AntigenAntigens, SurfaceCholestanetriol 26-MonooxygenaseCYP27A1 protein, humanCYP7B1 protein, humanCytochrome P450 Family 7ESR2 protein, humanEstrogen Receptor betaFOLH1 protein, humanGlutamate Carboxypeptidase IIKallikreinsKi-67 AntigenKLK3 protein, humanProstate-Specific AntigenReceptor, IGF Type 1Receptor, InsulinReceptors, AndrogenSteroid HydroxylasesAndrogen receptorCyp27A1Cyp7B1IGF-1 receptorInsulin receptorProstate cancer

Identifiers

PMID29249638
PMCPMC5985051
OpenAlexW2771351814

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.