Evidence map›Paper›PMID 34855273›Full record

ArticleThe Prostate2022

Advanced glycation end-products (AGEs) are lower in prostate tumor tissue and inversely related to proportion of West African ancestry.

Morgan L Zenner, Yves B Helou, Ryan J Deaton, Maria Sverdlov, Heng Wang, Andre Kajdacsy-Balla, Virgilia Macias, Cindy Voisine, Marcus Murray, Sarki A Abdulkadir and 2 more

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

12 authors at 4 institutions in 1 country.

Morgan L ZennerDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA.
Yves B HelouDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA.
Ryan J DeatonDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA.
Maria SverdlovDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA.
Heng WangDepartment of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, Illinois, USA.
Andre Kajdacsy-BallaDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA.
Virgilia MaciasDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA.
Cindy VoisineDepartment of Biology, Northeastern Illinois University, Chicago, Illinois, USA.
Marcus MurrayProject Brotherhood, Chicago, Illinois, USA.
Sarki A AbdulkadirDepartment of Urology, Northwestern University, Chicago, Illinois, USA.
Adam B MurphyDepartment of Urology, Northwestern University, Chicago, Illinois, USA.
Larisa NonnDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA.ORCID 0000-0002-0852-7726
University of Illinois Chicago · USNorthwestern University · USBrotherhood (United States) · USNortheastern Illinois University · US

Funding

Research Education CoreU54CA202997 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CIECIERSKI, CHRISTINA, FEINGLASS, JOSEPH M · 2015 to 2024
$13.8M
Research Education CoreU54CA203000 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CIECIERSKI, CHRISTINA, FEINGLASS, JOSEPH M · 2015 to 2024
$12.4M
The Chicago Cancer Health Equity Collaborative (ChicagoCHEC)U54CA202995 · NCI · NORTHEASTERN ILLINOIS UNIVERSITY · PI CIECIERSKI, CHRISTINA, FEINGLASS, JOSEPH M · 2015 to 2024
$9.5M
Institutional Career DevelopmentKL2TR002002 · NCATS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PHILLIPS, SHANE A · 2016 to 2024
$6.8M
Cancer Health Equity Career Development ProgramT32CA057699 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Marian L. Fitzgibbon · 2018 to 2026
$3.0M
Vitamin D Deficiency Leads to Increased Intra‐Prostatic Androgens in African American MenR21CA231610 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NONN, LARISA · 2018 to 2019
$480k
microRNAs in Prostate-derived Exosomes as Prognostic Biomarkers and Mediators of Intercellular CommunicationF30CA243197 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZENNER, MORGAN LEIGH · 2020 to 2023
$180k
Biological & Environmental Mediators of Vitamin D and Aggressive Prostate CancerIK2CX000926 · VA · JESSE BROWN VA MEDICAL CENTER · PI MURPHY, ADAM BRYANT · 2013 to 2019
–
CSRD VA IK2 CX000926NCATS NIH HHS KL2 TR002002NCI NIH HHS F30 CA243197NCI NIH HHS R21 CA231610NCI NIH HHS T32 CA057699NCI NIH HHS U54 CA202995NCI NIH HHS U54 CA202997NCI NIH HHS U54 CA203000
6 · The paper itself

Abstract

backgroundThe metabolism of normal prostate relies on glycolysis, with prostate cancer having reduced glycolysis and increased aerobic metabolism. Advanced glycation end products (AGEs) accumulate in tissues as a result of age and glycolytic rate. Differential AGE levels were recently observed in prostate cancer tissues. Herein we sought to quantify AGEs in benign and cancer prostate tissue in a diverse cohort of patients.

methodsLevels of the AGE Nε-(carboxylethyl)lysine (CML) were quantified by immunohistochemistry (IHC) in a tissue microarray which consisted of 3 cores from tumor and 2 cores from benign areas from 118 patients (87 African American and 31 European American). Ancestry informative markers for African Ancestry were available for 79 patients. Epithelial and stromal areas were quantified separately using an E-cadherin mask. CML levels were compared with clinical grade group and ancestry by mixed linear effect models. Age, prostate-specific antigen (PSA) levels, body mass index (BMI), and hemoglobin A1C were included as covariates.

resultsCML levels were lower in areas of the tumor, for both epithelium and surrounding stroma, compared with benign, but did not significantly change with tumor grade group. Age, PSA levels, BMI, and hemoglobin A1C did not associate with CML levels. CML levels were inversely associated with the percentage of African Ancestry in all tissues.

conclusionsThe low CML levels in cancer may reflect the reduced glycolytic state of the tissue. The inverse relationship between African Ancestry and CML levels in both benign and cancer areas suggests a state of reduced glycolysis. It is yet to be determined whether altered glycolysis and CML levels are bystanders or drivers of carcinogenesis.

Indexed as

Glycation End Products, AdvancedProstateProstatic HyperplasiaProstatic NeoplasmsWarburg Effect, OncologicAge FactorsBlack or African AmericanCorrelation of DataGlycated HemoglobinHumansImmunohistochemistryLysineMaleMiddle AgedProstate-Specific AntigenWhite PeopleGlycated HemoglobinGlycation End Products, Advancedhemoglobin A1c protein, humanLysineN(6)-carboxymethyllysineProstate-Specific Antigenadvanced glycation end products| cancer | cellular metabolism | CML | prostateWest-African ancestry

Identifiers

PMID34855273
PMCPMC8753724
OpenAlexW3216773565

What OpenQuestion holds

Textmetadata
LicenceTDM
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.