Evidence map›Paper›PMID 36093686›Full record

ArticleCancer biomarkers : section A of Disease markers2022

AhRR methylation contributes to disease progression in urothelial bladder cancer.

Nataly W El-Haddad, Michelle El Kawak, Khalil El Asmar, Michel E Jabbour, Mohamad A Moussa, Rima R Habib, Hassan R Dhaini

Open access · hybridAbstract read
In one paragraph

Article in Cancer biomarkers : section A of Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

7 authors at 3 institutions in 1 country.

Nataly W El-HaddadDepartment of Environmental Health, American University of Beirut, Beirut, Lebanon.
Michelle El KawakDepartment of Environmental Health, American University of Beirut, Beirut, Lebanon.
Khalil El AsmarDepartment of Epidemiology and Population Health, American University of Beirut, Beirut, Lebanon.
Michel E JabbourDepartment of Urology, St George Hospital University Medical Center, Beirut, Lebanon.
Mohamad A MoussaDepartment of Urology, Lebanese University, Beirut, Lebanon.
Rima R HabibDepartment of Environmental Health, American University of Beirut, Beirut, Lebanon.
Hassan R DhainiDepartment of Environmental Health, American University of Beirut, Beirut, Lebanon.
American University of Beirut · LBLebanese University · LBUniversity of Balamand · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBladder Cancer (BCa) is the tenth most incident malignancy worldwide. BCa is mostly attributed to environmental exposure and lifestyle, particularly tobacco smoking. The Aryl Hydrocarbon Receptor Repressor (AhRR) participates in the induction of many enzymes involved in metabolizing carcinogens, including tobacco smoke components. Additionally, studies have shown that smoking demethylates the (AhRR) gene in blood, suggesting AhRR demethylation as a specific serum smoking biomarker.

objectiveThis study aimed to validate AhRR demethylation as a smoking biomarker in the target tissue and investigate its contribution to bladder carcinogenesis.

methodsAhRR percent methylation was tested for its association with patient smoking status and oncogenic outcome indicators, particularly p53, RB1, and FGFR3 activating mutations, muscle-invasiveness, and tumor grade, in 180 BCa tissue-based DNA.

resultsResults showed significantly higher AhRR percent methylation in muscle-invasive compared to non-muscle invasive tumors (42.86% vs. 33.98%; p= 0.011), while lower AhRR methylation was significantly associated with FGFR3 Codon 248 mutant genotype compared to wild-type (28.11% ± 9.44 vs. 37.87% ± 22.53; p= 0.036). All other tested associations were non-statistically significant.

conclusionsAlthough AhRR methylation did not predict smoking status in BCa tumors, it may be a contributor to carcinogenesis and disease progression. Our findings constitute the basis for further research.

Indexed as

Carcinoma, Transitional CellTobacco Smoke PollutionUrinary Bladder NeoplasmsBasic Helix-Loop-Helix ProteinsBiomarkersCarcinogenesisCarcinogensDisease ProgressionDNA MethylationHumansReceptors, Aryl HydrocarbonRepressor ProteinsTumor Suppressor Protein p53AHRR protein, humanBasic Helix-Loop-Helix ProteinsBiomarkersCarcinogensReceptors, Aryl HydrocarbonRepressor ProteinsTobacco Smoke PollutionTumor Suppressor Protein p53FGFR3methylationmuscle-invasivenessp53tobacco smokingUrothelial bladder cancer

Identifiers

PMID36093686
PMCPMC9661316
OpenAlexW4294770705

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Registered trials

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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.