Evidence map›Paper›PMID 33906323›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2021

The Association of Aging-Related Polymorphisms with Susceptibility to Lung Cancer: A Case-Control Study in a Japanese Population.

Hironobu Furuie, Masako Arimura-Omori, Naoki Hamada, Toyoshi Yanagihara, Chikako Kiyohara

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 2 syntheses or guidelines pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer.International journal of molecular sciences · 2023
    Review
  5. 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

5 authors at 1 institution in 1 country.

Hironobu FuruieDepartment of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Masako Arimura-OmoriResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Naoki HamadaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Toyoshi YanagiharaResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Chikako KiyoharaDepartment of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTelomere length is associated with cancer as well as aging.  Telomerase reverse transcriptase (TERT), telomere RNA component (TERC) and oligonucleotide/oligosaccharide-binding fold containing 1 (OBFC1) are known to be involved in telomere length regulation. The tumor suppressor p53 (TP53), which has been shown to interact with tumor protein p53-binding protein 1 (TP53BP1), is implicated in the response to telomere shortening and aging.  Polymorphisms in the TP53 and TP53BP1 genes are associated with various types of cancer. The aim of this study is to evaluate the impact of aging-related polymorphisms on lung cancer risk. MATERIALS AND

methodsThis case-control study consists of 462 lung cancer cases and 379 controls from Japan.  We examined the effect of TERT rs2736100, TERC rs1881984, OBFC1 rs11191865, TP53 rs1042522 and TP53BP1 rs560191 on the risk of lung cancer using a Taq-Man real-time PCR assay. Unconditional logistic regression was used to assess the adjusted odds ratios (ORs) and 95% confidence intervals (CIs).

resultsNone of the main effects of any of the telomere-related polymorphisms were related to the risk of lung cancer.  Similarly, none of the interactive effects of any of the telomere-related polymorphisms with smoking were associated with lung cancer risk. The significant multiplicative interaction between TERT rs2736100 and TP53BP1 rs560191 was statistically significant (OR for interaction = 0.34, 95% CI = 0.14-0.84). The multiplicative interaction between OBFC1 rs11191865 and TP53BP1 rs560191 was also statistically significant (OR for interaction = 2.44, 95% CI = 1.02-5.87) but the OR for interaction was in the opposite direction.

conclusionsOur findings indicate that TP53BP1 rs560191 may predispose to lung cancer risk depending on the genotypes of telomere-related polymorphisms. Additional studies are warranted to confirm the findings suggested in the present study.<br />.

Indexed as

AgingCarcinomaCase-Control StudiesFemaleGenetic Predisposition to DiseaseHumansJapanLung NeoplasmsMalePolymorphism, GeneticRNATelomeraseTelomere-Binding ProteinsTumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53RNAStn1 protein, humanTelomerasetelomerase RNATelomere-Binding ProteinsTERT protein, humanTP53BP1 protein, humanTP53 protein, humanTumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53agingLung cancerOligonucleotide/oligosaccharide-binding fold containing 1Telomerase reverse transcriptaseTelomere RNA component

Identifiers

PMID33906323
PMCPMC8325147
OpenAlexW3157104102

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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.