Evidence map›Paper›PMID 23168701›Full record

ArticleThe Indian journal of medical research2012

Association between polymorphisms at N-acetyltransferase 1 (NAT1) & risk of oral leukoplakia & cancer.

Mousumi Majumder, Saurabh Ghosh, Bidyut Roy

Abstract read
In one paragraph

Article in The Indian journal of medical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
0.5field-weighted citation impact, top 36% 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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 12 citations in OpenAlex.

  1. Association ofMedicina (Kaunas, Lithuania) · 2021
    Pooled it
  2. N-acetyltransferase 2 genetic variants confer the susceptibility to head and neck carcinoma: evidence from 23 case-control studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  3. Article
  4. Article
  5. Article
  6. Genotypic distribution of single nucleotide polymorphisms in oral cancer: global scene.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  7. Review
  8. NAT1 polymorphisms and cancer risk: a systematic review and meta-analysis.International journal of clinical and experimental medicine · 2015
    Article
  9. Article
  10. 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

3 authors at 1 institution in 1 country.

Mousumi MajumderBiological Sciences Division, Indian Statistical Institute, Kolkata, India.
Saurabh Ghosh
Bidyut Roy
Indian Statistical Institute · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

objectivesN-acetyltransferases 1 and 2 (NAT1 and NAT2) are important enzymes for metabolism of tobacco carcinogens. Due to polymorphisms, improper activities of these enzymes might lead to the formation of DNA adducts that may modulate risk of tobacco related oral precancer and cancer. Previously, it was shown that NAT2 polymorphisms did not modulate the risk of oral precancer and cancer. We undertook this study to check whether polymorphisms at NAT1 can modulate the risk of oral leukoplakia and cancer either alone or in combination with NAT2.

methodsGenotypes at four SNPs on NAT1 were determined by TaqMan method in 389 controls, 224 leukoplakia and 310 cancer patients. Genotype data were analyzed to know haplotypes and acetylation status of individuals and, then to estimate the risk of diseases. Using our previously published NAT2 data, combination of NAT1 and NAT2 acetylation genotypes of patients and controls were also analyzed to estimate the risk of diseases.

resultsAnalysis of NAT1 genotype data revealed that 1088T and 1095C alleles exist in strong linkage disequilibrium (r 2 =0.97, P<0.0001) and SNPs are in Hardy-Weinberg Equilibrium (P=0.1). Wild type or normal acetylating and variant or rapid acetylating alleles were two major alleles (frequencies 0.62 and 0.36, respectively) present in the control population. NAT1 rapid acetylation could not modulate the risk of leukoplakia and cancer (OR=0.9, 95% CI: 0.6-1.3; OR=1.0, 95% CI: 0.7-1.4, respectively). Analysis of combined NAT1 and NAT2 acetylating data also showed no significant enhancement of the risk of diseases. INTERPRETATION &

conclusionsNAT1 rapid acetylation alone as well as combination of NAT1 rapid-NAT2 slow acetylation did not modulate the risk of oral precancer and cancer in our patient population. So, NAT1/NAT2 metabolized carcinogen products may not be involved in tobacco related oral precancer and cancer. It may be interpreted that large sample size as well as combination of polymorphisms at other candidate loci may be important to estimate the risk of a complex disease like oral cancer.

Indexed as

AcetylationArylamine N-AcetyltransferaseGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeHumansIndiaIsoenzymesLeukoplakia, OralLinkage DisequilibriumMouth NeoplasmsOdds RatioPolymorphism, Single NucleotideSmokingArylamine N-AcetyltransferaseIsoenzymesN-acetyltransferase 1NAT2 protein, human

Identifiers

PMID23168701
PMCPMC3516028
OpenAlexW1900360070

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.