Evidence map›Paper›PMID 26798414›Full record

ArticleOxidative medicine and cellular longevity2016

Epistatic Interaction of CYP1A1 and COMT Polymorphisms in Cervical Cancer.

Andreia Matos, Cindy Castelão, Alda Pereira da Silva, Irina Alho, Manuel Bicho, Rui Medeiros, Maria Clara Bicho

Abstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. 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
–field-weighted citation impact
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.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Frontiers in physiology · 2017
    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.

Andreia MatosGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal; Instituto de Investigação Científica Bento da Rocha Cabral, 1250-047 Lisbon, Portugal.ORCID 0000-0003-1551-9465
Cindy CastelãoGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal; Dermatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1250-047 Lisbon, Portugal.
Alda Pereira da SilvaGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal; Instituto de Investigação Científica Bento da Rocha Cabral, 1250-047 Lisbon, Portugal.
Irina AlhoClinical and Translational Oncology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1250-047 Lisbon, Portugal.
Manuel BichoGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal; Instituto de Investigação Científica Bento da Rocha Cabral, 1250-047 Lisbon, Portugal.
Rui MedeirosMolecular Oncology Group, Portuguese Institute of Oncology Porto Centre, 4200-072 Porto, Portugal.
Maria Clara BichoGenetics Laboratory and Environmental Health Institute, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisbon, Portugal; Dermatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1250-047 Lisbon, Portugal.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a clear association between the excessive and cumulative exposure to estrogens and the development of cancer in hormone-sensitive tissues, such as the cervix. We studied the association of CYP1A1 M1 (rs4646903) and COMT (rs4680) polymorphisms in 130 cervical cancer cases (c-cancer) and 179 controls. The CYP1A1 TT genotype was associated with a lower risk for c-cancer (OR = 0.39, p = 0.002). The allele C of CYP1A1 was a risk for c-cancer (OR = 2.29, p = 0.002). Women with COMT LL genotype had a higher risk of developing c-cancer (OR = 4.83, p < 0.001). For the interaction of the CYP1A1&COMT, we observed that TC&HL genotypes had a greater risk for c-cancer (OR = 6.07, p = 0.006) and TT&HL genotypes had a protection effect (OR = 0.24, p < 0.001). The CYP1A1 TT and COMT LL genotypes had higher estradiol levels in c-cancer (p < 0.001 and p = 0.037, resp.). C-cancer is associated with less production of 2-methoxy-estradiol resultant of functional polymorphisms of CYP1A1 and COMT, separately. CYP1A1 and COMT work in a metabolic sequence and their interaction could lead to an alternative pathway of estrogen metabolism with production of 16-OH-estrone that is more proliferative.

Indexed as

Epistasis, GeneticGenetic Predisposition to DiseaseAdultAgedCase-Control StudiesCatechol O-MethyltransferaseCytochrome P-450 CYP1A1EstradiolFemaleGenetic Association StudiesHumansMiddle AgedPolymorphism, Single NucleotideUterine Cervical NeoplasmsYoung AdultCatechol O-MethyltransferaseCOMT protein, humanCYP1A1 protein, humanCytochrome P-450 CYP1A1Estradiol

Identifiers

PMID26798414
PMCPMC4698955

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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.