Evidence map›Paper›PMID 28455582›Full record

ArticleClinical and experimental medicine2018

Glutathione S-transferases deletions may act as prognosis and therapeutic markers in breast cancer.

Clodoaldo Zago Campos, Roberta Losi Guembarovski, Carlos Eduardo Coral de Oliveira, Bruna Karina Banin Hirata, Glauco Akelinghton Freire Vitiello, Flávia Luísa Dias, Carlos Hiroji Hiroki, Maria Angelica Ehara Watanabe, Tânia Longo Mazzuco

Abstract read
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In one paragraph

Article in Clinical and experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 1 institution in 1 country.

Clodoaldo Zago CamposDepartment of Medicine, Health Sciences Center, Londrina State University, Londrina, Parana, Brazil.
Roberta Losi GuembarovskiDepartment of General Biology, Biological Sciences Center, Londrina State University, Londrina, Parana, Brazil.
Carlos Eduardo Coral de OliveiraLaboratory of Studies and Applications of DNA Polymorphisms, Department of Pathological Sciences, Biological Sciences Center, Londrina State University, Celso Garcia Cid Highway, PR 445, Km 380, Londrina, Parana, Brazil.
Bruna Karina Banin HirataLaboratory of Studies and Applications of DNA Polymorphisms, Department of Pathological Sciences, Biological Sciences Center, Londrina State University, Celso Garcia Cid Highway, PR 445, Km 380, Londrina, Parana, Brazil.
Glauco Akelinghton Freire VitielloLaboratory of Studies and Applications of DNA Polymorphisms, Department of Pathological Sciences, Biological Sciences Center, Londrina State University, Celso Garcia Cid Highway, PR 445, Km 380, Londrina, Parana, Brazil.
Flávia Luísa DiasLaboratory of Studies and Applications of DNA Polymorphisms, Department of Pathological Sciences, Biological Sciences Center, Londrina State University, Celso Garcia Cid Highway, PR 445, Km 380, Londrina, Parana, Brazil.
Carlos Hiroji HirokiLaboratory of Studies and Applications of DNA Polymorphisms, Department of Pathological Sciences, Biological Sciences Center, Londrina State University, Celso Garcia Cid Highway, PR 445, Km 380, Londrina, Parana, Brazil.
Maria Angelica Ehara WatanabeLaboratory of Studies and Applications of DNA Polymorphisms, Department of Pathological Sciences, Biological Sciences Center, Londrina State University, Celso Garcia Cid Highway, PR 445, Km 380, Londrina, Parana, Brazil. maewatuel@gmail.com.
Tânia Longo MazzucoEndocrine Interactions Research Group, Department of Medical Clinic, Health Sciences Center, Londrina State University, Londrina, Parana, Brazil.
Universidade Estadual de Londrina · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) is the main worldwide neoplasia in women. The metabolic balance between xenobiotic absorption and elimination rates plays an important role in preventing DNA damage and, consequently, tumor development. The glutathione S-transferases (GSTs), such as GSTM1 and GSTT1, and the NAD(P)H quinone oxidoreductase are important enzymes involved in phase II detoxification reactions. Deletions in GSTM1 and GSTT1, and single-nucleotide polymorphism (SNP) in NQO1 (rs1800655) have been investigated in cancer context, revealing conflicting results. The present study analyzed these genetic polymorphisms in 121 BC patients and 151 BC-free controls in order to verify if they could act as susceptibility modifiers and/or prognostic factors. Binary logistic regressions adjusted by age were performed to assess associations between allelic variants and interactions in polymorphisms combination with BC susceptibility, but no significant association was found. Genotypes distribution was also compared between BC subtypes, but no significant difference was observed (p > 0.05). GSTM1 deletion was significantly associated with histopathological grade, with a greater proportion of patients presenting grade III tumors (p = 0.007). Univariate analysis identified tumor size as the only clinicopathological parameter potentially associated with recurrence risk in patients that received adjuvant chemotherapy (p < 0.1). Thus, logistic regression analysis adjusted by tumor size revealed a positive association between GSTT1 deletion and recurrence risk in general BC (OR 4.25; p = 0.04), while GSTM1 was negatively associated with recurrence risk in ER/PR

Indexed as

Genetic Predisposition to DiseasePolymorphism, GeneticAdultAgedAged, 80 and overBiomarkers, TumorBreast NeoplasmsFemaleGlutathione TransferaseHumansMiddle AgedNAD(P)H Dehydrogenase (Quinone)PrognosisTreatment OutcomeBiomarkers, Tumorglutathione S-transferase T1Glutathione TransferaseNAD(P)H Dehydrogenase (Quinone)NQO1 protein, humanBreast cancerGenetic polymorphismsGSTM1GSTT1PrognosisRecurrence risk

Identifiers

PMID28455582
OpenAlexW2608134798

What OpenQuestion holds

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Read underepoch 390

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.