Evidence map›Paper›PMID 35715601›Full record

ArticleMolecular biology reports2022

Investigation of the relationship between MTRR A66G, MTR A2756G gene variations and cell anomalies in early diagnosis and progression of bladder cancer.

Nevra Alkanli, Arzu Ay, Pinar Koroglu Aydin, Gokhan Cevik

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Nevra AlkanliDepartment of Biophysics, Faculty of Medicine, Haliç University, Istanbul, Turkey. nevraalkanli@halic.edu.tr.ORCID http://orcid.org/0000-0002-3745-8838
Arzu AyDepartment of Biophysics, Faculty of Medicine, Trakya University, Edirne, Turkey.ORCID http://orcid.org/0000-0002-8412-091X
Pinar Koroglu AydinDepartment of Histology and Embriology, Faculty of Medicine, Haliç University, Istanbul, Turkey.ORCID http://orcid.org/0000-0002-3408-7867
Gokhan CevikDepartment of Urology, Faculty of Medicine, Trakya University, Edirne, Turkey.ORCID http://orcid.org/0000-0001-5221-5132

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aim of this study is to investigate the relationship between MTRR A66G, MTRA2756G gene variations and cell anomalies in the early diagnosis and progression of bladder cancer.

methodsPCR and RFLP methods were used to determine the genotype distributions of MTRR A66G and MTR A2756G gene variations. Peripheral smear preparations prepared from blood samples were fixed with methanol fixative and stained histochemically. Cellular morphological evaluations were made under the light microscope.

resultsIn our study, AA-GG haplotype was observed significantly more in the patient group than control group (OR: 3.304, 95% CI: 1.023-10.665, p = 0.046). The significant increase was determined in terms of histological damage parameters in the patient group compared to the control group (p < 0.05). For multiple vacuoles damage parameter (mild score), AA genotype of MTR A2756G gene variation was significantly different compared to AA genotype of MTRR A66G gene variation (OR: 0.211, 0.049-0.912, p = 0.037). AA genotype of MTR A2756G gene variation was observed more than AA homozygous genotype of MTR A66G gene variation for giant platelets with different sizes damage parameter (mild score) (OR: 0.062, 0.017-0.228, p < 0.001).

conclusionsIn conclusion, in Thrace population, AA genotype of the MTR A2756G gene variation was significantly higher than the AA homozygous genotype of the MTR A66G gene variation as a genetic risk factor for the multiple vacuoles damage parameter. In addition, AA genotype of MTR A2756G gene variation was determined as a genetic risk factor for giant platelets with different sizes damage parameter.

Indexed as

5-Methyltetrahydrofolate-Homocysteine S-MethyltransferaseUrinary Bladder NeoplasmsCase-Control StudiesEarly Detection of CancerFerredoxin-NADP ReductaseGenetic Predisposition to DiseaseGenotypeHumansMethylenetetrahydrofolate Reductase (NADPH2)Polymorphism, Single NucleotideRisk Factors5-Methyltetrahydrofolate-Homocysteine S-MethyltransferaseFerredoxin-NADP Reductasemethionine synthase reductaseMethylenetetrahydrofolate Reductase (NADPH2)MTR protein, humanBladder cancerGenetic variationHistological damage parametersPCR-RFLPPeripheral smear

Identifiers

What OpenQuestion holds

Textmetadata
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.