|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
GSTP1 and NAT2 polymorphisms studied have a significant contribution for the histological tumour types and the presence of metastases, at time of diagnosis, respectively, when males with smoking habits were considered.
|
25388590 |
2015 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Patients with N-acetyltransferase 2 slow genotypes were more likely to develop a high-grade and invasive tumor.
|
25376209 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Differential effects according to N-acetyltransferase (NAT2) status, BMI, alcohol consumption, and tumour subtypes were assessed.
|
24950597 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The N-acetyltransferase 2 (NAT2) gene is a marker for the study of interindividual susceptibility to developing neoplasias.
|
24023296 |
2013 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We were not able to find any correlation among smoking, dietary patterns, parameters of tumor aggressiveness or patient outcome and any NAT2 genotypes or phenotypes considered in separate or in different combinations.
|
22246524 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
NAT2 was associated with CIMP-positive/Ki-ras-mutated tumors but not with MSI tumors.
|
18992263 |
2009 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We showed that NAT2 genotypes and the NAT2 rapid acetylation phenotype are important susceptibility factors for DTC, suggesting that NAT2 detoxification system is involved in this tumor pathogenesis.
|
19118072 |
2009 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Furthermore, NAT2 slow-acetylator, GSTM1 null, and GSTM1/GSTT1-double null genotypes were associated with higher tumor grade (P=0.001, 0.022, and 0.036, respectively), and only NAT2 slow-acetylator genotype was associated with higher tumor stage (P=0.007).
|
19303722 |
2009 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
GSTM1 and NAT2 were generally not associated with rectal tumor alterations; however, we observed an interaction of ETS and NAT2 in TP53-mutated tumors (p < 0.01).
|
19358278 |
2009 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
A critical region of loss, close to the NAT2 locus and relatively far from FEZ1 gene currently postulated as tumor suppressor gene in this region.
|
17659675 |
2007 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We also evaluated differences in risk by estrogen receptor (ER) and progesterone receptor (PR) status in tumors, and the potential modification of the smoking association by N-acetyl transferase 2 (NAT2) genotype.
|
16721725 |
2006 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In 70.3% of the patients, there was a difference in NAT2 genotype between their tumors and blood cells.
|
16015704 |
2005 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Similar distribution of NAT2 acetylator genotypes both in tumor-prone and in tumor-resistant groups suggests that, despite the presence of NAT2 carcinogenic substrates in tobacco smoke, NAT2 polymorphism does not play a noticeable role in lung cancer susceptibility.
|
15808403 |
2005 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Our results suggest that SULT1A1 *1/*1 and NAT2 slow acetylator genotypes might modulate the effect of carcinogenic arylamines contained in tobacco smoke, and that the modulation of NAT2 intermediate and slow acetylator genotype has a tendency to present a higher risk for highly differentiated tumors among heavy-smokers.
|
14648207 |
2004 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In this study, we evaluate associations between the GSTM-1 genotype and the NAT2-imputed phenotype and acquired mutations in tumors.
|
12195642 |
2002 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The DNA from tumour and healthy tissue was evaluated for amplification of the 11q13 region and of the MYC and ERBB1 oncogenes, for integration of the Human Papillomavirus (HPV), and for loss of heterozygosity (LOH) at p53 and NAT2 loci.
|
12076699 |
2002 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
DNA from tumor and healthy tissue was evaluated for amplification of the oncogenes at 11q13 region (CCND1, FGF3, FGF4 and EMS1) and of the oncogenes MYC and ERBB1; for integration of the human papillomavirus (HPV) types 6b and 16; for loss of heterozygosity (LOH) at p53 and NAT2; and for the cellular DNA content.
|
11568558 |
2001 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
These results are supported by logistic regressions of patients allowing interactions between tumour type (or treatment) and PY (or age), and indicate that the GSTM1-null genotype could be an important susceptibility factor for SQ while the NAT2-slow genotype may have an impact on other types of lung cancer.
|
10607733 |
2000 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Analysis of the GSTM1 and NAT2 polymorphisms failed to show an association with any of the neoplasias, although a near significant increase in fast acetylators was also found in the leukaemia group (50.0 versus 35.9%, P = 0.06).
|
10383893 |
1999 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
There is agreement between loss of heterozygosity at the NAT2 locus and adjacent microsatellite marker loci in 11 of the tumours but two of the tumours appear to show retention at the NAT2 locus.
|
10208636 |
1999 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, fluorescence in situ hybridization (FISH) was used for study of the relationship between chromosome 8 deletions in the region of NAT1 and NAT2 and grade and stage of tumor in bladder cancer.
|
10398432 |
1999 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
It was also shown that bladder cancer patients with NAT2 slow genotypes were more likely to have a high grade tumor (G3) or an advanced stage tumor (pT2-pT4) [corrected].
|
10510890 |
1999 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In eleven out of 60 tumor samples (18.3%) we observed allelic loss at the NAT2 locus while in control DNA of blood from the same patients both alleles were still detectable.
|
9660060 |
1998 |