Our data does not support an association between SNPs of FSHR, CYP17, CYP1A1, CAPN10, INSR, SERPINE1 genes and susceptibility to PCOS or related traits in Turkish adolescent girls.
Apigenin (4',5,7-trihydroxyflavone) is one of the leading components supporting targeted treatment options. We explored the cytotoxic and apoptotic effects of various doses of apigenin administered alone and together with 5-fluorouracil (5-FU)-a chemotherapeutic agent with high cytotoxicity-for different incubation periods, on morphologic, DNA, RNA (messenger RNA [mRNA]), and protein levels on the p53 mutant HT29 human colon adenocarcinoma cell line. Treatment with apigenin alone for a 72-hour incubation at 90-μM dose resulted in an apoptotic percentage of 24.92% (P=.001). A higher percentage (29.13%) was observed after treatment with the same dose of apigenin plus 5-FU for the same incubation period (P=.001). These results were confirmed as mRNA and protein expression levels of caspase-3 increased 2.567-fold and mRNA expression levels of caspase-8 increased 3.689-fold compared with the control group. On the other hand, mRNA expression levels of mammalian target of rapamycin (mTOR) and cyclin D1 (CCND1) decreased by 0.423-fold and 0.231-fold, respectively. To our knowledge this is the first study showing that treatment with apigenin alone results in cell cycle arrest through activation of caspase cascade and stimulation of apoptosis in HT29 cells. It also shows that use of apigenin plus 5-FU further increases this effect. This study draws attention to the probable clinical effectiveness of apigenin plus a chemotherapeutic agent with high cytotoxicity. It also highlights the induction of desirable apoptotic effects by targeting the caspase cascade pathway through administration of reduced doses for shorter incubation periods.
Purpose Association of ESR1 gene PvuII, XbaI and (TA)n microsatellite polymorphisms and woman infertility was evaluated. Methods Infertile(n=104) and fertile(n=107) women were included in this study. We performed polymerase chain reaction-restriction fragment-length polymorphism analysis for detecting ESR1 polymorphisms. Result(s) PvuII and XbaI polymorphisms confered risk for infertility in a simple dominant manner in which a significant relationship was observed between infertile and control women. Infertile women had fewer(<18) short repeat alleles in promotor region. ESR1 genotypes were compared concerning maturation, fertilization, pregnancy rates and embryo quality. Although no difference was found in terms of pregnancy rates, maturation and fertilization rates were significantly smaller in pp and xx genotypes. Also, pp genotypes had significantly lower number of good quality embryos. Long TA repeat in promotor was found to be associated with low fertilization rate. Conclusion(s) Polymorphisms at the ESR1 gene are associated with infertility in this Turkish infertile women population.
Tumor growth, which employs a number of regulators, requires the formation of new blood vessels. The most important regulators are vascular endothelial growth factor (VEGF) and angiopoietin-2 (ANGPT-2). DNA sequence variations in VEGF and ANGPT-2 genes may lead to altered productions and/or activities of these genes. In this study, we aimed to determine the polymorphic effects of the changes in the VEGF -460 C/T, VEGF 936 C/T, and ANGPT-2 exon 4 G/A, which we perceive as risk factors in the progress and metastasis of cancer, on the gynecologic cancer patients in the Turkish population. Forty-seven ovarian, 32 cervical, and 21 endometrial cancer patients and 106 healthy controls were studied. The genomic DNA was extracted from the whole blood by using DNA extraction techniques. DNA samples were analyzed by polymerase chain reaction and restriction fragment length polymorphism. There were no significant differences between any of the three types of gynecologic cancer patients and controls in terms of the distribution of VEGF -460, VEGF 936, and ANGPT-2 genotypes and alleles (p > 0.05). Odds ratios (ORs) were calculated by logistic regression analysis in comparison with the most common homozygote genotype observed in the studied population. No evidence of a relationship that would constitute a risk factor (p > 0.05) was found between genotype and allele frequencies of patients and controls for VEGF -460, VEGF 936, and ANGPT-2 genes. A multivariable logistic regression analysis with the involvement of covariant factors, such as the history of gynecologic cancer and/or other cancer types in the family, stages of tumor, smoking habits, and existence of other diseases, did not change the results. The present study is the first case-control study of VEGF and ANGPT-2 polymorphisms in relation to ovarian, cervical, and endometrial cancers.
Hypoxia-inducible factor-1 (HIF-1), an important genetic component of angiogenesis, becomes stable as a response to tumor hypoxia and facilitates tumor survival. The polymorphisms of the HIF-1alphagene may cause changes in the activity of this protein, which serves as a transcription factor for many genes in tumorigenesis. In this study, we have investigated the relationship between seven HIF-1alphapolymorphisms [C > T substitution in intron 8 (rs10873142), T418I (rs41508050) in exon 10, P564P (rs41492849), L580L (rs34005929), P582S (rs11549465), A588T (rs11549467) in exon 12 and dinucleotide GT repeats in intron 13 (rs10645014)] among lung cancer patients in the Turkish population. Genomic DNA was isolated from 141 lung cancer cases and 156 controls and subjected to PCR for amplification. Genotyping was carried out with RFLP and DNA sequencing methods. There was no significant difference between the lung cancer cases and controls in terms of the distribution of genotyping frequencies of seven HIF-1alphapolymorphisms (P > 0.05). No significant relationship was found between the C > T substitution in intron 8 and P582S haplotypes and development of lung cancer. In addition, there were no significant associations between the genotypes and clinopathological characteristics of the cases examined. These findings show that polymorphisms in the HIF-1alphagene do not confer susceptibility to lung cancer.
The aim of this study was to analyse whether some cases of unexplained infertility and implantation failure after IVF could be explained by different expression levels of the matrix metalloproteinases (MMP-2, 9), their tissue inhibitors (TIMP-2, 3) and intercellular (ICAM-1) and vascular (VCAM-1) adhesion molecules in endothelial cells. Total RNA was extracted from the endometrial tissues of 41 women (unexplained infertile, group 1, n = 15; fertile volunteers, group 2, n = 15 and patients with implantation failure after IVF, group 3, n = 11). MMP-2, MMP-9, TIMP-2, TIMP-3, ICAM-1 and VCAM-1 mRNA expression levels were measured quantitatively using real-time polymerase chain reaction. In the endometrium from women with unexplained infertility and implantation failure after IVF, MMP-2 and TIMP-3 expression were significantly decreased when compared with the fertile group (P < 0.05 and P = 0.001 respectively). In addition, a marked decrease was observed in the expression of VCAM-1 in women with unexplained infertility. These results suggest that the expression of gelatinase A (MMP-2), TIMP-3 and VCAM-1, at least at the transcriptional level, might be regulated by common factors and signalling pathways. The present study adds new and important data in this field and highlights the complex preparation of the endometrium for implantation at the molecular level.
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