Analyses of EGF A61G Gene Variation and Serum EGF Level on Gastric Cancer Susceptibility and Clinicopathological Parameters.

Background: Epidermal growth factor (EGF) induces various biological signaling pathways, including proliferation and differentiation and it is the natural ligand of the epidermal growth factor receptor (EGFR) which is a member of tyrosine kinase transmembrane receptor family. EGF and EGFR control important processes in carcinogenesis and several differences in this signaling pathway are very common in certain types of cancers. In present study, we examined EGF A61G gene polymorphism as a marker of risk and progression in gastric cancer.

Genetic variants in the tumor necrosis factor-related apoptosis-inducing ligand and death receptor genes contribute to susceptibility to bladder cancer.

Aim: The aim of this study was to evaluate the role of polymorphisms of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor (DR4) genes in bladder cancer susceptibility in a Turkish population.

Materials And Methods: The study group included 91 bladder cancer patients, while the control group comprised 139 individuals with no evidence of malignancy. Gene polymorphisms of TRAIL C1595T (rs1131580) and DR4 C626G (rs4871857) were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis.

Chemopreventive effects of hydatid disease on experimental breast cancer.

Breast cancer is one of the most common and letal cancers in all over the world. Since there have been significant improvements in treatment of breast cancer, there is still a big need for alternative approaches. In this study, we aimed to investigate protective role of hydatid disease against breast cancer.

Functional genetic variants in apoptosis-associated FAS and FASL genes and risk of bladder cancer in a Turkish population.

Background: The present study aimed to evaluate the role of functional polymorphisms of apoptosis-associated Fatty acid synthase (FAS) and fatty acid synthase ligand (FASL) genes in bladder cancer susceptibility as first presentation in a Turkish population.

Patients And Methods: Genotypes of 91 patients with bladder cancer and 101 healthy controls were evaluated for the polymorphism of FAS-1377 G/A and FASL-844 T/C genes by polymerase chain reaction and restriction fragment length polymorphism analysis.

Results: The frequency of the FAS-1377 G allele was significantly higher in patients with bladder cancer compared to controls (p<0.

Association of the Cylin D1 G870A polymorphism with laryngeal cancer: are they really related?

Background: Cylin D1(CCDN1) is an important regulator of the cell cycle whose alterations are thought to be involved in cancer development. There have been many studies indicating CCDN1 amplification or over- expression in a variety of cancer types. In addition to gene amplification, the G870A polymorphism may be related with altered CCDN1 activity, and therefore with cancer development.

Association between FAS and FASL genetic variants and risk of primary brain tumor.

The purpose of this study was to investigate whether functional polymorphisms of apoptosis pathway genes FAS and FASL are associated with the development of primary brain tumors. The study constituted 83 patients with primary brain tumor and 108 healthy individuals. In the present case-control study, the primary brain tumors were divided into two groups: gliomas and meningiomas.

The exon 3-deleted/full-length growth hormone receptor polymorphism and response to growth hormone therapy in growth hormone deficiency and Turner syndrome: a multicenter study.

Background/aim: The exon 3-deleted/full-length (d3/fl) growth hormone (GH) receptor (GHR) polymorphism has been associated with responsiveness to GH therapy in some diagnostic groups. However, there are still controversies on this issue. To evaluate the effect of the GHR exon 3 polymorphism on growth after 1 and 2 years of GH therapy in Turkish patients with GH deficiency (GHD) and Turner's syndrome (TS) and the distribution of GHR exon 3 isoforms.