The Relationship Between eNOS Polymorphisms With Age, Smoking, Body Mass Index, and Clinicopathologic Parameters in Patients With Breast Cancer in Comparison With a Control Group.

INTRODUCTION: Nitric oxide (NO) is a free radical involved in carcinogenesis and is synthesized by endothelial nitric oxide synthase (eNOS). Genetic changes in the eNOS enzyme affect its activity, and the nitric oxide produced by inhibiting apoptosis can lead to cancer cell proliferation and metastasis. In this study, in addition to investigating the relationship between genetic changes in eNOS gene and the risk of breast cancer, the relationship between genotypes of polymorphisms, age, smoking, body mass index, and clinopathologic parameters was also investigated. MATERIAL AND METHODS: Three functional (Intron 4a/b, T786C, and G894T) and 1 tagging (G10T) polymorphisms of the eNOS gene were examined in 203 patients with breast cancer and 203 control subjects, and their genotypes were identified by restriction fragment length polymorphism polymerase chain reaction. RESULTS: The T allele in G10T polymorphism increased the risk of breast cancer by 1.503-fold, whereas allele a in Intron 4, T allele in G894T, and C allele in T786C decreased its risk by 0.678-, 0.440-, and 0.525-fold, respectively. GG, GT (G10T), bb and ab (Intron4), GG and TT (G894T), and TT and CC (T786C) genotypes were significantly correlated with body mass index. There was a significant relationship between age and bb genotype, cigarette smoking and genotype ab (Intron 4), and estrogen receptor and GG (G10T) genotype. Tumor invasion factor was also significantly associated with TT (G10T), bb (Intron 4), and TT (T786C) genotypes. CONCLUSION: Genetic changes in eNOS appear to have a dual role in breast cancer rate owing to changes in NO production and can be introduced as one of the genetic markers involved in breast cancer by evaluating the genotype of different populations.

The Relationship Between 6 Polymorphisms of Caveolin-1 Gene and the Risk of Breast Cancer.

BACKGROUND: Caveolae play a role in cell signal transduction, kinetic regulation of transport vesicles, and cellular physiology. In this study, we evaluated the role of caveolin-1 (CAV-1) genotypes in the risk of breast cancer. PATIENTS AND METHODS: We evaluated 6 single nucleotide polymorphisms of the CAV-1 gene in a sample size of 406 participants. Six polymorphisms-G32124A (rs3807992), T29107A (rs7804372), T28608A (rs3757733), G21985A (rs12672038), G14713A (rs3807987), and C521A (rs1997623)-were assessed using restriction fragment length polymorphism polymerase chain reaction. RESULTS: Regarding the distribution of genotypes, the relationship between cases and controls was significant for T29107A, G21985A, G14713A, and C521A polymorphisms, among which only C521A showed a significant difference in body mass index between the 2 groups. Moreover, the age of the 2 groups was significant in the case of G32124A and T28608A polymorphisms. CONCLUSION: Our results showed that genetic changes of CAV-1 might modify the risk for breast cancer and point out the importance of more studies for variants of this gene in breast cancer.

Epstein-Barr virus DNA in colorectal carcinoma in Iranian patients.

Colorectal cancer is an often fatal cancer with a rapidly increasing incidence. Current mortality is estimated to be approximately 600,000 per year, and both environmental and genetic factors are involved in its etiology. Viral and bacterial factors have a proven role in the incidence of approximately 20% of cancers. In the present study, the Epstein-Barr virus (EBV) was detected in 50 colorectal adenocarcinomas, 12 colon adenomas, and 38 control tissue samples using polymerase chain reaction (PCR). Epstein-Barr virus DNA was identified in 19 of the adenocarcinoma tissues, 1 adenoma tissue and 24 control specimens. In total, 15.8% (3/18) of the colorectal samples in the well-differentiated grade, 79% (15/30) in the moderately differentiated, and 5.2% (1/2) in the poorly differentiated grade tested positive for viral infection. Epstein-Barr virus was more prevalent in the moderately differentiated grade. Statistical analysis did not suggest a significant association between EBV and the incidence of colorectal cancer. However, it appears that the virus stimulates progression of the malignancy.

Lack of association between human papillomavirus infection and colorectal cancer.

INTRODUCTION: Colorectal cancer is the third leading cause of cancer-related deaths worldwide, with nearly one million new cases identified annually. Different factors might cause colorectal cancer, one of the most prevalent cancers among both men and women. Viral aetiology in cancerous malignancies is a very important issue and so far a number of viral strains have been identified as tumour oncogene viruses. Viral infections, such as human papillomavirus (HPV), have recently been suggested as a risk factor for colorectal cancer. However, the aetiology of the disease is still unknown. AIM: To assessed the association between HPV infection and colorectal cancer. MATERIAL AND METHODS: In this study, 50 cancer tissue samples and 50 samples without colon cancer were studied in order to identify HPV through polymerase chain reaction (PCR). Of 42 adenocarcinomas, 10 were well differentiated, 30 moderated differentiated, and 2 were poorly differentiated. DNA extraction was verified by beta globin gene amplification; specific PCR was carried out based on HPV L1 consensus primers MY09/MY11. RESULTS: HPV DNA was not identified in any of the normal, adenocarcinoma, or adenoma samples. CONCLUSIONS: In contrast with previous studies, the current research failed to establish a relationship between HPV infection and the incidence of colon cancer. Considering the existing inconsistencies, it is recommended that further studies be conducted with larger sample size.

Detection of human cytomegalovirus in patients with colorectal cancer by nested-PCR.

BACKGROUND: The association of colorectal cancer with human cytomegalovirus (HCMV) is a controversial issue in cancer research. This study aimed to identify the HCMV virus in colorectal cancer tissues and to investigate the association of HCMV with colorectal cancer. In this study, 50 cancer tissue samples and 50 samples without colon cancer were studied in order to identify the HCMV virus through nested-polymerase chain reaction. The virus was identified in 15 cases of colorectal cancer tissues (15/50) and in 5 cases of normal tissues (5/50). Eight cases of adenocarcinoma tissues were in a moderately differentiated stage, and 7 cases had well-differentiated stage tissues that were positive for viral DNA. The findings were statistically evaluated at a significance level of p<0.05. The HCMV virus could play a role in creating malignancy and the progress of cancer through the process of oncomodulation.