IntroductionColorectal 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.AimTo assessed the association between HPV infection and colorectal cancer.Material and methodsIn 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.ResultsHPV DNA was not identified in any of the normal, adenocarcinoma, or adenoma samples.ConclusionsIn 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.

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 cases of adenocarcinoma tissues were in a moderately differentiated stage, and 7 cases had well-differentiated of p<0.05. The HCMV virus could play a role in creating malignancy and the progress of cancer through the process of oncomodulation. 1455 DOI:http://dx.doi.org/10.7314/APJCP.2014.15.3 .1453 Detection of Human Cytomegalovirus in Patients with Colorectal Cancer by Nested-PCRadenocarcinoma tissues in the moderately differentiated stage and 7 cases in the well-differentiated stage were DiscussionIn vitro transform cells, and cause disruption along many cell to other studies on colorectal cancer, which point to a results, including; study limitations and methodology, kept in formalin for a long time will fail when compared to cell in the early stages of the infection, then transforms the in cancerous cells, cell cycle progress, stimulating intracellular signalling pathway, and increasing telomerase and more importantly, resistance against chemotherapy

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.

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Background: The mechanism of the relationship between obesity and the risk of breast cancer is still unknown. Objectives: The current study aimed at evaluating the relationship between the leptin receptor Q223R (Gln/Arg) polymorphism, body mass index (BMI), and histopathological changes in patients with breast cancer. Methods: A total of 158 patients with breast cancer and 158 healthy subjects within the same age range were recruited. After taking blood sample, DNAs were extracted using the salting-out method. Then, the polymerase chain reaction-restriction fragment length polymorphism technique was used for genotyping. The histopathological characteristics were determined by the immunohistochemistry technique. Results: Investigation of the relationship between BMI and alleles showed that the G (Arg) mutant elevated the risk of affection by 2.294 times, while the allele A had a descending effect by 0.375 times. The comparison of genotypes with histopathological changes showed a significant relationship between the GG (Arg/Arg) genotype and higher levels of progesterone receptor expression (P = 0.005), invasive type of cancer (P = 0.010), and stage of the disease (P = 0.003). Conclusions: People with higher BMI who also carried G (Arg) mutant of Q223R polymorphism were more prone to breast cancer. Also, tissue changes in the ones carrying this allele were more than those harboring the wild-type A (Gln) allele.

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