Gastric cancer is a disease which the cells forming the inner lining of the stomach start to divide uncontrollably, forming a mass called a tumor. Patients with gastric cancer from low facility provinces like North and South Khorasans may diagnose and registered in full featured provinces like Razavi-Khorasan; this causes misclassification error. The presence of this error makes the registry systems inaccurate and unreliable for estimating the burden of cancer and policy making. Two approaches are recommended for reducing the effects of misclassification; the first is using a small validation sample and the second is a Bayesian analysis which provides subjective prior information for the subset of the parameters to correct the statistics. Data for this study extracted from Iranian annual of national cancer registration report in 2008. The age standardized rate due to gastric cancer [ICD-10; C16] were expressed as rate per/100,000 population for male and female of North, South and Razavi Khorasans. To correct the misclassification effect, a Bayesian approach was used with Poisson count regression and beta prior. The reported expected coverage of cancer incidence for Razavi-Khorasan was 155.5% and exceeds than what expected, whereas the North and South Khorasans have just observed respectively 34.8% and 41.4% of their expected coverage. The results of the Bayesian analysis indicated that there was about 34% misclassification in gastric cancer incidence registry from North and South Khorasans in Razavi-Khorasan. In planning for resource allocation, authorities should consider that, low incidence of gastric cancer in North and South Khorasans, may be the effect of misclassification and it is needed to allocate them more health facilities and improve their address registration accuracy using National ID, electric bill, etc.
Most of signaling pathways play a basic role in controlling of embryonic development and cell proliferation in adult tissues. In recent years, mutations that affected on components in most of these pathways have been linked to a type of human cancer. For example, APC (adenomatosis polyposis coli) is the first of critical gene that mutated in the development of colon cancer, as part of the Wnt signaling pathway is known. Cancer development associated with genetic and epigenetic modifications. Studies show that APC including genes that involved through these modifications in cancer, such as gastric cancer. APC is a tumor suppressor protein that regulates part of the Wnt signaling pathway. The protein binds to I²-Catenin, Axin (a scaffold protein) and Gsk3 (glycogen synthase kinase 3) in the cytoplasm and promoted I²-Catenin phosphorylation via Gsk3. phosphorylated I²-Catenin destroyed by the proteasome and thereby inhibits Wnt signaling pathway. On the other hand APC has a nuclear localization signal (NLS) and nuclear export signal (NES). If in the presence of Wnt signal, accumulates I²-Catenin in cytoplasm enters into nucleus, APC connected to accumulated I²-Catenin in nucleus through binding domains and with its shuttling activity translocated I²-Catenin between nucleus and cytoplasm; therefore regulated level and transcriptional activity of I²-catenin in nucleus. If binding region to I²-Catenin of APC genes is mutated, does not occur Wnt signaling inhibition and caused uncontrolled proliferation of cells that lead to cancer cells. In general APC downregulated Wnt signaling pathway and caused cell proliferation inhibition, which indicates the important role of this protein as a tumor suppressor. In addition, APC is one of the genes that are commonly in gastric cancer hypermethylated and APC promoter hypermethylated helps activation of Wnt middle that is associated with development of gastric adenoma. Above shows that the APC as a tumor suppressor plays an important role in Wnt/I²_Catenin signaling pathway. Mutations in this gene can cause gastric cancer, but removing this gene did not influence in incidence of gastric cancer also involved in the development its.
Breast cancer as a heterogeneous sophisticated disease includes several group with discrete clinical consequences. The disease is the most prevalent malignancy after non-melanoma skin cancers and it is also considered as the second leading cause of death after lung cancer. In fact, breast cancer is account for 23% of all cancer cases and 14% of deaths from cancer. The major cause of breast cancer deaths is actually metastasis of the tumor. As a result, it is prominent to identify the disease mechanism and diagnose molecular tools in order to predict metastasis. The specimens were collected from 30 metastatic and 30 primary tumor tissues of breast cancer patients. After that, RNA extraction was accomplished by means of GeneAll kit and then was stored in -80 degrees. Then, cDNA synthesis was carried out by miscript II RT kit from Qiagenecompany. Finally, sybergreen Real Time PCR of all samples was done for miRNA124, miRNA130a and miRNA 16 as a reference by means of Pre-designed primers of Qiagene Company. The results of molecular expression study showed that the amount of miRNA 124 in metastatic tissues has approximately increased double of primary tumor tissues. It is also revealed that the amount of miRNA has similarly increased by about 1.7 times. According to recent results, it can be possible to regard molecule as a major cause of metastasis process in breast cancer.
Breast cancer is the second cause of mortality in women. The etiology of breast cancer is multi factorial. Genetic factors play an important role in the etimology of breast cancer. The FAS gene, has a critical role in the tumor growth and metastasis. Gene polymorphisms including -1377 G>A and -670 A/G in FAS gene have shown to change the transcription activities of this gene. The FAS genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 115 breast cancer patients, 115 healthy controls, all female and selected from city of Mashhad in north-eastern part of Iran. BstuI and ScrfI were used as endonuclease enzymes to detect -1377G/A and -670A/G gene polymorphisms, respectively. GG, GA and AA genotype frequencies for FAS -1377 polymorphism in patients were 30.4%, 49.6% and 20%, whereas in healthy controls were 26.1%, 50.4% and 23.5%, respectively and there was no significant difference between case and controls (p=0.7).Additionally, genotype frequencies of FAS -670 AA, AG and GG in patient groups were 52.2%, 39.1% and 8.7% respectively . The result of genotype frequency in controls for FAS -670 AA, AG and GG was 47%, 41% and 10.4%, which Showed insignificant difference as compared with patients genotypes (p=0.78). These results showed that FAS−1377G/A and FAS -670 A/G gene polymorphisms had a strong linkage disequilibrium with p value <0.001. These results indicated the lack of association between FAS−1377G>A and FAS -670 A/G gene polymorphisms and risk of breast cancer. Moreover, a significant linkage disequilibrium was found betweenFAS−1377G/A and FAS -670 A/G gene polymorphisms in case and control groups.