p53 proteins were the products of tumor-suppressor genes, which acted by modulating cell proliferation via control of the G1 arrest checkpoint of the cell cycle. bcl-2 and bax belonged to the bcl-2 family, and the latter was one of the most relevant classes of apoptosis regulatory molecules. The bcl-2 family were classified into two subfamilies: anti-apoptosis proteins and pro-apoptosis proteins. It has been shown that the bax to bcl-2 could affect the relative sensitivity or resistance of cells to apoptotic simuli. c-myc protein was a type of transcription factor. A previous study showed the c-myc expression was linked with cell proliferation. In this study, we evaluated the expression of biological markers such as p53, bcl-2, bax, and c-myc, correlated their expression to clinicopathological characteristics and evaluated their prognostic value. The identification of prognostic factors in gastric cancer was essential for predicting patients�� survival and determining optimal therapeutic strategies. Many studies have indicated that the depth of invasion and lymph node metastasis were the most important prognostic factors in gastric cancer. As a result of the variability of prognosis within same pathological stage of gastric cancer, there have been a lot of MG132 Abmole Acetylation targets HSD17B4 for degradation via the CMA pathway in response to estrone researches for specific biological markers to identify patients with poorer prognosis. Abmole Irinotecan Meanwhile, the expression of p53, bcl-2, bax, and c-myc were known for being related with tumorogenesis. Therefore, the aim of this study was to investigate whether these biological markers can be used as additional prognostic factors to traditional TNM stage in gastric cancer. In this study, the expression of these proteins was investigated in 501 cases of resected primary human gastric cancers. The immunohistochemical expression rates of p53, bcl-2, bax, and c-myc were 64.9%, 22.2%, 42.9%, 58.1%, respectively, and these results were consistent with the expression rates of other studies reported as 17�C84.1%, 12.7�C67%, 42.4�C58.0%, 23.5�C 72.9%, respectively. p53 played an important role in apoptosis. It altered most frequently in human cancer. Wild-type p53 protein induced growth arrest at the G1/S phase of cell cycle in response to DNA damage, thus preventing the proliferation of cells. Muted-type p53 lost the function, and allowed cells with damaged DNA to proliferate. In this study, a reverse correlation between p53 and histological type was found, which demonstrated that deregulation of p53 might result in uncontrolled proliferation in gastric cancer. It was consistent with a previous study.