The clinical importance of biologic markers remains elusive in gastric cancer. The aim of this study was to evaluate the prognostic value of p53, Ki-67, and COX-2 in gastric cancer. This retrospective study examined based on medical records of postoperative immunohistochemical test of 176 patients who demonstrated high expression of all three biological markers being tested (p53, Ki-67, and COX-2), among 357 gastric cancer patients who underwent surgical resection consecutively. This study demonstrates the correlation with biologic marker between clinical relationship and recurrence free survival (RFS). A positive correlation was observed between the expression of Ki-67 and p53, and a positive correlation was also observed between the expression of Ki-67 and COX-2 Expression of p53 did not correlate with any of the clinicopathological variables examined. Both Ki-67 and COX-2 expression significantly correlated with tumor depth, classified as early gastric cancer and advanced gastric cancer. The expression of COX-2 significantly correlated with tumor differentiation, with more tumors being of the undifferentiated type than of the differentiated type in the COX-2 positive group. A significant difference between p53 and RFS, also COX-2 expression and RFS was observed. This study showed that only p53 and COX-2 have significantly correlated with the RFS of gastric cancer.

Background : Ephedra Sinica has been used to treat obesity in Korean medicine and brown adipocytes also have potential in obesity treatment. Recently, p53 is considered as one of transcriptional regulators regarding thermogenesis of brown adipocytes. Methods and Results : E. Sinica extraction was made with DW and brown preadipocytes were differentiated with adipogenic reagents by incubating for 6 days in the absence or presence of E. Sinica extraction 5 ㎍/㎖ and 10 ㎍/㎖, non-cytotoxic concentration determined by MTT assay. Studies were conducted to see whether E. Sinica modulates the expression of thermogenic and adipogenic genes by qPCR and Western blot. Results showed that E. Sinica significantly activated thermogenesis of brown adipocytes by increasing the mRNA expressions of Uncoupling Protein 1 (UCP1), Cell Death-inducing DNA Fragmentation Factor Alpha-like Effector A (CIDEA), Interferon Regulatory Factor 4 (IRF4) and Beta-3 Adrenergic Receptor (ADRB3). However, major adipogenic genes such as Peroxisome Proliferator-activated Receptor Gamma (PPARλ) and PR Domain Containing 16 (PRDM16), showed no significant differences. In addition, the expression level of p53 was decreased by E. Sinica. Conclusion : It is suggest that E. Sinica stimulates the thermogenesis of brown adipocytes via p53 inhibition.

Regions of allelic loss on chromosomes in many tumors of human and some experimental animals are generally considered to harbor tumor-suppressor genes involved in tumorigenesis. Allelotype analyses have greatly improved our under-standing of the molecular mechanism of radiation lymphomagenesis. Previously, we and others found frequent loss of heterozygosity (LOH) on chromosomes 4, 11, 12, 16 and 19 in radiation-induced lymphomas from several F1, hybrid mice. To examine possible contributions of individual tumor-suppressor genes to tumorigenesis in p53 heterozygous deficiency, we investigated the genome-wide distribution and status of LOH in radiation-induced lymphomas from F1 mice with different p53 status. In this study, we found frequent LOH (more than 20%) on chromosomes 4 and 12 and on chromosomes 11, 12, 16 and 19 in radiation-induced lymphomas from (STS/A×MSM/Ms)F1 mice and (STS/A×MSM/Ms)F1-p53KO/+ mice, respectively. Low incidences of LOH (10-20%) were also observed on chromosomes 11 in mice with wild-type p53, and chromosomes 1, 2, 9, 17 and X in p53 heterozygous-deficient mice. The frequency of LOH on chromosomes 9 and 11 increased in the (STS/A×MSM/Ms)F1-p53KO/+ mice. Preferential losses of the STS-derived allele on chromosome 9 and wild-type p53 allele on chromosome 11 were also found in the p53 heterozygous-deficient mice. Thus, the putative tumor-suppressor gene regions responsible for lymphomagenesis might considerably differ due to the p53 status.