A Study on the Expression of SPRED1 and PBRM1 (Baf180) and their Clinical Significances in Patients with Gastric Cancer.

ola Kala shared this article with you from Inoreader A Study on the Expression of SPRED1 and PBRM1 (Baf180) and their Clinical Significances in Patients with Gastric Cancer. Μέσω pubmed: "clin lab"[jour] A Study on the Expression of SPRED1 and PBRM1 (Baf180) and their Clinical Significances in Patients with Gastric Cancer. Clin Lab. 2020 Oct 01;66(10): Authors: Liu W, Fang S, Zuo G Abstract BACKGROUND: To evaluate SPRED1 and PBRMl expression in patients with gastric cancer and determine the biological relationships of SPRED1 and PBRM1 with the occurrence and development of gastric cancer. METHODS: Tissue specimens of patients with gastric cancer at Jingzhou First People's Hospital were gathered from April 2016 to August 2018. SPRED1 and PBRMl (Baf180) protein expression levels were detected in the excised cancerous tissues and normal tissues (control group) of 80 patients with gastric cancer by immunohistochemical methods. RESULTS: The positive rates of SPRED1 and PBRMl protein expression in gastric cancer tissues were 55% and 75%, respectively. The positive rates of SPRED1 and PBRMl protein expression in the normal tissues without cancer were 84.6% and 92.3%, respectively. The expression in gastric cancer tissues was significantly lower than that of the control group (p < 0.05). Positive SPRED1 and PBRMl protein expression was related to histological type, depth of infiltration, presence of lymphatic metastasis, pathological grade, and clinical TNM phase (p < 0.05). SPRED1 expression and PBRMl expression were positively correlated. CONCLUSIONS: The expression of SPRED1 and PBRMl in gastric cancer tissues is low, unrelated to age and declines with increasing pathological grade and clinical phase of the gastric cancer tissues. SPRED1 and PBRMl expression may be related to the biological behavior of tumors, and the two may have a synergistic effect. PMID: 33073945 [PubMed - in process] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.