Objective To investigate the expression of phosphate and tension homology deleted on chromsome ten (PTEN) and Basigin1, as well as their relationships with clinicopathological factors and molecular subtypes in invasive ductal carcinoma of breast. Methods The expressions of PTEN and Basigin1 protein were examined in 76 invasive ductal carcinoma of breast tissues by immunohistochemical method, and 20 breast benign hyperplasia tissues as control. These 76 patients underwent surgery in our hospital from Jan. 2014 to Dec. 2015. Results The high-expression rate of PTEN protein in invasive ductal carcinoma of breast tissues was lower than that in benign hyperplasia tissues [56.6% (43/76) vs. 85.0% (17/20), χ2=5.457, P=0.019], while the high-expression rate of Basigin1 protein was higher than that of the benign hyperplasia tissues [51.3% (39/76) vs 25.0% (5/20), χ2=4.417, P=0.036]. The high-expression of PTEN protein was positively correlated with WHO grade and lymph node metastasis status (P<0.05). The high-expression of Basigin1 protein was positively correlated with WHO grade, lymph node metastasis status, and TNM stage (P<0.05). In addition, the high-expression of PTEN protein was associated with molecular subtypes of breast cancer (P<0.001), and its high-expression rate was higher in Luminal A and Luminal B patients; the high-expression of Basigin1 protein was associated with molecular subtypes of breast cancer too (P<0.001), and the high-expression rate of Basigin1 protein was higher in Her-2 overexpression and basal-like subtypes of breast cancer patients. Spearman correlation analysis shown that expression of PTEN protein was negatively correlated with expression of Basigin1 protein (rs=–0.481, P<0.001). Conclusion PTEN and Basigin1 protein may have some mechanisms to promote the occurrence and development of breast cancer, which provide a new basis for targeted treatment of breast cancer.
Continuous activation of Janus kinase (JAK)- signal transduction and activator of transcription (STAT) signaling pathway is prevalent in leukemia cells, and it has been found that this pathway plays an important role in acute leukemia (AL). JAK2/JAK1 gene mutations are found in both acute myelocytic leukemia and acute lymphoblastic leukemia and may have implications for the treatment and overall prognosis of the disease. Among the STAT family members, STAT3 and STAT5 proved to be key factors in AL. These gene mutations may provide new targets and new ideas for the treatment of AL. This article provides a review of the research progress of JAK-STAT signaling pathway, related gene mutations and AL.