Although reviewers of Tremblay＇s play For the Pleasure of Seeing Her Again （1998） focus on the monologues of the angry mother who rants about everyday concerns for the well-being of her child, a character much like...Although reviewers of Tremblay＇s play For the Pleasure of Seeing Her Again （1998） focus on the monologues of the angry mother who rants about everyday concerns for the well-being of her child, a character much like the one who initiated Tremblay＇s career （the old song）, the author will focus on how the narrator＇s memory of his mother stage by stage in his life enacted before our eyes, permits Tremblay to self-consciously explain that his artistry reaches far beyond bringing the people he knew best in his youth, who had no knowledge of theater history, acting, and directing and staging, to the stage. His growth as an artist and his ＂new songs＂ are a result of his own continuous development of that knowledge展开更多
Pancreatic ductal adenocarcinoma （PDAC） represents a biggest challenge in clinic oncology due to its invasiveness and lack of tar- geted therapeutics. Our recent study showed that schizophrenia susceptibility factor...Pancreatic ductal adenocarcinoma （PDAC） represents a biggest challenge in clinic oncology due to its invasiveness and lack of tar- geted therapeutics. Our recent study showed that schizophrenia susceptibility factor dysbindin exhibited significant higher level in serum of PDAC patients. However, the functional relevance of dysbindin in PDAC is still unclear. Here, we show that dysbindin pro- motes tumor growth both in vitro and in vivo by accelerating the G1/S phase transition in cell cycle via PI3K/AKT signaling path- way. Mechanistically, dysbindin interacts with PI3K and stimulates the kinase activity of PI3K. Moreover, overexpression of dysbindin in PDAC is correlated with clinicopathological characteristics significantly, such as histological differentiation （P = 0.011） and tumor size （P = 0.007）. Kaplan-Meier survival curves show that patients with high dysbindin expression exhibit poorer overall survival, compared to those with low dysbindin expression （P 〈 0.001）. Multivariate analysis reveals that dysbindin is an independ- ent prognostic factor for pancreatic ductal adenocarcinoma （P = 0.001）. Thus, our findings reveal that dysbindin is a novel PI3K acti- vator and promotes PDAC progression via stimulation of PI3K/AKT. Dysbindin therefore represents a potential target for prognosis and therapy of PDAC.展开更多
文摘Although reviewers of Tremblay＇s play For the Pleasure of Seeing Her Again （1998） focus on the monologues of the angry mother who rants about everyday concerns for the well-being of her child, a character much like the one who initiated Tremblay＇s career （the old song）, the author will focus on how the narrator＇s memory of his mother stage by stage in his life enacted before our eyes, permits Tremblay to self-consciously explain that his artistry reaches far beyond bringing the people he knew best in his youth, who had no knowledge of theater history, acting, and directing and staging, to the stage. His growth as an artist and his ＂new songs＂ are a result of his own continuous development of that knowledge
文摘Pancreatic ductal adenocarcinoma （PDAC） represents a biggest challenge in clinic oncology due to its invasiveness and lack of tar- geted therapeutics. Our recent study showed that schizophrenia susceptibility factor dysbindin exhibited significant higher level in serum of PDAC patients. However, the functional relevance of dysbindin in PDAC is still unclear. Here, we show that dysbindin pro- motes tumor growth both in vitro and in vivo by accelerating the G1/S phase transition in cell cycle via PI3K/AKT signaling path- way. Mechanistically, dysbindin interacts with PI3K and stimulates the kinase activity of PI3K. Moreover, overexpression of dysbindin in PDAC is correlated with clinicopathological characteristics significantly, such as histological differentiation （P = 0.011） and tumor size （P = 0.007）. Kaplan-Meier survival curves show that patients with high dysbindin expression exhibit poorer overall survival, compared to those with low dysbindin expression （P 〈 0.001）. Multivariate analysis reveals that dysbindin is an independ- ent prognostic factor for pancreatic ductal adenocarcinoma （P = 0.001）. Thus, our findings reveal that dysbindin is a novel PI3K acti- vator and promotes PDAC progression via stimulation of PI3K/AKT. Dysbindin therefore represents a potential target for prognosis and therapy of PDAC.
