Terials/analysis tools: CJH JFC YJL. Wrote the paper: MEL CPL SJT.Bcl-2 and Age-Related Gray Matter Volume Changes
Gastric cancer is the fourth most common cancer worldwide, and the second leading cause of cancer death in men and the fourth in women [1,2]. Although surgical techniques and adjuvant chemotherapy have substantially improved recently and rate of early detection by endoscopy has increased, the overall 5-year survival rate remains dismal [1]. A steady decline in gastric cancer incidence has been 25033180 observed in most developed countries and some developing countries over the past 50 years [2]. However,gastric cancer remains a major public health problem throughout the world. The carcinogenesis of gastric carcinoma is not well understood, but it exhibits a multi-hit process of genetic alterations involving suppressor genes and oncogenes [3,4]. The protein kinase C (PKC) family consists of serine-threonine kinases that act by phosphorylating their specific protein substrates. The PKC family members are classified into three major groups: classical (a, b, and c), novel (d, e, g, and h), and atypical (m, l, j). Activation of classical PKCs depends on calciumPKCa Protein Overexpression in Gastric Carcinomaand phospholipids. Novel PKCs are activated by phospholipids, and activation of atypical forms occurs independently of calcium or phospholipids. PKCs are involved in various cellular processes including regulating gene expression, proliferation, differentiation, apoptosis, migration, and tumor development [5?0]. Because of the existence of many PKC isoforms and their involvement in different cellular signaling pathways, the roles of PKC isoforms in carcinogenesis have not been clarified [8]. Among the PKC isoforms, PKCa is ubiquitously expressed in many tissues and has been associated with cell proliferation, apoptosis, and cell motility. PKCa activation results in increased cell motility and invasiveness in in vivo and in vitro cancer models [8]. PKCa has been found to be the most important PKC isoform in the formation and progression of malignancies in various cell lines [11]. Abnormal levels of PKCa have been found in transformed cell lines and human cancers [12]. Substantial evidence from gene knockout studies indicates that PKCa activity regulates cancer growth and progression. Selective targeting of PKCa thus has a potential therapeutic role in a wide variety of human cancers [13]. The specific role of PKCa in gastrointestinal tumors has not been well studied [14]. Among the PKC family, PKCa is the most 79983-71-4 biological activity abundant isoform in gastric epithelia, and might play an important role in the carcinogenesis and metastasis of gastric cancers [10]. Furthermore, PKCa is known to play a critical role in cancer cell proliferation and in maintaining the transformed phenotype and tumorigenic capacity of gastric cancer cells [10,14]. Our previous study using quantitative POR-8 price real-time PCR tests demonstrated that in gastric carcinoma, PKCa mRNA overexpression was correlated with distant metastasis, and might be an independent prognostic marker [15]. However, the expression of PKCa protein in gastric carcinoma and its clinicopathological correlations have not been investigated. Our study thus evaluated the expression of PKCa protein in gastric carcinoma using immunohistochemical method. The aims of this study were to assess the expression of PKCa protein in gastric carcinoma, and to correlate it with other clinicopathological parameters. The prognostic si.Terials/analysis tools: CJH JFC YJL. Wrote the paper: MEL CPL SJT.Bcl-2 and Age-Related Gray Matter Volume Changes
Gastric cancer is the fourth most common cancer worldwide, and the second leading cause of cancer death in men and the fourth in women [1,2]. Although surgical techniques and adjuvant chemotherapy have substantially improved recently and rate of early detection by endoscopy has increased, the overall 5-year survival rate remains dismal [1]. A steady decline in gastric cancer incidence has been 25033180 observed in most developed countries and some developing countries over the past 50 years [2]. However,gastric cancer remains a major public health problem throughout the world. The carcinogenesis of gastric carcinoma is not well understood, but it exhibits a multi-hit process of genetic alterations involving suppressor genes and oncogenes [3,4]. The protein kinase C (PKC) family consists of serine-threonine kinases that act by phosphorylating their specific protein substrates. The PKC family members are classified into three major groups: classical (a, b, and c), novel (d, e, g, and h), and atypical (m, l, j). Activation of classical PKCs depends on calciumPKCa Protein Overexpression in Gastric Carcinomaand phospholipids. Novel PKCs are activated by phospholipids, and activation of atypical forms occurs independently of calcium or phospholipids. PKCs are involved in various cellular processes including regulating gene expression, proliferation, differentiation, apoptosis, migration, and tumor development [5?0]. Because of the existence of many PKC isoforms and their involvement in different cellular signaling pathways, the roles of PKC isoforms in carcinogenesis have not been clarified [8]. Among the PKC isoforms, PKCa is ubiquitously expressed in many tissues and has been associated with cell proliferation, apoptosis, and cell motility. PKCa activation results in increased cell motility and invasiveness in in vivo and in vitro cancer models [8]. PKCa has been found to be the most important PKC isoform in the formation and progression of malignancies in various cell lines [11]. Abnormal levels of PKCa have been found in transformed cell lines and human cancers [12]. Substantial evidence from gene knockout studies indicates that PKCa activity regulates cancer growth and progression. Selective targeting of PKCa thus has a potential therapeutic role in a wide variety of human cancers [13]. The specific role of PKCa in gastrointestinal tumors has not been well studied [14]. Among the PKC family, PKCa is the most abundant isoform in gastric epithelia, and might play an important role in the carcinogenesis and metastasis of gastric cancers [10]. Furthermore, PKCa is known to play a critical role in cancer cell proliferation and in maintaining the transformed phenotype and tumorigenic capacity of gastric cancer cells [10,14]. Our previous study using quantitative real-time PCR tests demonstrated that in gastric carcinoma, PKCa mRNA overexpression was correlated with distant metastasis, and might be an independent prognostic marker [15]. However, the expression of PKCa protein in gastric carcinoma and its clinicopathological correlations have not been investigated. Our study thus evaluated the expression of PKCa protein in gastric carcinoma using immunohistochemical method. The aims of this study were to assess the expression of PKCa protein in gastric carcinoma, and to correlate it with other clinicopathological parameters. The prognostic si.