Epidermal growth factor receptor(EGFR)signaling has become an importanttarget for drug development becauseEGFR signaling enhances tumor cell proliferation,migration,and invasion and inhibits apoptosis.However,theresul...Epidermal growth factor receptor(EGFR)signaling has become an importanttarget for drug development becauseEGFR signaling enhances tumor cell proliferation,migration,and invasion and inhibits apoptosis.However,theresults of clinical trials using EGFR inhibitors in patients with solid tumors have been disappointing.Here,wereport a protective effect of the EGFR inhibitors AG1478 and PD153035 against cell death induced by acute hy-poxia,which contrasts with their proapoptotic effects under normoxia.Under hypoxic conditions,both agents re-展开更多
Objective To investigate the K562 cells biological function and related molecular changes in PTEN-PI3K/AKT signaling pathway of leukemia K562 cells by inhibiting the miRNA-21 expression to explore its pathogenesis of ...Objective To investigate the K562 cells biological function and related molecular changes in PTEN-PI3K/AKT signaling pathway of leukemia K562 cells by inhibiting the miRNA-21 expression to explore its pathogenesis of leukemia.Methods The chemical synthetic miRNA-展开更多
BACKGROUND:Pancreatic cancer(PCa)is one of the most aggressive human solid tumors,with rapid growth and metastatic spread as well as resistance to chemotherapeutic drugs,leading rapidly to virtually incurable disease....BACKGROUND:Pancreatic cancer(PCa)is one of the most aggressive human solid tumors,with rapid growth and metastatic spread as well as resistance to chemotherapeutic drugs,leading rapidly to virtually incurable disease.Over the last 20 years,however,significant advances have been made in our understanding of the molecular biology of PCa,with a focus on the cytogenetic abnormalities in PCa cell growth and differentiation. DATA SOURCES:A MEDLINE search and manual cross- referencing were utilized to identify published data for PCa molecular biology studies between 1986 and 2008, with emphasis on genetic alterations and developmental oncology. RESULTS:Activation of oncogenes,deregulation of tumor suppressor and genome maintenance genes,upregulation of growth factors/growth factor receptor signaling cascade systems,and alterations in cytokine expression,have been reported to play important roles in the process of pancreatic carcinogenesis.Alterations in the K-ras proto- oncogene and the p16INK4a,p53,FHIT,and DPC4 tumor suppressor genes occur in a high percentage of tumors. Furthermore,a variety of growth factors are expressed at increased levels.In addition,PCa often exhibits alterations in growth inhibitory pathways and evades apoptosis through p53 mutations and aberrant expression of apoptosis-regulating genes,such as members of the Bcl family.Additional pathways in the development of an aggressive phenotype,local infiltration and metastasis are still under ongoing genetic research.The present paper reviews recent studies on the pathogenesis of PCa,and includes a brief reference to alterations reported for other types of pancreatic tumor. CONCLUSIONS:Advances in molecular genetics and biology have improved our perception of the pathogenesis of PCa.However,further studies are needed to better understand the fundamental changes that occur in PCa,thus leading to better diagnostic and therapeutic management.展开更多
文摘Epidermal growth factor receptor(EGFR)signaling has become an importanttarget for drug development becauseEGFR signaling enhances tumor cell proliferation,migration,and invasion and inhibits apoptosis.However,theresults of clinical trials using EGFR inhibitors in patients with solid tumors have been disappointing.Here,wereport a protective effect of the EGFR inhibitors AG1478 and PD153035 against cell death induced by acute hy-poxia,which contrasts with their proapoptotic effects under normoxia.Under hypoxic conditions,both agents re-
文摘Objective To investigate the K562 cells biological function and related molecular changes in PTEN-PI3K/AKT signaling pathway of leukemia K562 cells by inhibiting the miRNA-21 expression to explore its pathogenesis of leukemia.Methods The chemical synthetic miRNA-
文摘BACKGROUND:Pancreatic cancer(PCa)is one of the most aggressive human solid tumors,with rapid growth and metastatic spread as well as resistance to chemotherapeutic drugs,leading rapidly to virtually incurable disease.Over the last 20 years,however,significant advances have been made in our understanding of the molecular biology of PCa,with a focus on the cytogenetic abnormalities in PCa cell growth and differentiation. DATA SOURCES:A MEDLINE search and manual cross- referencing were utilized to identify published data for PCa molecular biology studies between 1986 and 2008, with emphasis on genetic alterations and developmental oncology. RESULTS:Activation of oncogenes,deregulation of tumor suppressor and genome maintenance genes,upregulation of growth factors/growth factor receptor signaling cascade systems,and alterations in cytokine expression,have been reported to play important roles in the process of pancreatic carcinogenesis.Alterations in the K-ras proto- oncogene and the p16INK4a,p53,FHIT,and DPC4 tumor suppressor genes occur in a high percentage of tumors. Furthermore,a variety of growth factors are expressed at increased levels.In addition,PCa often exhibits alterations in growth inhibitory pathways and evades apoptosis through p53 mutations and aberrant expression of apoptosis-regulating genes,such as members of the Bcl family.Additional pathways in the development of an aggressive phenotype,local infiltration and metastasis are still under ongoing genetic research.The present paper reviews recent studies on the pathogenesis of PCa,and includes a brief reference to alterations reported for other types of pancreatic tumor. CONCLUSIONS:Advances in molecular genetics and biology have improved our perception of the pathogenesis of PCa.However,further studies are needed to better understand the fundamental changes that occur in PCa,thus leading to better diagnostic and therapeutic management.
