The Role of Phosphatidylinositol 3-Kinase Signaling Pathways in Pancreatic Cancer

被引:12
|
作者
Sun, Chen [4 ]
Rosendahl, Ann H.
Andersson, Roland [1 ,2 ]
Wu, DeQuan [3 ,4 ]
Wang, Xiangdong [5 ]
机构
[1] Skane Univ Hosp Lund, Dept Surg, SE-22185 Lund, Sweden
[2] Lund Univ, Dept Surg, SE-22185 Lund, Sweden
[3] Second Affiliated Hosp, Harbin, Peoples R China
[4] Harbin Med Univ, Harbin, Peoples R China
[5] Fudan Univ, Zhongshan Hosp Ctr Lab, Shanghai 200433, Peoples R China
关键词
Pancreatic cancer; PI3K; Signaling pathway; NF-KAPPA-B; SST2 SOMATOSTATIN RECEPTOR; FATTY-ACID SYNTHASE; GROWTH-FACTOR; INDUCED APOPTOSIS; C-MYC; DUCTAL ADENOCARCINOMA; ANTITUMOR-ACTIVITY; AKT ACTIVATION; CELL LUNG;
D O I
10.1159/000327715
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Pancreatic cancer is a highly malignant cancer and the fourth leading cause of cancer-related death. It is characterized by a rapid disease progression, a highly invasive tumor phenotype, and frequently resistance to chemotherapy. Despite significant advances in diagnosis, staging, and surgical management of the disease during the past decade, prognosis of pancreatic cancer is still dismal. Methods and Results: The phosphatidylinositol 3-kinase (PI3K) signaling pathways regulate cellular growth, metabolism, survival, and motility in pancreatic cancer. Pancreatic cancer is associated with a high degree of genetic alterations that can result in aberrant activation of the PI3K signaling pathway. Elucidating the role of the PI3K signaling pathway in pancreatic cancer may thus be both meaningful and necessary. Conclusion: Improved knowledge of the PI3K signaling pathway in pancreatic cancer would furthermore be helpful in understanding mechanisms of tumor initiation and progression, and in identifying appropriate targeted anticancer treatment in pancreatic cancer. Copyright (C) 2011 S. Karger AG, Basel and IAP
引用
收藏
页码:252 / 260
页数:9
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