NF-kappaB in pancreatic cancer.
NF-kappaB in pancreatic cancer.
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DOI：
10.1385/ijgc:33:1:15
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发表时间：
2003-01-01
期刊：
影响因子：
--
通讯作者：
Chiao, Paul J
中科院分区：
文献类型：
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作者：
Sclabas, Guido M;Fujioka, Shuichi;Chiao, Paul J
虽然胰腺癌的基因图谱是大量研究的结果，但启动肿瘤发生并产生局部侵袭性生长、转移和化疗耐药等主要临床特征的特定基因改变的作用仍未解决。近年来，一些研究表明，抑制胰腺癌中常见的分子变化之一的结构性核因子-kappaB的激活，可以抑制肿瘤的发生和转移。它还使胰腺癌细胞系对抗癌剂诱导的细胞凋亡敏感。因此，由于核因子-kappaB在胰腺癌中的重要作用，它是开发胰腺癌新的治疗策略的潜在靶点。在适当的组织学和分子水平上模拟致瘤表型的体内和体外模型对于确认胰腺癌标志性基因损害的可疑作用和更好地了解这种疾病的分子基础将非常有用。
Although the genetic profile of pancreatic cancer is emerging as a result of much research, the role of specific genetic alterations that initiate tumorigenesis and produce its cardinal clinical features of locally aggressive growth, metastasis, and chemotherapy resistance remains unresolved. Recently, a number of studies have shown that the inhibition of constitutive NF-kappaB activation, one of the frequent molecular alterations in pancreatic cancer, inhibits tumorigenesis and metastasis. It also sensitizes pancreatic cancer cell lines to anticancer agent-induced apoptosis. Therefore because of the crucial role of NF-kappaB in pancreatic cancer, it is a potential target for developing novel therapeutic strategies for the disease. In vivo and in vitro models that mimic the tumorigenic phenotypes in the appropriate histological and molecular concert would be very useful for confirming the suspected role of the pancreatic cancer signature genetic lesions and better understanding the molecular basis of this disease.