Molecular changes in pancreatic cancer

被引:19
作者
Buchholz, Malte [1 ]
Gress, Thomas M. [1 ]
机构
[1] Univ Klinikum Marburg, SP Gastroenterol, Klin F Innere Med, D-35043 Marburg, Germany
关键词
cellular origin; molecular alterations; mouse models; pancreatic cancer; preneoplastic lesions; ENDOTHELIAL GROWTH-FACTOR; GENE-EXPRESSION PROFILES; FOCAL ADHESION KINASE; TUMOR-SUPPRESSOR GENE; RECEPTOR IGF-IR; K-RAS MUTATION; DUCTAL ADENOCARCINOMA; TYROSINE KINASE; INHIBITS PROLIFERATION; CLINICAL-SIGNIFICANCE;
D O I
10.1586/ERA.09.107
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
As with many human malignancies, pancreatic cancer is a complex genetic disorder. Several thousand disease-associated alterations on the DNA, mRNA, miRNA and protein levels have been reported to date. Some of these alterations, including a number of gatekeeper mutations, which are of pre-eminent importance for the onset and progression of the disease, have been extensively studied in primary tissues, in vitro experiments and transgenic mouse models. For the vast majority of alterations, however, data about the functional significance are lacking. The situation is complicated by the fact that no certainty exists concerning the identity of the cells that originally undergo malignant transformation nor about the precise nature and fate of premalignant lesions that are observed in pancreatic tissues.
引用
收藏
页码:1487 / 1497
页数:11
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