Buchholz Malte, Gress Thomas M
Klinik f. Innere Medizin, SP Gastroenterologie, Universitätsklinikum Marburg, Baldingerstrasse 35043 Marburg, Germany.
Expert Rev Anticancer Ther. 2009 Oct;9(10):1487-97. doi: 10.1586/era.09.107.
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.
与许多人类恶性肿瘤一样,胰腺癌是一种复杂的基因疾病。迄今为止,已报道了DNA、mRNA、miRNA和蛋白质水平上数千种与疾病相关的改变。其中一些改变,包括一些对疾病的发生和进展至关重要的守门基因突变,已在原发性组织、体外实验和转基因小鼠模型中得到广泛研究。然而,对于绝大多数改变,关于其功能意义的数据仍然缺乏。情况因以下事实而变得复杂:对于最初发生恶性转化的细胞的身份以及在胰腺组织中观察到的癌前病变的精确性质和转归尚无定论。