Chromosomal instability in mouse metastatic pancreatic cancer--it's Kras and Tp53 after all.
A human pancreatic cancer progression model from intraepithelial neoplasia to ductal adenocarcinoma has been proposed. This process has been modeled in the mouse by activation of mutant Kras in pancreatic progenitor cells. In this issue of Cancer Cell, present a modification of their initial model by introducing a mutant Tp53. This combination of genetic alterations leads to rapid and increased frequency of neoplasia progression resulting in pancreatic cancers that manifest chromosomal instability in the presence of apparent intact telomeres. These findings introduce Tp53-mediated chromosomal instability as key event for carcinoma development in this mouse model.
Siveke
Jens T
JT
2nd Department of Internal Medicine, Technical University of Munich, Klinikum rechts der Isar, Ismaningerstrasse 22, 81675 Munich, Germany. roland.schmid@lrz.tum.de
Schmid
Roland M
RM
D000818:Animals; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics* / Q000473:pathology; D043171:Chromosomal Instability / Q000235:genetics*; D051379:Mice; D008954:Models, Biological; D009362:Neoplasm Metastasis; D017354:Point Mutation / Q000235:genetics; D016283:Proto-Oncogene Proteins p21(ras); D016615:Telomere / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D018631:ras Proteins / Q000235:genetics*
D016159:Tumor Suppressor Protein p53; C495971:Hras protein, mouse; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins