To insert individual citation into a bibliography in a word-processor,
select your preferred citation style below and drag-and-drop it into the document.
Oncogenic Kras activates a plethora of signaling pathways, but our understanding of critical Ras effectors is still very limited. We show that cell-autonomous phosphoinositide 3-kinase (PI3K) and 3-phosphoinositide-dependent protein kinase 1 (PDK1), but not Craf, are key effectors of oncogenic Kras in the pancreas, mediating cell plasticity, acinar-to-ductal metaplasia (ADM), and pancreatic ductal adenocarcinoma (PDAC) formation. This contrasts with Kras-driven non-small cell lung cancer, where signaling via Craf, but not PDK1, is an essential tumor-initiating event. These in vivo genetic studies together with pharmacologic treatment studies in models of human ADM and PDAC demonstrate tissue-specific differences of oncogenic Kras signaling and define PI3K/PDK1 as a suitable target for therapeutic intervention specifically in PDAC. ⺠PI3K (p110αH1047R)-induced neoplasia phenocopies KrasG12D-driven ADM, PanINs, and PDAC ⺠Deletion of Pdk1 blocks KrasG12D-induced PDAC but not NSCLC ⺠Craf is dispensable for Kras-induced PanIN and PDAC development ⺠The PI3K/PDK1 pathway is a target for therapeutic intervention in Kras-driven PDAC
CiteULike organises scholarly (or academic) papers or literature and provides bibliographic
(which means it makes bibliographies) for universities and higher education establishments.
It helps undergraduates and postgraduates. People studying for PhDs or in postdoctoral (postdoc) positions.
The service is similar in scope to EndNote or RefWorks or any other reference manager
like BibTeX, but it is a social bookmarking service for scientists and humanities researchers.
There are no reviews yet
Find related articles from these CiteULike users
