Open AccessReciprocal regulation of pancreatic ductal adenocarcinoma growth and molecular subtype by HNF4α and SIX1/4
Author(s) -
Soledad A. Camolotto,
Veronika K Belova,
Luke A. Torre-Healy,
Jeffery M. Vahrenkamp,
Kristofer C. Berrett,
Hannah Conway,
Jill E. Shea,
Chris Stubben,
Richard A. Moffitt,
Jason Gertz,
Eric L. Snyder
Publication year - 2020
Publication title -
gut
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 8.413
H-Index - 293
eISSN - 1468-3288
pISSN - 0017-5749
DOI - 10.1136/gutjnl-2020-321316
Subject(s) - hepatocyte nuclear factor 4 , cancer research , biology , psychological repression , transcriptome , hepatocyte nuclear factors , basal (medicine) , gene expression profiling , gene expression , pancreatic cancer , gene , genetics , cancer , nuclear receptor , endocrinology , transcription factor , insulin
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a 5-year survival of less than 5%. Transcriptomic analysis has identified two clinically relevant molecular subtypes of PDAC: classical and basal-like. The classical subtype is characterised by a more favourable prognosis and better response to chemotherapy than the basal-like subtype. The classical subtype also expresses higher levels of lineage specifiers that regulate endodermal differentiation, including the nuclear receptor hepatocyte nuclear factor 4 α (HNF4α). The objective of this study is to evaluate the role of HNF4α, SIX4 and SIX1 in regulating the growth and molecular subtype of PDAC.