TY - JOUR
T1 - Back to the drawing board
T2 - Re-thinking the role of GLI1 in pancreatic carcinogenesis
AU - Hogenson, Tara L.
AU - Lauth, Matthias
AU - diMagliano, Marina Pasca
AU - Fernandez-Zapico, Martin E.
N1 - Funding Information:
This work was supported by National Institutes of Health Grant CA136526, Division of Oncology Research (Mayo Clinic), Mayo Clinic Pancreatic SPORE P50 Grant CA102701 and Mayo Clinic Center for Cell Signaling in Gastroenterology Grant P30 DK84567 (to M.E.F.-Z.).
Publisher Copyright:
© 2016 Hogenson TL et al.
PY - 2016
Y1 - 2016
N2 - Aberrant activation of the transcription factor GLI1, a central effector of the Hedgehog (HH) pathway, is associated with several malignancies, including pancreatic ductal adenocarcinoma (PDAC), one of most deadly human cancers. GLI1 has been described as an oncogene in PDAC, making it a promising target for drug therapy. Surprisingly, clinical trials targeting HH/GLI1 axis in advanced PDAC were unsuccessful, leaving investigators questioning the mechanism behind these failures. Recent evidence suggests the loss of GLI1 in the later stages of PDAC may actually accelerate disease. This indicates GLI1 may play a dual role in PDAC, acting as an oncogene in the early stages of disease and a tumor-suppressor in the late stages.
AB - Aberrant activation of the transcription factor GLI1, a central effector of the Hedgehog (HH) pathway, is associated with several malignancies, including pancreatic ductal adenocarcinoma (PDAC), one of most deadly human cancers. GLI1 has been described as an oncogene in PDAC, making it a promising target for drug therapy. Surprisingly, clinical trials targeting HH/GLI1 axis in advanced PDAC were unsuccessful, leaving investigators questioning the mechanism behind these failures. Recent evidence suggests the loss of GLI1 in the later stages of PDAC may actually accelerate disease. This indicates GLI1 may play a dual role in PDAC, acting as an oncogene in the early stages of disease and a tumor-suppressor in the late stages.
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U2 - 10.12688/f1000research.5324.1
DO - 10.12688/f1000research.5324.1
M3 - Review article
AN - SCOPUS:85010919229
SN - 2046-1402
VL - 3
SP - 238
JO - F1000Research
JF - F1000Research
ER -