Abstract
KRAS above and beyond - EGFR in pancreatic cancer
Highlights
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal of all malignancies with a frightening resistance to chemotherapeutic and targeted approaches
Along with the central role of KRAS-dependent signaling, receptor tyrosine kinases and especially the EGF receptor (EGFR) and its ligands are strongly upregulated in PDAC and chronic pancreatitis (CP), a risk factor for PDAC
In vitro studies show that treatment of acinar cells with EGFR ligands induces a phenotypic conversion to a ductlike cell, a process later confirmed to be true acinar-to-ductal metaplasia (ADM) [2]
Summary
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal of all malignancies with a frightening resistance to chemotherapeutic and targeted approaches. Along with the central role of KRAS-dependent signaling, receptor tyrosine kinases and especially the EGF receptor (EGFR) and its ligands are strongly upregulated in PDAC and chronic pancreatitis (CP), a risk factor for PDAC. In vitro studies show that treatment of acinar cells with EGFR ligands induces a phenotypic conversion to a ductlike cell, a process later confirmed to be true ADM [2].
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