remains one of the most lethal of all malignancies with a frightening resistance to chemotherapeutic and targeted approaches. Recent evidence defines how EGF receptor is involved in tumor formation, which may lead to novel approaches for PDAC prevention and therapy. Besides lung cancer and some colon cancers, PDAC is one of the few primarily oncogene-driven solid tumors, with oncogenic KRAS mutations found in up to 95 % of cases. 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. The relevance of this upregulation was hinted at with the advent of a transgenic mouse model overexpressing TGFA, one of the main EGFR ligands.
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Siveke et al. (2012) studied this question.
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