Molecular markers for novel therapeutic strategies in pancreatic endocrine tumors

JA Gilbert, LJ Adhikari, RV Lloyd, TR Halfdanarson… - Pancreas, 2013 - journals.lww.com
JA Gilbert, LJ Adhikari, RV Lloyd, TR Halfdanarson, MH Muders, MM Ames
Pancreas, 2013journals.lww.com
Objectives Pancreatic endocrine tumors (PETs) share numerous features with
gastrointestinal neuroendocrine (carcinoid) tumors. Targets of novel therapeutic strategies
previously assessed in carcinoid tumors were analyzed in PETs (44 cases). Methods
Activating mutations in EGFR, KIT, and PDGFRA and nonresponse mutations in KRAS were
evaluated. Copy number of EGFR and HER-2/neu was quantified by fluorescence in situ
hybridization. Expression of EGFR, PDGFRA, VEGFR1, TGFBR1, Hsp90, SSTR2A, SSTR5 …
Abstract
Objectives
Pancreatic endocrine tumors (PETs) share numerous features with gastrointestinal neuroendocrine (carcinoid) tumors. Targets of novel therapeutic strategies previously assessed in carcinoid tumors were analyzed in PETs (44 cases).
Methods
Activating mutations in EGFR, KIT, and PDGFRA and nonresponse mutations in KRAS were evaluated. Copy number of EGFR and HER-2/neu was quantified by fluorescence in situ hybridization. Expression of EGFR, PDGFRA, VEGFR1, TGFBR1, Hsp90, SSTR2A, SSTR5, IGF1R, mTOR, and MGMT was measured immunohistochemically.
Results
Elevated EGFR copy number was found in 38% of cases but no KRAS nonresponse mutations. VEGFR1, TGFBR1, PDGFRA, SSTR5, SSTR2A, and IGF1R exhibited the highest levels of expression in the largest percentages of PETs.
Lippincott Williams & Wilkins
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