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Profiling of a global cohort of 1,250 neuroendocrine tumors to identify multiple potential drug targets
Journal article   Peer reviewed

Profiling of a global cohort of 1,250 neuroendocrine tumors to identify multiple potential drug targets

Igor A. Astsaturov, Steven J. Cohen, Paul F. Engstrom, Zoran Gatalica, Ryan P. Bender, Gargi Dan Basu and Sherri Z. Millis
Journal of clinical oncology, Vol.32(3_suppl), pp.214-214
01/20/2014

Abstract

Abstract only 214 Background: Identification of new drug targets may extend treatment options for NET, regardless of histologic classification or primary organ site. Methods: 1,250 cases of infradiaphragmatic neuroendocrine tumors (all grades and sites) were identified among >50,000 cases profiled in a CLIA certified laboratory. Biomarker profiling utilized multiple platforms: gene sequencing (next generation sequencing, Sanger or pyrosequencing), gene copy number by in-situ hybridization, and protein expression by immunohistochemistry. The results are shown relative to the total number of tests performed. Results: Overall, drug therapy-relevant alterations were identified in 1,130 of 1,250 (90%) of cases. Low or absent (0 or 1+ by IHC) MGMT, a biomarker of sensitivity to alkylating agents, was found in 130/219 pancreatic cases (59%), and in 450/991 (45%) of non-pancreatic NET. Low or absent (0 or 1+ by IHC) expression of RRM1, a biomarker of gemcitabine sensitivity, was found in 813/1,100 of NET (74%) and low or absent thymidine synthase, TS, a biomarker of fluoropyrimidine sensitivity, was shown for 793/1,096 (72%) of NET by IHC. Sequencing of tumors showed oncogenic mutations in BRAF (4/369 (V600E in 3 and G596R in 1), CTNNB1 (2/150), KIT (3/281), EGFR (1/178), FGFR2 (1/150), GNAS (1/150), HRAS (2/150), PIK3CA (6/343), RB (2/150) VHL (1/150), KRAS (10/125), NRAS (2/274), and APC (2/150) and amplifications of EGFR (46/686) and MET (4/236). Ki67 status and correlation between the site of origin and biomarkers will be presented. Therapies guided by mechanism-based biomarkers produced durable responses in documented cases: partial response (PR) >1 year to imatinib in a patient with KIT-mutant metastatic NET, and in cases of MGMT low /TS low treated with streptozocine or temizolomide plus fluoropyrimidine chemotherapy, thus supporting the clinical relevance of target profiling in NET. Conclusions: Comprehensive multiplatform profiling of a large series (n=1,250) of NET, despite low frequency of individual biomarkers, identified clinically relevant targets in the majority of patients. Our results provide the basis for future clinical trials to assess the efficacy of biomarker-based therapy for NET.

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