An integrated cellular and molecular model of gastric neuroendocrine cancer evolution highlights therapeutic targets
Authors
- J. Griger
- S.A. Widholz
- M. Jesinghaus
- N. de Andrade Krätzig
- S. Lange
- T. Engleitner
- J.J. Montero
- E. Zhigalova
- R. Öllinger
- V. Suresh
- W. Winkler
- S. Lier
- O. Baranov
- R. Trozzo
- N. Ben Khaled
- S. Chakraborty
- J. Yu
- B. Konukiewitz
- K. Steiger
- N. Pfarr
- A. Rajput
- D. Sailer
- G. Keller
- P. Schirmacher
- C. Röcken
- K.W. Fagerstedt
- J. Mayerle
- M. Schmidt-Supprian
- G. Schneider
- W. Weichert
- D.P. Calado
- T. Sommermann
- G. Klöppel
- K. Rajewsky
- D. Saur
- R. Rad
Journal
- Cancer Cell
Citation
- Cancer Cell 41 (7): 1327-1344.e10
Abstract
Gastric neuroendocrine carcinomas (G-NEC) are aggressive malignancies with poorly understood biology and a lack of disease models. Here, we use genome sequencing to characterize the genomic landscapes of human G-NEC and its histologic variants. We identify global and subtype-specific alterations and expose hitherto unappreciated gains of MYC family members in a large part of cases. Genetic engineering and lineage tracing in mice delineate a model of G-NEC evolution, which defines MYC as a critical driver and positions the cancer cell of origin to the neuroendocrine compartment. MYC-driven tumors have pronounced metastatic competence and display defined signaling addictions, as revealed by large-scale genetic and pharmacologic screening of cell lines and organoid resources. We create global maps of G-NEC dependencies, highlight critical vulnerabilities, and validate therapeutic targets, including candidates for clinical drug repurposing. Our study gives comprehensive insights into G-NEC biology.