TY - JOUR
T1 - An integrated cellular and molecular model of gastric neuroendocrine cancer evolution highlights therapeutic targets
AU - Griger, Joscha
AU - Widholz, Sebastian A.
AU - Jesinghaus, Moritz
AU - de Andrade Krätzig, Niklas
AU - Lange, Sebastian
AU - Engleitner, Thomas
AU - Montero, Juan José
AU - Zhigalova, Ekaterina
AU - Öllinger, Rupert
AU - Suresh, Veveeyan
AU - Winkler, Wiebke
AU - Lier, Svenja
AU - Baranov, Olga
AU - Trozzo, Riccardo
AU - Ben Khaled, Najib
AU - Chakraborty, Shounak
AU - Yu, Jiakun
AU - Konukiewitz, Björn
AU - Steiger, Katja
AU - Pfarr, Nicole
AU - Rajput, Ashish
AU - Sailer, David
AU - Keller, Gisela
AU - Schirmacher, Peter
AU - Röcken, Christoph
AU - Fagerstedt, Klaus W.
AU - Mayerle, Julia
AU - Schmidt-Supprian, Marc
AU - Schneider, Günter
AU - Weichert, Wilko
AU - Calado, Dinis P.
AU - Sommermann, Thomas
AU - Klöppel, Günter
AU - Rajewsky, Klaus
AU - Saur, Dieter
AU - Rad, Roland
N1 - Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/7/10
Y1 - 2023/7/10
N2 - 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.
AB - 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.
KW - CRISPR screen
KW - MANEC
KW - NEC
KW - WGS
KW - gastric cancer
KW - genetic screening
KW - mouse model
KW - neuroendocrine cancer
KW - pharmacologic screening
KW - stomach
UR - http://www.scopus.com/inward/record.url?scp=85164291778&partnerID=8YFLogxK
U2 - 10.1016/j.ccell.2023.06.001
DO - 10.1016/j.ccell.2023.06.001
M3 - Article
C2 - 37352862
AN - SCOPUS:85164291778
SN - 1535-6108
VL - 41
SP - 1327-1344.e10
JO - Cancer Cell
JF - Cancer Cell
IS - 7
ER -