Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive Plus
ORGANISM(S): Homo Sapiens (human)
DISEASE(S): Pancreatic Cancer
SUBMITTER: Roberta Noberini
LAB HEAD: Tiziana Bonaldi
PROVIDER: PXD043559 | Pride | 2024-06-16
REPOSITORIES: Pride
Action | DRS | |||
---|---|---|---|---|
Cortesi.zip | Other | |||
Experimental_design.txt | Txt | |||
QEP220510_RN_1.raw | Raw | |||
QEP220510_RN_10.raw | Raw | |||
QEP220510_RN_11.raw | Raw |
Items per page: 5 1 - 5 of 18 |
Cortesi Alice A Gandolfi Francesco F Arco Fabiana F Di Chiaro Pierluigi P Valli Emanuele E Polletti Sara S Noberini Roberta R Gualdrini Francesco F Attanasio Sergio S Citron Francesca F Ho I-Lin IL Shah Rutvi R Yen Er-Yen EY Spinella Mara Cetty MC Ronzoni Simona S Rodighiero Simona S Mitro Nico N Bonaldi Tiziana T Ghisletti Serena S Monticelli Silvia S Viale Andrea A Diaferia Giuseppe Riccardo GR Natoli Gioacchino G
Science advances 20240327 13
While pancreatic ductal adenocarcinomas (PDACs) are addicted to KRAS-activating mutations, inhibitors of downstream KRAS effectors, such as the MEK1/2 kinase inhibitor trametinib, are devoid of therapeutic effects. However, the extensive rewiring of regulatory circuits driven by the attenuation of the KRAS pathway may induce vulnerabilities of therapeutic relevance. An in-depth molecular analysis of the transcriptional and epigenomic alterations occurring in PDAC cells in the initial hours after ...[more]