Proteomics

Dataset Information

0

Activation of endogenous retroviruses and induction of viral mimicry by MEK1/2 inhibition in pancreatic cancer


ABSTRACT: While pancreatic ductal adenocarcinomas (PDAC) are addicted to KRAS-activating mutations, inhibitors of downstream effectors in the KRAS pathway, such as the clinically approved MEK1/2 kinases inhibitor Trametinib, are devoid of significant therapeutic effects. Nevertheless, the extensive rewiring of regulatory circuits driven by the attenuation of the KRAS pathway can induce novel functional states and vulnerabilities of potential therapeutic relevance. Here, we performed a quantitative histone post-translatinal modification analysis of PDAC cells in the initial hours after MEK1/2 inhibition by Trametinib.

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

Dataset's files

Source:
Action DRS
Cortesi.zip Other
Experimental_design.txt Txt
QEP220510_RN_1.raw Raw
QEP220510_RN_10.raw Raw
QEP220510_RN_11.raw Raw
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Publications


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]

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