Complete loss of ATM function augments replication catastrophe induced by ATR inhibition and gemcitabine in pancreatic cancer models
Charles R. Dunlop; Yann Wallez; Timothy Isaac Johnson; Sandra Bernaldo de Quirós Fernández; Stephen T. Durant; Elaine Cadogan; Alan Lau; Frances M. Richards · 2020 · British Journal of Cancer
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
BACKGROUND: Personalised medicine strategies may improve outcomes in pancreatic ductal adenocarcinoma (PDAC), but validation of predictive biomarkers is required. Having developed a clinical trial to assess the ATR inhibitor, AZD6738, in combination with gemcitabine (ATRi/gem), we investigated ATM loss as a predictive biomarker of response to ATRi/gem in PDAC. METHODS: Through kinase inhibition, siRNA depletion and CRISPR knockout of ATM, we assessed how ATM targeting affected the sensitivity of PDAC cells to ATRi/gem. Using flow cytometry, immunofluorescence and immunoblotting, we investigate
Abstract by Charles R. Dunlop; Yann Wallez; Timothy Isaac Johnson; Sandra Bernaldo de Quirós Fernández; Stephen T. Durant; Elaine Cadogan; Alan Lau; Frances M. Richards, British Journal of Cancer (2020) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1038/s41416-020-1016-2