Back

Pooled CRISPR screening in pancreatic cancer cells implicates co-repressor complexes as a cause of multiple drug resistance via regulation of epithelial-to-mesenchymal transition

Ramaker, R. C.; Hardigan, A. A.; Gordon, E. R.; Wright, C. A.; Myers, R. M.; Cooper, S. J.

2020-10-27 genomics
10.1101/648709 bioRxiv
Show abstract

Pancreatic ductal adenocarcinoma (PDAC) patients suffer poor outcomes in part due to therapeutic resistance. We conducted four genome-wide CRISPR activation (CRISPRact) and CRISPR knock out (CRISPRko) screens to identify novel resistance mechanisms to four cytotoxic chemotherapies (gemcitabine, 5-fluorouracil, irinotecan, and oxaliplatin). ABCG2, a well-described efflux pump was the strongest mediator of resistance. We showed that overexpressing HDAC1 altered promoter occupancy and expression of genes involved in the epithelial-to-mesenchymal transition. Using the results of our CRISPR screens, we predicted drug sensitivity for patients and cell lines based on gene expression profiles. These predictions could be clinically useful for treatment selection.

Matching journals

The top 4 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.