Supplementary Materials

MTAP deletion confers enhanced dependency on the PRMT5 arginine methyltransferase in cancer cells

Gregory V. Kryukov, Frederick H. Wilson, Jason R. Ruth, Joshiawa Paulk, Aviad Tsherniak, Sara E. Marlow, Francisca Vazquez, Barbara A. Weir, Mark E. Fitzgerald, Minoru Tanaka, Craig M. Bielski, Justin M. Scott, Courtney Dennis, Glenn S. Cowley, Jesse S. Boehm, David E. Root, Todd R. Golub, Clary B. Clish, James E. Bradner, William C. Hahn, Levi A. Garraway

Materials/Methods, Supplementary Text, Tables, Figures, and/or References

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  • Materials and Methods
  • Figs. S1 to S10
  • Tables S1 and S2
  • References
Data Table S1
MTAP and CDKN2A copy number and expression data for 216 cell lines used in the initial screening data set.
Data Table S2
Metrics of correlation between MTAP loss and cell viability for 50,529 shRNAs used for the initial screening data set.
Data Table S3
Two lowest P values for point biserial correlation between MTAP status and effect on cell viability for shRNAs targeting the same gene.
Data Table S4
MTAP and CDKN2A copy number and expression data for 275 cell lines used in the validation dataset.
Data Table S5
Normalized metabolite levels profiled in 40 cancer cell lines.
Data Table S6
Metrics of correlation between MTAP loss and abundance of 73 metabolites profiled across 40 cancer cell lines.
Data Table S7
Normalized metabolite levels and shPRMT5 #1 sensitivity scores across 40 cancer cell lines.
Data Table S8
Details of methyltransferase assay, including identity and source of profiled methyltransferases, corresponding substrates, and assay buffers.