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We have developed faithful patient-derived RMC models and using whole-genome sequencing, we identified loss-of-function intronic fusion events in one\n                    <jats:italic>SMARCB1<\/jats:italic>\n                    allele with concurrent loss of the other allele. Biochemical and functional characterization of these models revealed that RMC requires the loss of\n                    <jats:italic>SMARCB1<\/jats:italic>\n                    for survival. Through integration of RNAi and CRISPR-Cas9 loss-of-function genetic screens and a small-molecule screen, we found that the ubiquitin-proteasome system (UPS) was essential in RMC. Inhibition of the UPS caused a G2\/M arrest due to constitutive accumulation of cyclin B1. These observations extend across cancers that harbor\n                    <jats:italic>SMARCB1<\/jats:italic>\n                    loss, which also require expression of the E2 ubiquitin-conjugating enzyme,\n                    <jats:italic>UBE2C<\/jats:italic>\n                    . Our studies identify a synthetic lethal relationship between\n                    <jats:italic>SMARCB1<\/jats:italic>\n                    -deficient cancers and reliance on the UPS which provides the foundation for a mechanism-informed clinical trial with proteasome inhibitors.\n                  <\/jats:p>","DOI":"10.7554\/elife.44161","type":"journal-article","created":{"date-parts":[[2019,3,12]],"date-time":"2019-03-12T09:00:15Z","timestamp":1552381215000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.44161","source":"Crossref","is-referenced-by-count":47,"title":["Renal medullary carcinomas depend upon SMARCB1 loss and are sensitive to proteasome inhibition"],"prefix":"10.7554","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0374-1667","authenticated-orcid":true,"given":"Andrew L","family":"Hong","sequence":"first","affiliation":[{"name":"Boston Children\u2019s Hospital, Boston, United States"},{"name":"Dana-Farber Cancer Institute, Boston, United 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