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BB65-RCC

RRID:CVCL_1078

Organism

Homo sapiens

Comments

Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: COSMIC cell lines project. From: Ludwig Institute for Cancer Research, Brussels Branch; Brussels; Belgium. Microsatellite instability: Stable (MSS) (Sanger). Sequence variation: Heterozygous for TP53 p.Arg248Trp (c.742C>T) (Cosmic-CLP). Omics: CNV analysis. Omics: Deep exome analysis. Omics: DNA methylation analysis. Omics: SNP array analysis. Omics: Transcriptome analysis. Genome ancestry: African=0.53%; Native American=1.94%; East Asian, North=1.65%; East Asian, South=0%; South Asian=0.38%; European, North=59.69%; European, South=35.82% (PubMed=30894373). DT Created: 04-04-12; Last updated: 06-09-19; Version: 23

Proper Citation

RRID:CVCL_1078

Category

Cancer cell line DT Created: 04-04-12; Last updated: 06-09-19; Version: 23

Sex

DT Created: 04-04-12; Last updated: 06-09-19; Version: 23

Synonyms

BB65 RCC, BB65RCC, BB65 DT Created: 04-04-12, Last updated: 06-09-19, Version: 23

Cross References

ArrayExpress; E-MTAB-3610 CCLE; BB65RCC_KIDNEY Cell_Model_Passport; SIDM00191 ChEMBL-Cells; CHEMBL3308283 ChEMBL-Targets; CHEMBL2366247 Cosmic; 753533 Cosmic-CLP; 753533 DepMap; ACH-002090 GDSC; 753533 GEO; GSM1669609 IARC_TP53; 21188 IARC_TP53; 26919 LINCS_LDP; LCL-1763 PharmacoDB; BB65RCC_76_2019 Wikidata; Q54795073 DT Created: 04-04-12; Last updated: 06-09-19; Version: 23

Hierarchy

DT Created: 04-04-12; Last updated: 06-09-19; Version: 23

Originate from Same Individual

DT Created: 04-04-12; Last updated: 06-09-19; Version: 23

Publications that use this research resource

Loss of functional BAP1 augments sensitivity to TRAIL in cancer cells.

  • Kolluri KK
  • Elife
  • 2018 Jan 18

Literature context:


Abstract:

Malignant mesothelioma (MM) is poorly responsive to systemic cytotoxic chemotherapy and invariably fatal. Here we describe a screen of 94 drugs in 15 exome-sequenced MM lines and the discovery of a subset defined by loss of function of the nuclear deubiquitinase BRCA associated protein-1 (BAP1) that demonstrate heightened sensitivity to TRAIL (tumour necrosis factor-related apoptosis-inducing ligand). This association is observed across human early passage MM cultures, mouse xenografts and human tumour explants. We demonstrate that BAP1 deubiquitinase activity and its association with ASXL1 to form the Polycomb repressive deubiquitinase complex (PR-DUB) impacts TRAIL sensitivity implicating transcriptional modulation as an underlying mechanism. Death receptor agonists are well-tolerated anti-cancer agents demonstrating limited therapeutic benefit in trials without a targeting biomarker. We identify BAP1 loss-of-function mutations, which are frequent in MM, as a potential genomic stratification tool for TRAIL sensitivity with immediate and actionable therapeutic implications.

Funding information:
  • Cancer Research UK - A17341()
  • NINDS NIH HHS - R01NS043915(United States)
  • Wellcome - WT097452MA()
  • Wellcome Trust - 106555/Z/14/Z()
  • Wellcome Trust - WT107963AIA()