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Homo sapiens


Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: COSMIC cell lines project. Part of: MD Anderson Cell Lines Project. Microsatellite instability: Instable (MSI-low) (Sanger). Sequence variation: Homozygous for BAP1 p.Arg146Alafs*48 (c.438-24_438-2del23) (PubMed=21642991; PubMed=26011428). Omics: Array-based CGH. Omics: Deep exome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: SNP array analysis. Omics: Transcriptome analysis. Genome ancestry: African=65.11%; Native American=0.21%; East Asian, North=3.2%; East Asian, South=0%; South Asian=0%; European, North=16.44%; European, South=15.05% (PubMed=30894373). Discontinued: KCLB; 90028. Derived from sampling site: Pleural effusion. DT Created: 04-04-12; Last updated: 05-07-19; Version: 25

Proper Citation

KCLB Cat# 90028, RRID:CVCL_1555


Cancer cell line DT Created: 04-04-12; Last updated: 05-07-19; Version: 25


DT Created: 04-04-12; Last updated: 05-07-19; Version: 25


H28, H-28, NCIH28, HUT-28, HUT 28, HuT 28, HUT28, Hut28, HuT28 DT Created: 04-04-12, Last updated: 05-07-19, Version: 25



Cat Num


Cross References

CLO; CLO_0008079 EFO; EFO_0006686 ArrayExpress; E-MTAB-2706 ArrayExpress; E-MTAB-2770 ArrayExpress; E-MTAB-3610 ATCC; CRL-5820 BioSample; SAMN03471010 BioSamples; SAMEA100874 BioSample; SAMN10987612 CCLE; NCIH28_PLEURA Cell_Model_Passport; SIDM00720 ChEMBL-Cells; CHEMBL3308775 ChEMBL-Targets; CHEMBL1075541 Cosmic; 688059 Cosmic; 733814 Cosmic; 877108 Cosmic; 877350 Cosmic; 886387 Cosmic; 908470 Cosmic; 980995 Cosmic; 1032386 Cosmic; 1146909 Cosmic; 1152495 Cosmic; 1481543 Cosmic; 1522766 Cosmic; 1541208 Cosmic; 1749556 Cosmic; 1963325 Cosmic; 1995572 Cosmic; 2474149 Cosmic-CLP; 908470 DepMap; ACH-000648 GDSC; 908470 GEO; GSM434272 GEO; GSM726267 GEO; GSM794268 GEO; GSM850284 GEO; GSM887425 GEO; GSM888504 GEO; GSM1670236 IGRhCellID; H28GEO KCLB; 90028 LiGeA; CCLE_571 Wikidata; Q54908002 DT Created: 04-04-12; Last updated: 05-07-19; Version: 25


DT Created: 04-04-12; Last updated: 05-07-19; Version: 25

Originate from Same Individual

DT Created: 04-04-12; Last updated: 05-07-19; Version: 25

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:


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()