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NCI-H1650

RRID:CVCL_1483

Organism

Homo sapiens

Comments

Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: COSMIC cell lines project. Part of: MD Anderson Cell Lines Project. Doubling time: 42 hours (PubMed=25984343). Microsatellite instability: Stable (MSS) (Sanger). Sequence variation: EGFR p.Glu746_Ala750del (PubMed=17332333). Omics: Deep exome analysis. Omics: Deep RNAseq analysis. Omics: DNA methylation analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: shRNA library screening. Omics: SNP array analysis. Omics: Transcriptome analysis. Derived from metastatic site: Pleural effusion.

Proper Citation

ICLC Cat# HTL06002, RRID:CVCL_1483

Category

Cancer cell line

Sex

Male

Synonyms

H1650, H-1650, H1650_CO, NCIH1650

Vendor

ICLC

Cat Num

HTL06002

Cross References

BTO; BTO:0005243 CLO; CLO_0008007 EFO; EFO_0002260 CLDB; cl7182 AddexBio; C0016015/4961 ArrayExpress; E-MTAB-2706 ATCC; CRL-5883 BioSample; SAMN03472182 CCLE; NCIH1650_LUNG CCRID; 3111C0001CCC000251 CCRID; 3131C0001000700152 ChEMBL-Cells; CHEMBL3308800 ChEMBL-Targets; CHEMBL1075518 Cosmic; 687800 Cosmic; 877429 Cosmic; 903598 Cosmic; 1017829 Cosmic; 1028942 Cosmic; 1047096 Cosmic; 1128242 Cosmic; 1146883 Cosmic; 1212188 Cosmic; 1239904 Cosmic; 1571738 Cosmic; 1600606 Cosmic; 1741779 Cosmic; 1795296 Cosmic; 1802299 Cosmic; 1891894 Cosmic; 1995530 Cosmic; 2042866 Cosmic; 2125236 Cosmic-CLP; 687800 GDSC; 687800 GEO; GSM206474 GEO; GSM253384 GEO; GSM274795 GEO; GSM274828 GEO; GSM434313 GEO; GSM782115 GEO; GSM784207 GEO; GSM794324 GEO; GSM827475 GEO; GSM844623 GEO; GSM887373 GEO; GSM888451 GEO; GSM1374703 GEO; GSM1670181 ICLC; HTL06002 IGRhCellID; H1650_COGEO IGRhCellID; NCIH1650 KCLB; 91650 LINCS_LDP; LCL-1612

Publications that use this research resource

Epigenetic Therapy Ties MYC Depletion to Reversing Immune Evasion and Treating Lung Cancer.

  • Topper MJ
  • Cell
  • 2017 Nov 30

Literature context: NCI-H1650 ATCC RRID:CVCL_1483 NCI-H1975 ATCC RRID: CVCL_1511


Abstract:

Combining DNA-demethylating agents (DNA methyltransferase inhibitors [DNMTis]) with histone deacetylase inhibitors (HDACis) holds promise for enhancing cancer immune therapy. Herein, pharmacologic and isoform specificity of HDACis are investigated to guide their addition to a DNMTi, thus devising a new, low-dose, sequential regimen that imparts a robust anti-tumor effect for non-small-cell lung cancer (NSCLC). Using in-vitro-treated NSCLC cell lines, we elucidate an interferon α/β-based transcriptional program with accompanying upregulation of antigen presentation machinery, mediated in part through double-stranded RNA (dsRNA) induction. This is accompanied by suppression of MYC signaling and an increase in the T cell chemoattractant CCL5. Use of this combination treatment schema in mouse models of NSCLC reverses tumor immune evasion and modulates T cell exhaustion state towards memory and effector T cell phenotypes. Key correlative science metrics emerge for an upcoming clinical trial, testing enhancement of immune checkpoint therapy for NSCLC.

Funding information:
  • NCI NIH HHS - P30 CA006973()
  • NCI NIH HHS - R01 CA121113()
  • NCI NIH HHS - R01 CA166348()
  • NIDA NIH HHS - R01 DA007427(United States)