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Homo sapiens


Part of: Cancer Cell Line Encyclopedia (CCLE) project. Part of: EGFR genetic alteration cell panel (ATCC TCP-1027). Sequence variation: EGFR p.Leu747_Glu749del. Omics: Deep exome analysis. Omics: Deep proteome analysis. Omics: Deep RNAseq analysis. Omics: Protein expression by reverse-phase protein arrays. Omics: SNP array analysis. Omics: Transcriptome analysis. Derived from metastatic site: Pleural effusion.

Proper Citation

ATCC Cat# CRL-2871, RRID:CVCL_1269


Cancer cell line







Cat Num


Cross References

BTO; BTO:0004081 CLO; CLO_0003657 EFO; EFO_0003132 AddexBio; C0016012/4917 ArrayExpress; E-MTAB-2706 ATCC; CRL-2871 BioSample; SAMN03471807 BioSample; SAMN03473288 CCLE; HCC4006_LUNG Cosmic; 903602 Cosmic; 1028938 Cosmic; 1128250 Cosmic; 1146936 Cosmic; 1802302 Cosmic; 2015233 GEO; GSM63351 GEO; GSM253408 GEO; GSM434286 GEO; GSM794399 GEO; GSM844552 GEO; GSM887055 GEO; GSM888125 IGRhCellID; HCC4006GEO PRIDE; PXD002556

Publications that use this research resource

TGF-β reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24- cancer cells.

  • Pal D
  • Elife
  • 2017 Jan 16

Literature context: HCC4006 (RRID:CVCL_1269), H23 (RRI


Many lines of evidence have indicated that both genetic and non-genetic determinants can contribute to intra-tumor heterogeneity and influence cancer outcomes. Among the best described sub-population of cancer cells generated by non-genetic mechanisms are cells characterized by a CD44+/CD24- cell surface marker profile. Here, we report that human CD44+/CD24- cancer cells are genetically highly unstable because of intrinsic defects in their DNA-repair capabilities. In fact, in CD44+/CD24- cells, constitutive activation of the TGF-beta axis was both necessary and sufficient to reduce the expression of genes that are crucial in coordinating DNA damage repair mechanisms. Consequently, we observed that cancer cells that reside in a CD44+/CD24- state are characterized by increased accumulation of DNA copy number alterations, greater genetic diversity and improved adaptability to drug treatment. Together, these data suggest that the transition into a CD44+/CD24- cell state can promote intra-tumor genetic heterogeneity, spur tumor evolution and increase tumor fitness.

Funding information:
  • NCI NIH HHS - P01 CA129243()
  • NCI NIH HHS - P30 CA045508()