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Homo sapiens


AG 51Y

Proper Citation

KCLB Cat# 90023, RRID:CVCL_1547


AG 51Y Cancer cell line


Male AG 51Y



Cat Num


Cross References

BTO; BTO:0003238 CLO; CLO_0008071 EFO; EFO_0002286 AddexBio; C0016005/4861 ATCC; CRL-5800 BioSample; SAMN03471316 BioSample; SAMN03471735 CCLE; NCIH23_LUNG CCRID; 3111C0001CCC000255 ChEMBL-Cells; CHEMBL3307750 ChEMBL-Targets; CHEMBL614997 Cosmic; 687818 Cosmic; 722038 Cosmic; 801587 Cosmic; 844829 Cosmic; 852004 Cosmic; 875849 Cosmic; 876142 Cosmic; 877237 Cosmic; 905942 Cosmic; 910561 Cosmic; 914948 Cosmic; 917993 Cosmic; 953983 Cosmic; 961834 Cosmic; 974292 Cosmic; 1004697 Cosmic; 1089217 Cosmic; 1092619 Cosmic; 1146906 Cosmic; 1154591 Cosmic; 1175864 Cosmic; 1188590 Cosmic; 1219060 Cosmic; 1239881 Cosmic; 1305347 Cosmic; 1312332 Cosmic; 1436010 Cosmic; 1802313 Cosmic; 1870271 Cosmic; 1995567 Cosmic; 1998461 Cosmic; 2125183 Cosmic; 2433751 Cosmic; 2630416 Cosmic-CLP; 905942 GDSC; 905942 GEO; GSM2106 GEO; GSM50214 GEO; GSM50277 GEO; GSM206487 GEO; GSM253310 GEO; GSM274790 GEO; GSM274820 GEO; GSM353232 GEO; GSM385519 GEO; GSM385530 GEO; GSM434335 GEO; GSM482108 GEO; GSM513961 GEO; GSM514346 GEO; GSM750803 GEO; GSM794267 GEO; GSM799341 GEO; GSM799404 GEO; GSM827478 GEO; GSM847075 GEO; GSM844643 GEO; GSM887421 GEO; GSM888500 GEO; GSM1153412 GEO; GSM1181268 GEO; GSM1181312 GEO; GSM1374733 GEO; GSM1374734 GEO; GSM1374735 GEO; GSM1670229 GEO; GSM2124674 IGRhCellID; NCIH23 KCLB; 90023 LINCS_LDP; LCL-1619 NCI-DTP; NCI-H23 PRIDE; PXD005942 SKY/M-FISH/CGH; 2796 AG 51Y


AG 51Y

Originate from Same Individual

AG 51Y

Publications that use this research resource

O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate.

  • Schoenfeld JD
  • Cancer Cell
  • 2017 Apr 10

Literature context: ollection RRID:CVCL_1547 H292 Ameri


Pharmacological ascorbate has been proposed as a potential anti-cancer agent when combined with radiation and chemotherapy. The anti-cancer effects of ascorbate are hypothesized to involve the autoxidation of ascorbate leading to increased steady-state levels of H2O2; however, the mechanism(s) for cancer cell-selective toxicity remain unknown. The current study shows that alterations in cancer cell mitochondrial oxidative metabolism resulting in increased levels of O2⋅- and H2O2 are capable of disrupting intracellular iron metabolism, thereby selectively sensitizing non-small-cell lung cancer (NSCLC) and glioblastoma (GBM) cells to ascorbate through pro-oxidant chemistry involving redox-active labile iron and H2O2. In addition, preclinical studies and clinical trials demonstrate the feasibility, selective toxicity, tolerability, and potential efficacy of pharmacological ascorbate in GBM and NSCLC therapy.

Funding information:
  • NCI NIH HHS - P30 CA086862()
  • NCI NIH HHS - R01 CA169046()
  • NCI NIH HHS - R01 CA182804()
  • NCI NIH HHS - R01 CA184051()
  • NCI NIH HHS - T32 CA078586()
  • NCI NIH HHS - U01 CA140206()
  • NCI NIH HHS - U01 CA166800()
  • NIGMS NIH HHS - T32 GM007337()

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: 23 (RRID:CVCL_1547) were obta


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()