Literature DB >> 23856246

The exomes of the NCI-60 panel: a genomic resource for cancer biology and systems pharmacology.

Ogan D Abaan1, Eric C Polley, Sean R Davis, Yuelin J Zhu, Sven Bilke, Robert L Walker, Marbin Pineda, Yevgeniy Gindin, Yuan Jiang, William C Reinhold, Susan L Holbeck, Richard M Simon, James H Doroshow, Yves Pommier, Paul S Meltzer.   

Abstract

The NCI-60 cell lines are the most frequently studied human tumor cell lines in cancer research. This panel has generated the most extensive cancer pharmacology database worldwide. In addition, these cell lines have been intensely investigated, providing a unique platform for hypothesis-driven research focused on enhancing our understanding of tumor biology. Here, we report a comprehensive analysis of coding variants in the NCI-60 panel of cell lines identified by whole exome sequencing, providing a list of possible cancer specific variants for the community. Furthermore, we identify pharmacogenomic correlations between specific variants in genes such as TP53, BRAF, ERBBs, and ATAD5 and anticancer agents such as nutlin, vemurafenib, erlotinib, and bleomycin showing one of many ways the data could be used to validate and generate novel hypotheses for further investigation. As new cancer genes are identified through large-scale sequencing studies, the data presented here for the NCI-60 will be an invaluable resource for identifying cell lines with mutations in such genes for hypothesis-driven research. To enhance the utility of the data for the greater research community, the genomic variants are freely available in different formats and from multiple sources including the CellMiner and Ingenuity websites. ©2013 AACR.

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Year:  2013        PMID: 23856246      PMCID: PMC4893961          DOI: 10.1158/0008-5472.CAN-12-3342

Source DB:  PubMed          Journal:  Cancer Res        ISSN: 0008-5472            Impact factor:   12.701


  50 in total

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2.  CHEK2 genomic and proteomic analyses reveal genetic inactivation or endogenous activation across the 60 cell lines of the US National Cancer Institute.

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10.  Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants.

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  131 in total

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3.  rcellminer: exploring molecular profiles and drug response of the NCI-60 cell lines in R.

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4.  Phosphorylated fraction of H2AX as a measurement for DNA damage in cancer cells and potential applications of a novel assay.

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5.  Overcoming Resistance to DNA-Targeted Agents by Epigenetic Activation of Schlafen 11 (SLFN11) Expression with Class I Histone Deacetylase Inhibitors.

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6.  A common cancer-associated DNA polymerase ε mutation causes an exceptionally strong mutator phenotype, indicating fidelity defects distinct from loss of proofreading.

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7.  Cancer immunology. Mutational landscape determines sensitivity to PD-1 blockade in non-small cell lung cancer.

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8.  Ovarian cancer-associated mutations disable catalytic activity of CDK12, a kinase that promotes homologous recombination repair and resistance to cisplatin and poly(ADP-ribose) polymerase inhibitors.

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Review 10.  Bioinformatic approaches to augment study of epithelial-to-mesenchymal transition in lung cancer.

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