Cancer genomics articles within Nature

Featured

  • Letter |

    An in vivo transposon screen in a pancreatic cancer model identifies frequent inactivation of Usp9x; deletion of Usp9x cooperates with KrasG12D to accelerate rapidly pancreatic tumorigenesis in mice, validating their genetic interaction.

    • Pedro A. Pérez-Mancera
    • , Alistair G. Rust
    •  & David A. Tuveson

  • Letter |

    The Cancer Cell Line Encyclopedia presents the first results from a large-scale screen of some 947 cancer cell lines with 24 anticancer drugs, with the aim of identifying specific genomic alterations and gene expression profiles associated with selective sensitivity or resistance to potential therapeutic agents.

    • Jordi Barretina
    • , Giordano Caponigro
    •  & Levi A. Garraway

  • News & Views |

    Debates over the role of sirtuin proteins in ageing are maturing into functional assessments of the individual proteins. It seems that overexpression of a specific sirtuin can extend lifespan in male mice. See Letter p.218

    • David B. Lombard
    •  & Richard A. Miller

  • News & Views |

    A genetic study of brain cancers in mice and humans reveals distinct mutations in primary tumours and their metastases, suggesting that the two disease 'compartments' may require different treatments.

    • Steven C. Clifford

  • News & Views |

    Prognosis for patients with pancreatic cancer is bleak, often owing to late diagnosis. The estimate that at least 15 years pass from tumour initiation to malignancy offers hope for early detection and prevention. See Letters p.1109 & p.1114

    • E. Georg Luebeck

  • Letter |

    Pancreatic cancer is highly aggressive, usually because of widespread metastasis. Here, next-generation DNA sequencing has been used to detect genomic rearrangements in 13 patients with pancreatic cancer and to explore clonal relationships among metastases. The results reveal not only considerable inter-patient heterogeneity, but also ongoing genomic instability and evolution during the development of metastases.

    • Peter J. Campbell
    • , Shinichi Yachida
    •  & P. Andrew Futreal

  • Letter |

    Gastrointestinal stromal tumours (GIST) are believed to arise in interstitial cells of Cajal (ICC). These authors show that the transcription factor ETV1 is required for ICC development and promotes the development of GIST. KIT, which is often activated by mutations in GIST, cooperates with ETV1 in the transformation of ICCs, in part by promoting ETV1 stabilization. Thus, a normal developmental lineage factor is switched into a tumour-promoting factor by a cooperating oncogene.

    • Ping Chi
    • , Yu Chen
    •  & Charles L. Sawyers

  • Letter |

    Complete genome sequencing has already provided insights into the mutation spectra of several cancer types. Here, the first complete sequences are provided of a primary lung tumour and adjacent normal tissue. Comparison of the two reveals a variety of somatic mutations in the cancer genome, including changes in the KRAS proto-oncogene. The results reveal a distinct pattern of selection against mutations within expressed genes compared to non-expressed genes, and selection against mutations in promoter regions.

    • William Lee
    • , Zhaoshi Jiang
    •  & Zemin Zhang

  • Article |

    Massively parallel DNA sequencing allows entire genomes to be screened for genetic changes associated with tumour progression. Here, the genomes of four DNA samples from a 44-year-old African-American patient with basal-like breast cancer were analysed. The samples came from peripheral blood, the primary tumour, a brain metastasis and a xenograft derived from the primary tumour. The findings indicate that cells with a distinct subset of the primary tumour mutation might be selected during metastasis and xenografting.

    • Li Ding
    • , Matthew J. Ellis
    •  & Elaine R. Mardis

  • News & Views |

    Cancer cells that invade other parts of the body do so by accumulating genomic aberrations. Analysis of the genomic differences between primary and metastatic tumours should aid the understanding of this process.

    • Joe Gray

  • News Feature |

    Databases could soon be flooded with genome sequences from 25,000 tumours. Heidi Ledford looks at the obstacles researchers face as they search for meaning in the data.

    • Heidi Ledford

  • Article
    | Open Access

    Homozygous gene deletions in cancer cells occur over recessive cancer genes (where they can confer selective growth advantage) or over genes at fragile sites of the genome (where they are thought to reflect increased DNA breakage). Here, a large number of homozygous deletions in a collection of cancer cell lines are identified and analysed to derive structural signatures for the two different types of deletion. More deletions are found in inherently fragile regions, and fewer overlying recessive genes.

    • Graham R. Bignell
    • , Chris D. Greenman
    •  & Michael R. Stratton

  • News |

    Some argue that tumour cells obtained directly from patients are the best way to study cancer genomics.

    • Brendan Borrell

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