Gastrointestinal cancer articles within Nature

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  • News & Views |

    New clinical trials report the efficacy of two mechanism-based therapies for treating human pancreatic neuroendocrine tumours. Studies in mouse models have contributed to these success stories, and continue to do so.

    • David Tuveson
    •  & Douglas Hanahan

  • Letter |

    This study shows, via a mouse model of intestinal cancer, that in the absence of CKIα, the loss of p53 dramatically enhances tumour progression and metastasis. p53 is shown to normally limit cancer cell invasion via the regulation of p21 and a set of invasion genes that include Prox1. This study adds important insights to the emerging picture that during tumour development the p53 tumour suppressor gene not only controls cell death and proliferation but also metastasis.

    • Ela Elyada
    • , Ariel Pribluda
    •  & Yinon Ben-Neriah

  • 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 |

    Here, whole-genome sequencing has been used to analyse primary pancreatic tumours and one or more metastases from the same patients. The findings show that tumours are composed of several geographically distinct subclones, and allow maps to be produced showing how metastatic cancer clones evolve within the primary tumour. Moreover, a quantitative analysis of the timing of the genetic evolution of pancreatic cancer has been performed.

    • Shinichi Yachida
    • , Siân Jones
    •  & Christine A. Iacobuzio-Donahue

  • News & Views |

    In certain types of gastrointestinal cell, mutations in the protein KIT give rise to gastrointestinal stromal tumours. Why are other cell types that express KIT not affected? The answer lies with a second protein. See Letter p.849

    • Michael C. Heinrich
    •  & Christopher L . Corless

  • 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 |

    Cancer 'chemoprevention' uses substances to reverse, suppress or prevent the initial phase of carcinogenesis or the progression of neoplastic cells to cancer cells. Here it is shown that treatment with TRAIL proteins and all-trans-retinyl acetate can cause the death, in vitro and in vivo, of premalignant cells deficient in the adenomatous polyposis coli gene. Normal cells are unaffected. Selectively eliminating premalignant tumour cells in this way is thus an effective method for chemoprevention.

    • Ling Zhang
    • , Xiaoyang Ren
    •  & Xiangwei Wu

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