Oncogenesis articles within Nature

Featured

  • Letter |

    DNA damage induces translocation of cyclic GMP–AMP synthase to the nucleus, where it suppresses homologous recombination by interfering with the formation of the PARP1–Timeless complex.

    • Haipeng Liu
    • , Haiping Zhang
    •  & Baoxue Ge

  • Article |

    Comparison of multiple lesions from individual pancreases sheds light on how ancestral clones can spread through the ductal system and give rise to precursor lesions, with acquisition of further mutations leading to pancreatic cancer.

    • Alvin P. Makohon-Moore
    • , Karen Matsukuma
    •  & Christine A. Iacobuzio-Donahue

  • Article
    | Open Access

    Analyses of genomes from 914 children, adolescents, and young adults provide a comprehensive resource of genomic alterations across a spectrum of common childhood cancers.

    • Susanne N. Gröbner
    • , Barbara C. Worst
    •  & Stefan M. Pfister

  • Article |

    A high-fat diet increases the number of intestinal stem cells in mammals, both in vivo and in intestinal organoids; a pathway that involves PPAR-δ confers organoid-initiating capacity to non-stem cells and induces them to form in vivo tumours after loss of the Apc tumour suppressor.

    • Semir Beyaz
    • , Miyeko D. Mana
    •  & Ömer H. Yilmaz

  • Letter |

    A cell-autonomous role for the COUP-TFII transcription factor in prostate cancer cells is identified, in which COUP-TFII inhibits TGF-β signalling by binding to SMAD4; COUP-TFII promotes prostate tumorigenesis and metastasis in a mouse model, and is associated with more aggressive disease in human prostate cancers.

    • Jun Qin
    • , San-Pin Wu
    •  & Sophia Y. Tsai

  • Letter |

    Individuals with the red hair/fair skin phenotype usually carry a polymorphism in the gene encoding the melanocortin 1 receptor (Mc1r) that results in the production of pigment containing a high pheomelanin-to-eumelanin ratio; here it is shown in a mouse model that inactivation of Mc1r promotes melanoma formation in the presence of the Braf oncogene, thus suggesting that pheomelanin synthesis is carcinogenic by an ultraviolet-radiation-independent mechanism.

    • Devarati Mitra
    • , Xi Luo
    •  & David E. Fisher

  • News & Views |

    The identification of a signalling protein that regulates the accumulation of fat and connective tissue in breasts may help to explain why high mammographic density is linked to breast-cancer risk. It may also provide a marker for predicting this risk.

    • Victoria L. Seewaldt

  • Letter |

    IL-22 is one of the factors that, although important for wound healing, also promote tumorigenesis; the regulation of IL-22BP, the IL-22 binding protein, via the NLRP3 and NLRP6 inflammasomes provides an unanticipated mechanism, controlling IL-22 and thereby the development of colon cancer.

    • Samuel Huber
    • , Nicola Gagliani
    •  & Richard A. Flavell

  • News & Views |

    A tightly regulated enzyme balances energy production and the synthesis of macromolecules from glucose in cancer cells. Upsetting this balance by stimulating the enzyme's activity can suppress tumour growth in mice.

    • Lei Jiang
    •  & Ralph J. DeBerardinis

  • Letter |

    A mouse model is developed in which the pro-apoptotic activity of DCC is silenced and the mice are more prone to intestinal tumour progression, giving insight into the role of DCC in human colorectal cancer.

    • Marie Castets
    • , Laura Broutier
    •  & Patrick Mehlen

  • News & Views |

    In 2–3% of cancers, a single genetic event may have led to hundreds of genomic rearrangements confined to just one or a few chromosomes. This finding challenges the conventional view of how mutations accumulate in oncogenesis.

    • Jose M. C. Tubio
    •  & Xavier Estivill

  • Letter |

    This study finds frequent mutations in MYD88 in the activated B-cell-like subtype of diffuse large B-cell lymphoma and, with lower frequency, in mucosa-associated lymphoid tissue lymphomas. MYD88 mediates signalling by Toll-like receptors, and the mutations, most of which affect the same amino acid, are shown to activate the pathway and promote cancer cell survival.

    • Vu N. Ngo
    • , Ryan M. Young
    •  & Louis M. Staudt

  • Letter |

    Progestins, used in hormone replacement therapy and contraceptives, have been suggested to promote the development of breast cancer. These authors show that the ability of progestins to induce mammary tumours in mouse models is mediated by RANKL (receptor activator of NF-KB ligand). Inhibition of RANKL could reduce tumorigenesis in hormone-induced and other mouse mammary gland tumour models, suggesting a new therapeutic approach.

    • Eva Gonzalez-Suarez
    • , Allison P. Jacob
    •  & William C. Dougall

  • Article |

    Cellular senescence — an irreversible cell-cycle arrest — has been implicated in suppressing tumour formation or growth. A new cellular signalling pathway that drives senescence has now been identified. This pathway does not involve most known mediators of senescence, and instead signals via the proteins Atf4, p27 and p21. Inactivating the proto-oncogene Skp2 in the context of oncogenic signalling can induce senescence through this new pathway, indicating that drugs that target Skp2 might be useful in cancer treatment.

    • Hui-Kuan Lin
    • , Zhenbang Chen
    •  & Pier Paolo Pandolfi

  • Letter |

    In response to oncogenic stress, the tumour suppressor ARF activates the p53 protein. ARF protein is highly stable in most human cell lines, so it has been thought that ARF activation occurs mainly at the level of transcription. Here, however, ARF is shown to be unstable in normal human cells but stable in cancer cells, through a transcription-independent mechanism. A ubiquitin ligase for ARF is identified and shown to promote ARF degradation in normal cells. This activity is prevented in cancer cells, stabilizing ARF.

    • Delin Chen
    • , Jing Shan
    •  & Wei Gu

  • Letter |

    In human tumours, complex cell interactions in the tumour and its microenvironment are thought to have an important role in tumorigenesis and cancer progression. In a genetically well-defined model system in Drosophila, clones of cells bearing different mutations are now shown to cooperate to promote tumour growth and invasion. This interaction involves JNK signalling propagation and JNK-induced upregulation of JAK/STAT-activating cytokines.

    • Ming Wu
    • , José Carlos Pastor-Pareja
    •  & Tian Xu

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