Cancer articles within Nature

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  • News & Views |

    Cellular senescence is a physiological mechanism for thwarting the proliferation of tumour cells. Encouraging cancer-prone cells to senesce might therefore be a way to nip this disease in the bud.

    • Manuel Serrano

  • News & Views |

    Inhibitors of RAF enzymes can suppress or activate the same signalling pathway. The details of how this happens provide a cautionary note for those targeting the pathway for anticancer drug discovery.

    • Karen Cichowski
    •  & Pasi A. Jänne

  • Letter |

    In a mouse model of prostate cancer it is shown that infiltrating B cells promote tumorigenesis by secreting lymphotoxin. Lymphotoxin accelerates the emergence of castration-resistant prostate tumours in this model. Interfering with this pathway may offer therapeutic strategies for androgen-independent prostate cancer.

    • Massimo Ammirante
    • , Jun-Li Luo
    •  & Michael Karin

  • News |

    Immune cells seem to spark recurrent prostate cancer in mice.

    • Brian Vastag

  • 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 |

    Each human cell contains hundreds of copies of mitochondrial DNA (mtDNA), making it difficult to characterize mtDNA completely. Here, massively parallel sequencing-by-synthesis of mtDNA reveals widespread heterogeneity (heteroplasmy) in the mtDNA of normal human cells, and homoplasmic and heteroplasmic mutations in cancer cells. The findings provide new insight into the nature and variability of mtDNA sequences, with implications for forensic analysis and the development of biomarkers for cancer.

    • Yiping He
    • , Jian Wu
    •  & Nickolas Papadopoulos

  • Letter |

    The RAS–RAF signalling pathway is an attractive target for drug development in oncology, and several RAF inhibitors are being tested in clinical trials. Here and in an accompanying paper, RAF inhibitors are shown to have opposing roles, functioning as either inhibitors or activators of RAF depending on the cellular context and mutational status of RAF. The mechanistic basis for these opposing roles is dissected. The results have implications for the clinical use of these inhibitors and for the design of kinase inhibitors.

    • Poulikos I. Poulikakos
    • , Chao Zhang
    •  & Neal Rosen

  • Letter |

    Genomic instability has been implicated in tumour development. Here, a new mouse model of Kras-driven lung tumours has been developed, in which genomic instability is caused by overexpression of the mitotic checkpoint protein Mad2. In this model, inhibiting Kras leads to tumour regression, as shown previously. But tumours recur at a much higher rate.

    • Rocio Sotillo
    • , Juan-Manuel Schvartzman
    •  & Robert Benezra

  • Article |

    One way of discovering genes with key roles in cancer development is to identify genomic regions that are frequently altered in human cancers. Here, high-resolution analyses of somatic copy-number alterations (SCNAs) in numerous cancer specimens provide an overview of regions of focal SCNA that are altered at significant frequency across several cancer types. An oncogenic function is also found for the anti-apoptosis genes MCL1 and BCL2L1, which reside in amplified genome regions in many cancers.

    • Rameen Beroukhim
    • , Craig H. Mermel
    •  & Matthew Meyerson

  • News |

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

    • Brendan Borrell

  • Letter |

    Chronic myeloid leukaemia is caused by a BCR-ABL fusion, a constitutively active tyrosine kinase that, it is believed, leads to suppression of the forkhead O transcription factors (FOXO). Although the use of the tyrosine kinase inhibitor imatinib is a breakthrough for CML therapy, imatinib does not deplete the leukaemia-initiating cells (LICs) that drive the recurrence of CML. Foxo3a is now shown to have an essential role in the maintenance of CML LICs in a mouse model.

    • Kazuhito Naka
    • , Takayuki Hoshii
    •  & Atsushi Hirao

  • Books & Arts |

    Steve Silberman enjoys a moving account that probes racial and ethical issues in medicine through the story of the young mother whose death from cancer led to the first immortal cell line.

    • Steve Silberman

  • News & Views |

    Embryonic stem cells can create copies of themselves, but can also mature into almost any type of cell in the body. Tiny gene regulators called microRNAs are now shown to have a role in directing these properties.

    • Frank J. Slack

  • Letter |

    The RAS–RAF signalling pathway is an attractive target for drug development in oncology, and several RAF inhibitors are being tested in clinical trials. Here and in an accompanying paper, RAF inhibitors are shown to have opposing roles, functioning as either inhibitors or activators of RAF depending on the cellular context and mutational status of RAF. The mechanistic basis for these opposing roles is dissected. The results have implications for the clinical use of these inhibitors and for the design of kinase inhibitors.

    • Georgia Hatzivassiliou
    • , Kyung Song
    •  & Shiva Malek

  • News Feature |

    Alan Ashworth took a cancer drug from Petri dish to patients in near record speed. Daniel Cressey meets a biologist who is evangelical about translational research.

    • Daniel Cressey

  • Letter |

    Heat shock protein 70 (Hsp70) is a molecular chaperone which, by inhibiting lysosomal membrane permeabilization, promotes the survival of stressed cells. Hsp70 is now shown to stabilize lysosomes by binding to an anionic phospholipid, BMP, resulting in stimulation of acid sphingomyelinase (ASM) activity. Notably, the decreased ASM activity and lysosomal stability seen in patients with Niemann–Pick disease can be corrected by treatment with recombinant Hsp70.

    • Thomas Kirkegaard
    • , Anke G. Roth
    •  & Marja Jäättelä

  • 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

  • Letter |

    The role of B-cell-receptor (BCR) signalling in human B cell lymphomas has been a long-standing question, with genetic and functional evidence for its oncogenic role in human lymphomas lacking. Here, a form of 'chronic active' BCR signalling that is required for cell survival in the activated B-cell-like subtype of diffuse large B-cell lymphoma is described and analysed, with potential implications for future therapeutic strategies.

    • R. Eric Davis
    • , Vu N. Ngo
    •  & Louis M. Staudt

  • Letter |

    Clear cell renal carcinoma, the most common form of adult kidney cancer, is often characterized by the presence of inactivating mutations in the VHL gene. A large survey for somatic mutations now identifies inactivating mutations in two genes encoding enzymes involved in histone modification, highlighting the role of mutations in components of the chromatin modification machinery in human cancer.

    • Gillian L. Dalgliesh
    • , Kyle Furge
    •  & P. Andrew Futreal

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