Cancer articles within Nature Medicine

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  • News & Views |

    Mammalian genomes harbor regulatory elements from ancient retroviral infections. These retroviral remnants are normally silenced by DNA methylation—but this can change. Reactivation of one such element triggers the expression of a nearby oncogene during the development of Hodgkin's lymphoma (571–579).

    • Michael E Engel
    •  & Scott W Hiebert

  • News & Views |

    T lymphocytes engineered to produce T cell receptors specific for tumor antigens lead to an antitumor immune response. New findings draw attention to a potentially deadly problem with this strategy. The transgenic T cell receptors can shuffle components with native receptors to produce hybrid molecules with specificity against self antigens (pages 565–570).

    • Malcolm Brenner

  • Letter |

    Chromosomal translocations involving the gene encoding MOZ, a transcriptional regulator, can result in the production of fusion proteins that promote acute myeloid leukemia. In a mouse model of acute myeloid leukemia induced by a MOZ-containing fusion protein, Yukiko Aikawa et al. now identify a potential new therapeutic target, the cytokine receptor CSF1R, which is present on leukemia stem cells and is needed for leukemia induction and progression.

    • Yukiko Aikawa
    • , Takuo Katsumoto
    •  & Issay Kitabayashi

  • Technical Report |

    McMillin et al. describe a drug screening platform that takes into account the tumor microenvironment, in particular tumor-stromal interactions, enabling the screening of the antitumor activity of candidate anticancer agents in the context of such interactions. The in vitro tumor cell–specific bioluminescence imaging assay is both high throughput and scalable.

    • Douglas W McMillin
    • , Jake Delmore
    •  & Constantine S Mitsiades

  • Article |

    Metastasis is a fatal complication of prostate cancer, but its mechanisms remain largely unknown. In this report, the authors identify a signaling pathway commonly deregulated in human prostate cancer and describe how it can foster both primary growth and metastatic tumor progression. Epigenetic silencing of the RasGAP DAB2IP by EZH2 overexpression results in aberrant activation of Ras signaling, but also of NF-κB. These two events are mediated by different DAB2IP domains and have distinct roles in localized growth and distant dissemination.

    • Junxia Min
    • , Alexander Zaslavsky
    •  & Karen Cichowski

  • News & Views |

    Inflammatory cells can promote tumor cell proliferation, but the range of mechanisms has not been fully explored. A proteinase produced by neutrophils is now shown to enter tumor cells and promote their proliferation (pages 219–223).

    • Barbara Fingleton

  • Between Bedside and Bench |

    Muscle diseases can take many forms, from the progressive muscle degeneration of dystrophies to the childhood cancer rhabdomyosarcoma. In 'Bench to Bedside', Joel R. Chamberlain and Jeffrey S. Chamberlain discuss studies using antisense oligonucleotides to treat Duchenne muscular dystrophy and myotonic dystrophy. In 'Bedside to Bench', Simone Hettmer and Amy J. Wagers examine the implications of clinical studies describing a type of rhabdomyosarcoma that resembles acute leukemia. The findings dovetail with other studies suggesting that some of these cancers might originate outside of muscle tissue and highlight the need for a better understanding of the cells that give rise to this condition.

    • Joel R Chamberlain
    •  & Jeffrey S Chamberlain

  • Article |

    The protein kinase mTOR is known to contribute to cancer development. However, existing drugs targeting mTOR, such as rapamycin, have not been very effective at inhibiting cancer cell survival and also have the unwanted side effect of immunosuppression. Studying preclinical models of leukemia driven by the BCR-ABL oncogene, Matthew Janes et al. now show that a new mTOR inhibitor—which unlike previous ones is an ATP competitive inhibitor that targets the active site of the enzyme—can overcome these drawbacks.

    • Matthew R Janes
    • , Jose J Limon
    •  & David A Fruman

  • News & Views |

    Tumors use many strategies to evade the immune system. A new study adds a new trick to the list—inhibiting the migration of dendritic cells from tumors toward lymph nodes (pages 98–105).

    • Cornelis Melief

  • News |

    The epigenome consists of a system of chemical tags that attach to our DNA and its associated molecules, switching genes on and off. But the system is not without glitches—and scientists think that the misplacement of these tags can cause disease. This idea has led to new drugs that aim to correct gene activity (and obliterate disease) by altering the proteins around which DNA winds. Cassandra Willyard examines whether this approach will unlock the long-awaited promise of epigenetic therapy.

    • Cassandra Willyard

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