Oncogenes articles within Nature

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  • Article |

    A mouse model of invasive breast cancer in which Pten and Trp53 are simultaneously inactivated links PTEN loss with STAT3 activation and indicates that immune escape in PTEN-null tumours is mediated by PI3Kβ.

    • Johann S. Bergholz
    • , Qiwei Wang
    •  & Jean J. Zhao

  • Article
    | Open Access

    An analysis of whole-genome sequencing data from patients with Barrett’s oesophagus or oesophageal ademocarcinoma shows that extrachromosomal DNA (ecDNA) is strongly associated with cancer progression, and that a wide range of oncogenes are amplified on ecDNAs.

    • Jens Luebeck
    • , Alvin Wei Tian Ng
    •  & Paul S. Mischel

  • Article |

    MYC dissociation from active promoters alters its interactions with proteins involved in transcription termination and RNA processing, influencing DNA repair and thus, potentially, tumour cell growth.

    • Daniel Solvie
    • , Apoorva Baluapuri
    •  & Martin Eilers

  • Article |

    Cryogenic electron microscopy analyses reveal a new, compact structure of telomeric chromatin, providing mechanistic insight into telomere maintenance and function.

    • Aghil Soman
    • , Sook Yi Wong
    •  & Lars Nordenskiöld

  • Article |

    Extrachromosomal DNA (ecDNA) congregates in clusters called ecDNA hubs that promote intermolecular interactions between gene-regulatory regions and thereby amplify the expression of oncogenes such as MYC in cancer cell lines.

    • King L. Hung
    • , Kathryn E. Yost
    •  & Howard Y. Chang

  • Article |

    In mouse models of pancreatic cancer, a cooperative interaction between tissue damage and Kras gene mutation rapidly induces cancer-associated chromatin states in pre-malignant tissue, leading to gene dysregulation and neoplastic transformation.

    • Direna Alonso-Curbelo
    • , Yu-Jui Ho
    •  & Scott W. Lowe

  • Letter |

    Oncogenic FGFR3–TACC3 gene fusions signal through phosphorylated PIN4 to trigger biogenesis of peroxisomes and synthesis of new proteins, enabling mitochondrial respiration and tumour growth.

    • Véronique Frattini
    • , Stefano M. Pagnotta
    •  & Antonio Iavarone

  • Article |

    The cryo-electron microscopy and crystal structures of several mTORC1 complexes, and accompanying biochemical analyses, shed light on how mTORC1 is regulated and how cancer mutations lead to its hyperactivation.

    • Haijuan Yang
    • , Xiaolu Jiang
    •  & Nikola P. Pavletich

  • Letter |

    Structural variations disrupting the 3′ region of PD-L1 are shown to aid immune evasion in a number of human cancers, including adult T-cell leukaemia/lymphoma, and in a mouse tumour model, CRISPR/Cas9-mediated deletion of the 3'-UTR of Pd-l1 is also shown to result in immune escape, suggesting that PD-L1 3′-UTR disruption could provide a diagnostic marker to identify patients who will benefit from anti-PD-1/PD-L1 therapy.

    • Keisuke Kataoka
    • , Yuichi Shiraishi
    •  & Seishi Ogawa

  • Letter |

    A novel ALK transcript expressed in a subset of human cancers, arising from a de novo alternative transcription initiation site within the ALK gene, is described; the ALK transcript encodes three protein isoforms that stimulate tumorigenesis in vivo in mouse models; resultant tumours are sensitive to treatments with ALK inhibitors, indicating a possible therapeutic avenue for patients expressing these isoforms.

    • Thomas Wiesner
    • , William Lee
    •  & Ping Chi

  • Letter |

    Splicing factors such as BUD31 are identified in a synthetic-lethal screen with cells overexpressing the transcription factor MYC; oncogenic MYC leads to an increase in pre-mRNA synthesis, and spliceosome inhibition impairs the growth and tumorigenicity of MYC-dependent breast cancers, suggesting that spliceosome components may be potential therapeutic targets for MYC-driven cancers.

    • Tiffany Y.-T. Hsu
    • , Lukas M. Simon
    •  & Thomas F. Westbrook

  • Letter |

    PIK3CA mutations are associated with distinct types of human breast cancers but the cellular origin and mechanisms responsible for this heterogeneity were unclear; here, using a genetic approach in mice, PIK3CA mutations are shown to activate a genetic program directing multiple cell fates in normally lineage-restricted cell types.

    • Alexandra Van Keymeulen
    • , May Yin Lee
    •  & Cédric Blanpain

  • Letter |

    A novel anti-microRNA delivery platform that targets the acidic tumour microenvironment, in which a chosen anti-miRNA is coupled to a peptide that can transport the anti-miRNA across cell membranes specifically in an acidic environment.

    • Christopher J. Cheng
    • , Raman Bahal
    •  & Frank J. Slack

  • Letter |

    The nature of the retinal cell-type-specific circuitry that predisposes to retinoblastoma is demonstrated, in which a program that is unique to post-mitotic human cone precursors sensitizes to the oncogenic effects of retinoblastoma (Rb) protein depletion; hence, the loss of Rb collaborates with the molecular framework of cone precursors to initiate tumorigenesis.

    • Xiaoliang L. Xu
    • , Hardeep P. Singh
    •  & David Cobrinik

  • Letter |

    Using a structure-based approach, small molecule inhibitors that selectively target the GTPase Ral are identified and characterized; these first-generation inhibitors will be valuable tools for elucidating the Ral signalling pathway and constitute a step towards developing Ral-specific agents for cancer therapy.

    • Chao Yan
    • , Degang Liu
    •  & Dan Theodorescu

  • Outlook |

    Even as cancer therapies improve, basic questions about drug resistance, tumour spread and the role of normal tissue remain unanswered.

    • Katherine Bourzac

  • Letter |

    SMYD3 is a methyltransferase overexpressed in several human tumours; here methylation of the MAP3K2 kinase by SMYD3 is shown to be critical for Ras-induced tumour development in mouse models and human tumour cells, showing an unexpected role for methylation in a kinase signalling pathway and revealing a candidate therapeutic target.

    • Pawel K. Mazur
    • , Nicolas Reynoird
    •  & Or Gozani

  • Letter |

    Tumorigenesis driven by the oncogene BRAFV600E is shown both to depend on the BRAF substrates MEK1/2 associating with copper, and to be sensitive to copper-chelating drugs, suggesting merit in testing such drugs for the treatment of BRAF mutation-positive cancers.

    • Donita C. Brady
    • , Matthew S. Crowe
    •  & Christopher M. Counter

  • Letter |

    KRAS is one of the most frequently mutated oncogenes and a major target in anticancer drug discovery, but small molecule modulators that work in the clinic have been elusive; here a new approach to target KRAS is described, based on interfering with its binding to the prenyl-binding protein PDEδ.

    • Gunther Zimmermann
    • , Björn Papke
    •  & Herbert Waldmann

  • 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 |

    Here, single nucleotide variants within the LMO1 locus are shown to be associated with inherited susceptibility to neuroblastoma, a childhood cancer of the sympathetic nervous system. Acquired structural variation in the same locus was also frequently found in neuroblastoma patients, leading to the suggestion that loci identified through genome-wide association studies might be also prone to somatic alterations and therefore identify potential therapy targets and/or biomarkers of tumour aggressiveness.

    • Kai Wang
    • , Sharon J. Diskin
    •  & John M. Maris

  • 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

  • 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

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