Cancer genomics articles within Nature

Featured

  • Article |

    RNA sequencing data and tumour pathology observations of non-small-cell lung cancers indicate that the immune cell microenvironment exerts strong evolutionary selection pressures that shape the immune-evasion capacity of tumours.

    • Rachel Rosenthal
    • , Elizabeth Larose Cadieux
    •  & Andrew Kidd

  • Article |

    Analyses of samples from patients with acute myeloid leukaemia reveal that drug response is associated with mutational status and gene expression; the generated dataset provides a basis for future clinical and functional studies of this disease.

    • Jeffrey W. Tyner
    • , Cristina E. Tognon
    •  & Brian J. Druker

  • Article |

    A large-scale genomics study shows that the cell of origin and founding mutations determine disease subtype and lead to the expression of multiple haematopoietic lineage-defining antigens in mixed phenotype acute leukaemia.

    • Thomas B. Alexander
    • , Zhaohui Gu
    •  & Charles G. Mullighan

  • 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

  • Brief Communications Arising |

    • Song Wu
    • , Wei Zhu
    •  & Yusuf A. Hannun

  • Article |

    The authors describe a two-cell-type CRISPR screen to identify tumour-intrinsic genes that regulate the sensitivity of cancer cells to effector T cell function.

    • Shashank J. Patel
    • , Neville E. Sanjana
    •  & Nicholas P. Restifo

  • Article
    | Open Access

    Genomic analysis of 491 medulloblastoma samples, including methylation profiling of 1,256 cases, effectively assigns candidate drivers to most tumours across all molecular subgroups.

    • Paul A. Northcott
    • , Ivo Buchhalter
    •  & Peter Lichter

  • Article |

    High-depth sequencing of targeted regions in primary breast cancer identifies mutated promoter elements with recurrent mutations at specific and/or nearby bases, suggesting selection of certain non-coding events.

    • Esther Rheinbay
    • , Prasanna Parasuraman
    •  & Gad Getz

  • Article |

    The genomes of 102 primary pancreatic neuroendocrine tumours have been sequenced, revealing mutations in genes with functions such as chromatin remodelling, DNA damage repair, mTOR activation and telomere maintenance, and a greater-than-expected contribution from germ line mutations.

    • Aldo Scarpa
    • , David K. Chang
    •  & Sean M. Grimmond

  • Article |

    Genomic analyses of localized, non-indolent prostate cancer identify recurrent aberrations that can predict relapse, and also highlight differences between early prostate cancer and metastatic, castration-resistant disease.

    • Michael Fraser
    • , Veronica Y. Sabelnykova
    •  & Paul C. Boutros

  • Article
    | Open Access

    The Cancer Genome Atlas Research Network report integrated genomic and molecular analyses of 164 squamous cell carcinomas and adenocarcinomas of the oesophagus; they find genomic and molecular features that differentiate squamous and adenocarcinomas of the oesophagus, and strong similarities between oesophageal adenocarcinomas and the chromosomally unstable variant of gastric adenocarcinoma, suggesting that gastroesophageal adenocarcinoma is a single disease entity.

    • Jihun Kim
    • , Reanne Bowlby
    •  & Jiashan Zhang

  • Letter |

    Genomic analyses show that primary germ-cell tumours are highly enriched for chromosomal reciprocal loss of heterozygosity, mutations in KRAS and have high mitochondrial priming, providing insight into chemosensitivity and the evolution of chemoresistance in this disease.

    • Amaro Taylor-Weiner
    • , Travis Zack
    •  & Eliezer M Van Allen

  • 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

  • Analysis |

    Large-scale analyses of the drug sensitivity of cancer cell lines have been previously reported to yield conflicting conclusions; this Analysis uses independently generated data to demonstrate that consistency can be achieved if key laboratory and data analysis practices are considered when future studies are undertaken.

    • Peter M. Haverty
    • , Eva Lin
    •  & Richard Bourgon

  • Article |

    Whole-genome sequencing of tumours from 560 breast cancer cases provides a comprehensive genome-wide view of recurrent somatic mutations and mutation frequencies across both protein coding and non-coding regions; several mutational signatures in these cancer genomes are associated with BRCA1 or BRCA2 function and defective homologous-recombination-based DNA repair.

    • Serena Nik-Zainal
    • , Helen Davies
    •  & Michael R. Stratton

  • Letter |

    An analysis of cancer genomic data reveals an increased rate of somatic mutations at active transcription factor binding sites located both within promoter regions and distal from genes; the increased mutation rate at these genomic regions can be explained by reduced accessibility of the protein-bound DNA to nucleotide excision repair machinery.

    • Radhakrishnan Sabarinathan
    • , Loris Mularoni
    •  & Núria López-Bigas

  • Article |

    An integrated genomic analysis of 456 human pancreatic ductal adenocarcinomas identifies four subtypes defined by transcriptional expression profiles and show that these are associated with distinct histopathological characteristics and differential prognosis.

    • Peter Bailey
    • , David K. Chang
    •  & Sean M. Grimmond

  • Article |

    Genomic studies of the paediatric brain tumour medulloblastoma have revealed four clinically distinct molecular subgroups; here active gene regulatory elements in 28 primary medulloblastoma tissues are mapped to reveal differentially regulated enhancers across the different subgroups, allowing insights into the transcription factors that characterize subgroup divergence and the cellular origin of the poorly characterized Group 3 and 4 subgroups.

    • Charles Y. Lin
    • , Serap Erkek
    •  & Paul A. Northcott

  • Article |

    To address the question of whether a recurrent tumour is genetically similar to the tumour at diagnosis, the evolution of medulloblastoma has been studied in both an in vivo mouse model of clinical tumour therapy as well as in humans with recurrent disease; targeted tumour therapies are usually based on targets present in the tumour at diagnosis but the results from this study indicate that post-treatment recurring tumours (compared with the tumour at diagnosis) have undergone substantial clonal divergence of the initial dominant tumour clone.

    • A. Sorana Morrissy
    • , Livia Garzia
    •  & Michael D. Taylor

  • Analysis |

    In panels of cancer cell lines analysed for their response to drug libraries, some studies have proposed distinct pharmacological sensitivities for some cell lines while other studies have not seen the same trends; here the data in the Cancer Cell Line Encyclopedia and the Genomics of Drug Sensitivity in Cancer are reassessed, and the authors report a stronger degree of concordance between the two data sets than that in a previous study.

    • Nicolas Stransky
    • , Mahmoud Ghandi
    •  & Julio Saez-Rodriguez

  • Article |

    This study reports exome sequencing of samples from 538 individuals with chronic lymphocytic leukaemia (CLL), including 278 collected as part of a prospective clinical trial; recurrently mutated genes are identified and pathways involved in CLL are highlighted, as well as their evolution in progression and disease relapse.

    • Dan A. Landau
    • , Eugen Tausch
    •  & Catherine J. Wu

  • Article |

    A ChIP-seq analysis of the DNA-binding properties of mutant gain-of-function p53 protein compared to wild-type p53 reveals the gain-of-function proteins bind to and activate a distinct set of genes including chromatin modifying enzymes such as the histone methyltransferase MLL; small molecular inhibitors of MLL function may represent a new target for cancers with mutant p53.

    • Jiajun Zhu
    • , Morgan A. Sammons
    •  & Shelley L. Berger

  • Article |

    Genomic sequencing of 110 human small cell lung cancers identifies genomic signatures including nearly ubiquitous bi-allelic inactivation of TP53 and RB1, a role for NOTCH family genes, and somatic rearrangements that create an oncogenic version of TP73.

    • Julie George
    • , Jing Shan Lim
    •  & Roman K. Thomas

  • Article |

    The mechanism for chromothripsis, “shattered” chromosomes that can be observed in cancer cells, is unknown; here, using live-cell imaging and single-cell sequencing, chromothripsis is shown to occur after a chromosome is isolated into a micronucleus, an abnormal nuclear structure.

    • Cheng-Zhong Zhang
    • , Alexander Spektor
    •  & David Pellman

  • Article |

    Whole-genome sequencing of tumour and germline DNA samples from 92 patients with high-grade serous ovarian cancer identifies frequent gene breakages that inactivate the tumour suppressors RB1, NF1, RAD51B and PTEN, and contribute to chemotherapy resistance; acquired resistance was associated with diverse mechanisms such as reversions of germline BRCA1/2 mutations and overexpression of the drug efflux pump MDR1.

    • Ann-Marie Patch
    • , Elizabeth L. Christie
    •  & David D. L. Bowtell

Browse broader subjects

Browse Cancer genomics across other nature.com journals