Cancer genomics articles within Nature

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  • Article
    | Open Access

    We uncover key processes of the genomic evolution of small cell lung cancer under therapy, identify the common ancestor as the source of clonal diversity at relapse and show central genomic patterns associated with drug response.

    • Julie George
    • , Lukas Maas
    •  & Roman K. Thomas

  • Article
    | Open Access

    Analyses of single epithelial cells from early-stage lung adenocarcinoma and normal lung identifies a population of intermediate cells that may have an increased likelihood of transforming to tumour cells after injury such as tobacco exposure.

    • Guangchun Han
    • , Ansam Sinjab
    •  & Humam Kadara

  • Article |

    The Chinese Liver Cancer Atlas project depicts a panoramic genomic landscape of hepatocellular carcinoma, covering candidate coding and non-coding drivers, mutational signatures, extrachromosomal circular DNA, subclonal catastrophic events and detailed evolutionary history.

    • Lei Chen
    • , Chong Zhang
    •  & Hongyang Wang

  • Article
    | Open Access

    By using phylogenetic analyses of multiple microdissected samples from both cancer and non-cancer lesions, unique evolutionary histories of breast cancers harbouring a common driver alteration are shown, providing new insight into how breast cancer evolves.

    • Tomomi Nishimura
    • , Nobuyuki Kakiuchi
    •  & Seishi Ogawa

  • Article |

    A study reports the development of an algorithm, BISCUT, that detects genomic loci under selective pressure by relying on the distribution of breakpoints across chromosome arms, and uses it to explore how aneuploidies affect tumorigenesis.

    • Juliann Shih
    • , Shahab Sarmashghi
    •  & Rameen Beroukhim

  • Article |

    Chromothriptically produced pieces of a micronucleated chromosome are shown to be tethered together in mitosis by a protein complex consisting of MDC1, TOPBP1 and CIP2A, thus enabling their inheritance by a single daughter cell.

    • Prasad Trivedi
    • , Christopher D. Steele
    •  & Don W. Cleveland

  • Article
    | Open Access

    Micronuclei, which are common features of nuclei in cancer cells, can generate heritable sources of transcriptional suppression, a finding that establishes an inherent relationship between chromosomal instability and variation in chromatin state and gene expression.

    • Stamatis Papathanasiou
    • , Nikos A. Mynhier
    •  & David Pellman

  • Article
    | Open Access

    We model occult preneoplasia by biallelic inactivation of TP53, a common early event in gastric cancer, in human gastric organoids, the results implying predictability in the earliest stages of tumorigenesis.

    • Kasper Karlsson
    • , Moritz J. Przybilla
    •  & Christina Curtis

  • Article
    | Open Access

    An analysis of 780 breast cancer genomes shows that focal amplifications are frequently preceded by dicentric chromosome formation from inter-chromosomal translocations associated with oestrogen receptor binding, which leads to chromosome bridge formation and breakage, initiating the amplification process.

    • Jake June-Koo Lee
    • , Youngsook Lucy Jung
    •  & Peter J. Park

  • Article
    | Open Access

    This study illustrates long interspersed nuclear element-1 retrotransposition-induced somatic mosaicism in normal cells and provides insights into the genomic and epigenomic regulation of transposable elements over the human lifetime.

    • Chang Hyun Nam
    • , Jeonghwan Youk
    •  & Young Seok Ju

  • Article
    | Open Access

    Computational and machine-learning approaches that integrate genomic and transcriptomic variation from paired primary and metastatic non-small cell lung cancer samples from the TRACERx cohort reveal the role of transcriptional events in tumour evolution.

    • Carlos Martínez-Ruiz
    • , James R. M. Black
    •  & Nicholas McGranahan

  • 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
    | Open Access

    A longitudinal evolutionary analysis of 126 lung cancer patients with metastatic disease reveals the timing of metastatic divergence, modes of dissemination and the genomic events subject to selection during the metastatic transition.

    • Maise Al Bakir
    • , Ariana Huebner
    •  & Charles Swanton

  • Article |

    Combination of epidemiology, preclinical models and ultradeep DNA profiling of clinical cohorts unpicks the inflammatory mechanism by which air pollution promotes lung cancer

    • William Hill
    • , Emilia L. Lim
    •  & Charles Swanton

  • Article
    | Open Access

    Multi-modal analysis of genomically unstable ovarian tumours characterizes the contribution of anatomical sites and mutational processes to evolutionary phenotypic divergence and immune resistance mechanisms.

    • Ignacio Vázquez-García
    • , Florian Uhlitz
    •  & Sohrab P. Shah

  • Article |

    Results are presented that indicate that alterations to gene regulatory three-dimensional architecture are a critical mechanism that enables structural variant-based oncogene activation in cancer genomes and sheds light on the essential elements for such gene activation events.

    • Zhichao Xu
    • , Dong-Sung Lee
    •  & Jesse R. Dixon

  • Article
    | Open Access

    Single-cell whole-genome sequencing shows that 'foreground' cell-to-cell structural variation and alterations in copy number are associated with genomic diversity and evolution in triple-negative breast and high-grade serous ovarian cancers.

    • Tyler Funnell
    • , Ciara H. O’Flanagan
    •  & Samuel Aparicio

  • Article
    | Open Access

    A study maps genetic and epigenetic heterogeneity of primary colorectal adenomas and cancers at single-clone resolution through spatial multi-omic profiling of individual glands and adjacent normal tissue.

    • Timon Heide
    • , Jacob Househam
    •  & Andrea Sottoriva

  • Article |

    Extensive genomic analyses of the chromatin architecture in acute myeloid leukaemia reveals several characteristics, including subtype-specific distal enhancers and silencers, that may represent new anticancer therapeutic targets.

    • Jie Xu
    • , Fan Song
    •  & Feng Yue

  • Article
    | Open Access

    Intratumour genetic ancestry only infrequently affects gene expression traits and subclonal evolution in colorectal cancer, with most genetic intratumour variation having no detected phenotypic consequence and transcriptional plasticity being widespread within a tumour.

    • Jacob Househam
    • , Timon Heide
    •  & Trevor A. Graham

  • Article
    | Open Access

    A study examining DNA transfer from mitochondria to the nucleus using whole-genome sequences from 66,083 people shows that this is an ongoing dynamic process in normal cells with distinct roles in different types of cancer.

    • Wei Wei
    • , Katherine R. Schon
    •  & Patrick F. Chinnery

  • Article |

    The nuclear mitotic apparatus protein NuMA helps to protect genes from oxidative damage by occupying regions around transcription start sites, binding DNA repair factors and promoting transcription following damage.

    • Swagat Ray
    • , Arwa A. Abugable
    •  & Sherif F. El-Khamisy

  • Article
    | Open Access

    A molecular taxonomy for prostate cancer reveals a subtype associated with copy-number loss found in African and European populations that predicts poor outcomes and two subtypes—one associated with high mutational noise and one with copy-number gain—specific to African populations.

    • Weerachai Jaratlerdsiri
    • , Jue Jiang
    •  & Vanessa M. Hayes

  • Article
    | Open Access

     Malignant evolution enabled by p53 inactivation in mice proceeds through an ordered and predictable pattern of Trp53 loss of heterozygosity, accumulation of deletions, genome doubling and the emergence of gains and amplifications.

    • Timour Baslan
    • , John P. Morris IV
    •  & Scott W. Lowe

  • Article
    | Open Access

    Endogenous APOBEC3 deaminases generate prevalent mutational signatures in human cancer cells, and APOBEC3A is the main driver of these mutations.

    • Mia Petljak
    • , Alexandra Dananberg
    •  & John Maciejowski

  • Article |

    Deep whole-genome sequencing of serial blood samples and matched metastatic tissue reveals that circulating tumour DNA profiling enables detailed study of treatment-driven subclone dynamics, epigenomics and genome-wide somatic evolution in metastatic human cancers.

    • Cameron Herberts
    • , Matti Annala
    •  & Alexander W. Wyatt

  • Article |

    Active super-enhancers are highly and specifically hypermutated in 92% of diffuse large B cell lymphoma samples and display signatures of activation-induced cytidine deaminase activity, leading to the dysregulation of genes encoding B cell developmental regulators and oncogenes.

    • Elodie Bal
    • , Rahul Kumar
    •  & Riccardo Dalla-Favera

  • Article
    | Open Access

    A new framework enables a pan-cancer reference set of copy number signatures derived from allele-specific profiles from different experimental assays.

    • Christopher D. Steele
    • , Ammal Abbasi
    •  & Nischalan Pillay

  • Article
    | Open Access

    Whole-genome sequencing is used to analyse the landscape of somatic mutation in intestinal crypts from 16 mammalian species, revealing that rates of somatic mutation inversely scale with the lifespan of the animal across species.

    • Alex Cagan
    • , Adrian Baez-Ortega
    •  & Iñigo Martincorena

  • Article
    | Open Access

    An analysis of clustered substitutions and indels across 30 cancer types provides insight into the role of APOBEC3 in giving rise to clustered mutation events through its activity on extrachromosomal DNA.

    • Erik N. Bergstrom
    • , Jens Luebeck
    •  & Ludmil B. Alexandrov

  • Article |

    Whole-genome sequencing of 1,013 clonal haematopoietic colonies from myeloproliferative neoplasms of 12 individuals reveals haematopoietic phylogenies and indicates that driver mutations are acquired sequentially, starting early in life.

    • Nicholas Williams
    • , Joe Lee
    •  & Jyoti Nangalia

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