Lung cancer 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 |

    A study identifies the AT1 cell as a cell of origin for lung adenocarcinoma, and demonstrates that expression of oncogenic KRAS in differentiated AT1 cells reprograms them back into AT2 stem cells that generate indolent lepidic tumours.

    • Nicholas H. Juul
    • , Jung-Ki Yoon
    •  & Tushar J. Desai

  • Article |

    Induction of APOBEC3A in response to targeted therapies drives evolution of drug-tolerant persister cells, suggesting that its suppression may represent a potential therapeutic strategy in the prevention of acquired resistance to lung cancer targeted therapy.

    • Hideko Isozaki
    • , Ramin Sakhtemani
    •  & Aaron N. Hata

  • Article |

    Measurements of subclonal expansion of ctDNA in the plasma before surgery may enable the prediction of future metastatic subclones, offering the possibility for early intervention in patients with non-small-cell lung cancer.

    • Christopher Abbosh
    • , Alexander M. Frankell
    •  & Charles Swanton

  • 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

    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

    A study describing an approach that combines imaging and profiling techniques to structurally and functionally analyse lung cancer in vivo, revealing heterogeneous mitochondrial networks and an association between bioenergetic phenotypes and mitochondrial organization and function.

    • Mingqi Han
    • , Eric A. Bushong
    •  & David B. Shackelford

  • Article
    | Open Access

    Using imaging mass cytometry, the tumour and immunological spatial landscapes of 416 lung adenocarcinomas are characterized, which, when combined with deep learning, can predict clinical outcomes with high accuracy.

    • Mark Sorin
    • , Morteza Rezanejad
    •  & Logan A. Walsh

  • Article |

    Whole-transcriptome sequencing of a subset of 75 non-small-cell lung cancer specimens in a multi-institutional genome screening study identified a fusion of the CLIP1 and LTK genes with transformational potential due to constitutive LTK kinase activity.

    • Hiroki Izumi
    • , Shingo Matsumoto
    •  & Koichi Goto

  • Article
    | Open Access

    Structural classification of mutations in the epidermal growth factor receptor causing non-small cell lung cancer is a better predictor of patient outcomes following drug treatment than traditional exon-based classification.

    • Jacqulyne P. Robichaux
    • , Xiuning Le
    •  & John V. Heymach

  • Article |

    Current outcomes are reported from the ongoing National Lung Matrix Trial, an umbrella trial for the treatment of non-small-cell lung cancer in which patients are triaged according to their tumour genotype and matched with targeted therapeutic agents.

    • Gary Middleton
    • , Peter Fletcher
    •  & Lucinda Billingham

  • Article |

    Circulating tumour DNA in blood is analysed to identify genomic features that distinguish early-stage lung cancer patients from risk-matched controls, and these are integrated into a machine-learning method for blood-based lung cancer screening.

    • Jacob J. Chabon
    • , Emily G. Hamilton
    •  & Maximilian Diehn

  • Article |

    Populations of KRAS(G12C)-mutant cancer cells can rapidly bypass the effects of treatment with KRAS(G12C) inhibitors because a subset of cells escapes drug-induced quiescence by producing new KRAS(G12C) that is maintained in its active, drug-insensitive state.

    • Jenny Y. Xue
    • , Yulei Zhao
    •  & Piro Lito

  • Article |

    A positron emission tomography imaging tracer is developed to image mitochondrial function in vivo, and application of this tracer to a mouse model of lung cancer identifies distinct functional mitochondrial heterogeneity between tumour cells.

    • Milica Momcilovic
    • , Anthony Jones
    •  & David B. Shackelford

  • Letter |

    Loss of RB promotes both malignant progression and the development of metastatic disease; however, whereas reactivation of the RB pathway can revert metastatic tumour cell states to non-metastatic cell states, malignant cell proliferation is supported by MAPK–CDK2-dependent suppression of RB.

    • David M. Walter
    • , Travis J. Yates
    •  & David M. Feldser

  • 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

  • Letter |

    Kinase-inactive Braf mutants can initiate the development of lung adenocarcinoma in mice; co-expression of activated Kras enhances tumour initiation and progression, and wild-type Braf is required to sustain tumorigenesis.

    • Patricia Nieto
    • , Chiara Ambrogio
    •  & David Santamaría

  • Article |

    Circulating tumour DNA profiling in early-stage non-small-cell lung cancer can be used to track single-nucleotide variants in plasma to predict lung cancer relapse and identify tumour subclones involved in the metastatic process.

    • Christopher Abbosh
    • , Nicolai J. Birkbak
    •  & Charles Swanton

  • Article |

    A systematic screen identifies FGFR1 signalling reactivation as an adaptive resistance mechanism after MEK inhibition specific for KRAS tumours, which can be targeted by combined inhibition with the clinically approved drugs trametinib and ponatinib.

    • Eusebio Manchado
    • , Susann Weissmueller
    •  & Scott W. Lowe

  • Letter |

    An allosteric inhibitor, EAI045, is reported that is selective for certain drug-resistant EGFR mutants, but spares the wild-type receptor; combination therapy of EAI045 with EGFR-dimerization-blocking antibodies is effective in mouse models of lung cancer driven by mutant versions of EGFR that are resistant to all previously developed inhibitors.

    • Yong Jia
    • , Cai-Hong Yun
    •  & Michael J. Eck

  • 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

  • Letter |

    Whole-exome sequencing is used to compare the mutational landscape of adenomas from three mouse models of non-small-cell lung cancer, induced either by exposure to carcinogens or by genetic mutation of Kras; the results reveal that the two types of tumour have different mutational profiles and adopt different routes to tumour development.

    • Peter M. K. Westcott
    • , Kyle D. Halliwill
    •  & Allan Balmain

  • Letter |

    The CRISPR/Cas system has been used to induce the Eml4–Alk chromosomal inversion in mice, a characteristic chromosomal rearrangement seen in human non-small cell lung cancers; the mice developed lung cancer and responded to the ALK inhibitor crizotinib, which is used to treat lung cancer patients with the EML4–ALK rearrangement; this general strategy can be used to engineer other disease-associated chromosomal rearrangements in mice and potentially in other organisms.

    • Danilo Maddalo
    • , Eusebio Manchado
    •  & Andrea Ventura

  • Letter |

    The CRISPR/Cas system has been used in mice for genome editing to introduce genetic alterations found in human lung tumours, and these genome modifications resulted in mouse lung tumours showing different histopathologies depending on the genes altered; the CRISPR/Cas system offers improved and faster ways to create animal models of human diseases such as cancer.

    • Francisco J. Sánchez-Rivera
    • , Thales Papagiannakopoulos
    •  & Tyler Jacks

  • Outlook |

    Carcinogens are all around us, so scientists are broadening their ideas of environmental risk.

    • Rebecca Kessler

  • Letter |

    HMGA2 promotes lung cancer progression in mice and humans; in mouse and human lung cancer cells, HMGA2 competes with mRNAs like TGFBR3 for the let-7 microRNA family, and in human non-small-cell lung cancer tissue, expression levels of HMGA2 and TGFBR3 are correlated, suggesting that HMGA2 functions both as a protein-coding gene and as a non-coding RNA.

    • Madhu S. Kumar
    • , Elena Armenteros-Monterroso
    •  & Julian Downward

  • Article
    | Open Access

    Comprehensive analyses of 178 lung squamous cell carcinomas by The Cancer Genome Atlas project show that the tumour type is characterized by complex genomic alterations, with statistically recurrent mutations in 11 genes, including TP53 in nearly all samples; a potential therapeutic target is identified in most of the samples studied.

    • Peter S. Hammerman
    • , Michael S. Lawrence
    •  & Matthew Meyerson

  • News & Views |

    Anticancer 'co-clinical' trials, in which mice carrying known mutations are treated in parallel with patients enrolled in a simultaneous clinical study, could help to improve therapeutic outcome. See Letter p.613

    • Leisa Johnson

  • Outlook |

    Being able to determine an individual's chances of developing cancer will greatly improve risk management strategies and recruitment to clinical trials.

    • Vicki Brower

  • Letter |

    Lung cancers with activating mutations in EGFR can be treated with EGFR inhibitors, but not all tumours respond and some develop resistance. In an RNAi screen, this study searches for modifiers of the EGFR inhibitor response. It is found that inhibition of FAS and NF-κB signalling enhances the response in vitro and in vivo. In a cohort of lung cancer patients treated with EGFR inhibitors, expression of the NF-κB inhibitor IκB is associated with a better response and longer survival, indicating that combining NF-κB pathway and EGFR inhibitors may prove clinically useful.

    • Trever G. Bivona
    • , Haley Hieronymus
    •  & Charles L. Sawyers

  • Editorial |

    Irresponsible policies could cause an epidemic of malignant lung disease.

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