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Showing 1–50 of 531 results
Advanced filters: Author: Dana D. Miller Clear advanced filters
  • Pharmacologic inhibition of dihydroorotate dehydrogenase (DHODH) shows limited efficacy in pancreatic ductal adenocarcinoma (PDAC) models. Here the authors find that targeting the anti-apoptotic protein BCL-XL synergizes with DHODH inhibition in promoting apoptosis in PDAC cells, patient-derived organoids, and PDAC mouse models.

    • Huan Zhang
    • Naiara Santana-Codina
    • Joseph D. Mancias
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-18
  • Sequencing analysis of tamoxifen-associated uterine cancers and further in vivo analyses suggest that the drug tamoxifen can activate the PI3K pathway in the absence of oncogenic mutations.

    • Kirsten Kübler
    • Agostina Nardone
    • Rinath Jeselsohn
    ResearchOpen Access
    Nature Genetics
    Volume: 57, P: 2192-2202
  • Analyses of 2,658 whole genomes across 38 types of cancer identify the contribution of non-coding point mutations and structural variants to driving cancer.

    • Esther Rheinbay
    • Morten Muhlig Nielsen
    • Christian von Mering
    ResearchOpen Access
    Nature
    Volume: 578, P: 102-111
  • Integrated single-cell transcriptomic and genetic characterization of 121 adult glioblastomas identifies heterogeneity at cell type, cell state and baseline expression program levels associated with specific mutations that form three stereotypical ecosystems.

    • Masashi Nomura
    • Avishay Spitzer
    • Itay Tirosh
    ResearchOpen Access
    Nature Genetics
    Volume: 57, P: 1155-1167
  • Analysis of cancer genome sequencing data has enabled the discovery of driver mutations. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium the authors present DriverPower, a software package that identifies coding and non-coding driver mutations within cancer whole genomes via consideration of mutational burden and functional impact evidence.

    • Shimin Shuai
    • Federico Abascal
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-12
  • Multi-omics datasets pose major challenges to data interpretation and hypothesis generation owing to their high-dimensional molecular profiles. Here, the authors develop ActivePathways method, which uses data fusion techniques for integrative pathway analysis of multi-omics data and candidate gene discovery.

    • Marta Paczkowska
    • Jonathan Barenboim
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-16
  • Understanding deregulation of biological pathways in cancer can provide insight into disease etiology and potential therapies. Here, as part of the PanCancer Analysis of Whole Genomes (PCAWG) consortium, the authors present pathway and network analysis of 2583 whole cancer genomes from 27 tumour types.

    • Matthew A. Reyna
    • David Haan
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-17
  • The authors present SVclone, a computational method for inferring the cancer cell fraction of structural variants from whole-genome sequencing data.

    • Marek Cmero
    • Ke Yuan
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-15
  • Whole-genome sequencing data for 2,778 cancer samples from 2,658 unique donors across 38 cancer types is used to reconstruct the evolutionary history of cancer, revealing that driver mutations can precede diagnosis by several years to decades.

    • Moritz Gerstung
    • Clemency Jolly
    • Christian von Mering
    ResearchOpen Access
    Nature
    Volume: 578, P: 122-128
  • Integrative analyses of transcriptome and whole-genome sequencing data for 1,188 tumours across 27 types of cancer are used to provide a comprehensive catalogue of RNA-level alterations in cancer.

    • Claudia Calabrese
    • Natalie R. Davidson
    • Christian von Mering
    ResearchOpen Access
    Nature
    Volume: 578, P: 129-136
  • Viral pathogen load in cancer genomes is estimated through analysis of sequencing data from 2,656 tumors across 35 cancer types using multiple pathogen-detection pipelines, identifying viruses in 382 genomic and 68 transcriptome datasets.

    • Marc Zapatka
    • Ivan Borozan
    • Christian von Mering
    ResearchOpen Access
    Nature Genetics
    Volume: 52, P: 320-330
  • In somatic cells the mechanisms maintaining the chromosome ends are normally inactivated; however, cancer cells can re-activate these pathways to support continuous growth. Here, the authors characterize the telomeric landscapes across tumour types and identify genomic alterations associated with different telomere maintenance mechanisms.

    • Lina Sieverling
    • Chen Hong
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-13
  • Whole-genome sequencing data from more than 2,500 cancers of 38 tumour types reveal 16 signatures that can be used to classify somatic structural variants, highlighting the diversity of genomic rearrangements in cancer.

    • Yilong Li
    • Nicola D. Roberts
    • Christian von Mering
    ResearchOpen Access
    Nature
    Volume: 578, P: 112-121
  • In this study the authors consider the structural variants (SVs) present within cancer cases of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. They report hundreds of genes, including known cancer-associated genes for which the nearby presence of a SV breakpoint is associated with altered expression.

    • Yiqun Zhang
    • Fengju Chen
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-14
  • Some cancer patients first present with metastases where the location of the primary is unidentified; these are difficult to treat. In this study, using machine learning, the authors develop a method to determine the tissue of origin of a cancer based on whole sequencing data.

    • Wei Jiao
    • Gurnit Atwal
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-12
  • Cancers evolve as they progress under differing selective pressures. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, the authors present the method TrackSig the estimates evolutionary trajectories of somatic mutational processes from single bulk tumour data.

    • Yulia Rubanova
    • Ruian Shi
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-12
  • Myoepithelial cells prevent tumour growth and invasion in DCIS. Here, the authors show that p63 and TCF7 cooperate to regulate a transcription factor network for the maintenance of normal myoepithelial function and altered expression of these genes perturb myoepithelial function in DCIS to promote invasive progression.

    • Lina Ding
    • Ying Su
    • Kornelia Polyak
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-16
  • With the generation of large pan-cancer whole-exome and whole-genome sequencing projects, a question remains about how comparable these datasets are. Here, using The Cancer Genome Atlas samples analysed as part of the Pan-Cancer Analysis of Whole Genomes project, the authors explore the concordance of mutations called by whole exome sequencing and whole genome sequencing techniques.

    • Matthew H. Bailey
    • William U. Meyerson
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-27
  • The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 cancer whole genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.

    • Lauri A. Aaltonen
    • Federico Abascal
    • Christian von Mering
    ResearchOpen Access
    Nature
    Volume: 578, P: 82-93
  • Leptomeningeal disease (LMD) is a serious complication of metastatic solid tumors with a poor prognosis. Here, by using single-cell RNA sequencing of cerebrospinal fluid, the authors report genomic and immune correlates of response to immunotherapy in two cohorts of patients with LMD treated with immune checkpoint inhibitors.

    • Sanjay M. Prakadan
    • Christopher A. Alvarez-Breckenridge
    • Alex K. Shalek
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-10
  • There’s an emerging body of evidence to show how biological sex impacts cancer incidence, treatment and underlying biology. Here, using a large pan-cancer dataset, the authors further highlight how sex differences shape the cancer genome.

    • Constance H. Li
    • Stephenie D. Prokopec
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-24
  • Many tumours exhibit hypoxia (low oxygen) and hypoxic tumours often respond poorly to therapy. Here, the authors quantify hypoxia in 1188 tumours from 27 cancer types, showing elevated hypoxia links to increased mutational load, directing evolutionary trajectories.

    • Vinayak Bhandari
    • Constance H. Li
    • Christian von Mering
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-10
  • The characterization of 4,645 whole-genome and 19,184 exome sequences, covering most types of cancer, identifies 81 single-base substitution, doublet-base substitution and small-insertion-and-deletion mutational signatures, providing a systematic overview of the mutational processes that contribute to cancer development.

    • Ludmil B. Alexandrov
    • Jaegil Kim
    • Christian von Mering
    ResearchOpen Access
    Nature
    Volume: 578, P: 94-101
  • In vivo CRISPR screening reveals that loss of Ptpn2 increases the response of tumour cells to immunotherapy and increases IFNγ signalling, suggesting that PTPN2 inhibition may potentiate the effect of immunotherapies that invoke an IFNγ response.

    • Robert T. Manguso
    • Hans W. Pope
    • W. Nicholas Haining
    Research
    Nature
    Volume: 547, P: 413-418
  • The genomic features of precursor conditions of multiple myeloma provide multiple biological insights into disease origins and evolution, together with opportunities to identify those at highest risk of progression.

    • Jean-Baptiste Alberge
    • Ankit K. Dutta
    • Irene M. Ghobrial
    ResearchOpen Access
    Nature Genetics
    Volume: 57, P: 1493-1503
  • An analysis of data from the Sherlock-Lung study provides insight into the mutational processes that contribute to lung cancer in never smokers, and looks at the possible role of factors such as air pollution and passive smoking.

    • Marcos Díaz-Gay
    • Tongwu Zhang
    • Maria Teresa Landi
    Research
    Nature
    Volume: 644, P: 133-144
  • Analysis of whole-genome sequencing data across 2,658 tumors spanning 38 cancer types shows that chromothripsis is pervasive, with a frequency of more than 50% in several cancer types, contributing to oncogene amplification, gene inactivation and cancer genome evolution.

    • Isidro Cortés-Ciriano
    • Jake June-Koo Lee
    • Christian von Mering
    ResearchOpen Access
    Nature Genetics
    Volume: 52, P: 331-341
  • Wu et al. perform single-cell analyses to explore the switch from low-grade to high-grade isocitrate-dehydrogenase-mutant glioma and show that it is characterized by oligodendrocyte progenitor cell-like cells transitioning to proliferative neural progenitor cell-like cells.

    • Jingyi Wu
    • L. Nicolas Gonzalez Castro
    • Bradley E. Bernstein
    Research
    Nature Cancer
    Volume: 6, P: 145-157
  • PPM1D is a known mediator of p53 signalling, and has been linked to treatment resistance in glioma. In this work, the authors utilise genomics, proteomics, and mouse models to determine the role of PPM1D in the development of diffuse midline glioma.

    • Prasidda Khadka
    • Zachary J. Reitman
    • Pratiti Bandopadhayay
    ResearchOpen Access
    Nature Communications
    Volume: 13, P: 1-18
  • A study of myeloid cells in gliomas, a type of brain tumour, used a factor-based computational framework to reveal four immunomodulatory gene-expression programs that are expressed across myeloid cell types, driven by microenvironmental cues and predictive of therapeutic response.

    • Tyler E. Miller
    • Chadi A. El Farran
    • Bradley E. Bernstein
    ResearchOpen Access
    Nature
    Volume: 640, P: 1072-1082