Peter Van Loo
United States
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Articles by Peter Van Loo
A guide to transcriptomic deconvolution in cancer - Nature Reviews Cancer
Abstract Cancer tissues are heterogeneous mixtures of tumour, stromal and immune cells, where each component comprises multiple distinct cell types and/or states. Mapping this heterogeneity and understanding the unique contributions of each cell type to the tumour transcriptome is crucial for advancing cancer biology, yet high-throughput expression profiles from tumour tissues only represent combined signals from all cellular sources.
DNA methylation cooperates with genomic alterations during non-small cell lung cancer evolution - Nature Genetics
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Abstract Aberrant DNA methylation has been described in nearly all human cancers, yet its interplay with genomic alterations during tumor evolution is poorly understood. To explore this, we performed reduced representation bisulfite sequencing on 217 tumor and matched normal regions from 59 patients with non-small cell lung cancer from the TRACERx study to deconvolve tumor methylation. We developed two metrics for integrative evolutionary analysis with DNA and RNA sequencing data.
By Elizabeth Larose Cadieux, Takahiro Karasaki, Carlos Martinez-Ruiz, Alexander Frankell, Georgia Stavrou, Wei-Ting Lu, Daniele Marinelli, Pawan Dhami, Robert Hynds, Özgen Deniz, Mariam Jamal-Hanjani, Nicholas McGranahan, TRACERx consortium, Stephan Beck, Jonas Demeulemeester, Miljana Tanić, Charles Swanton, Peter Van Loo
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Nature
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ImmuneLENS characterizes systemic immune dysregulation in aging and cancer - Nature Genetics
Abstract Recognition and elimination of pathogens and cancer cells depend on the adaptive immune system. Thus, accurate quantification of immune subsets is vital for precision medicine. We present immune lymphocyte estimation from nucleotide sequencing (ImmuneLENS), which estimates T cell and B cell fractions, class switching and clonotype diversity from whole-genome sequencing data at depths as low as 5× coverage.
Aneuploidy and Complex Genomic Rearrangements in Cancer Evolution
Mutational processes that alter large genomic regions occur frequently in developing tumors. They range from simple copy number gains and losses to the shattering and reassembly of entire chromosomes. These catastrophic events, such as chromothripsis, chromoplexy and the formation of extrachromosomal DNA, affect the expression of many genes and therefore have a substantial effect on the fitness of the cells in which they arise.
MHC Hammer reveals genetic and non-genetic HLA disruption in cancer evolution - Nature Genetics
Abstract Disruption of the class I human leukocyte antigen (HLA) molecules has important implications for immune evasion and tumor evolution. We developed major histocompatibility complex loss of heterozygosity (LOH), allele-specific mutation and measurement of expression and repression (MHC Hammer). We identified extensive variability in HLA allelic expression and pervasive HLA alternative splicing in normal lung and breast tissue.
Author Correction: The evolution of lung cancer and impact of subclonal selection in TRACERx - Nature
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Correction to: Nature https://doi.org/10.1038/s41586-023-05783-5 Published online 12 April 2023 In the version of the article initially published, the symbols for death (x) and censored (>) were swapped in the graphs in Fig. 1. The figure has now been corrected in the HTML and PDF versions of the article.
By Alexander Frankell, Michelle Dietzen, Maise Al Bakir, Takahiro Karasaki, Sophia Ward, Emma Colliver, Ariana Huebner, Abigail Bunkum, Mark Hill, Kristiana Grigoriadis, David Moore, Oriol Pich, Daniel Cook, Mihaela Angelova, Carlos Martinez-Ruiz, Christopher Abbosh, John Le Quesne, Dhruva Biswas, Sonya Hessey, Claudia Lee, Jerome Nicod, Gary Middleton, Javier Herrero, Sergio A Quezada, Peter Van Loo, Nicolai J. Birkbak, Allan Hackshaw, Simone Zaccaria, TRACERx consortium, Mariam Jamal-Hanjani, Nicholas McGranahan
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Nature
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Crowd-sourced benchmarking of single-sample tumor subclonal reconstruction - Nature Biotechnology
Abstract Subclonal reconstruction algorithms use bulk DNA sequencing data to quantify parameters of tumor evolution, allowing an assessment of how cancers initiate, progress and respond to selective pressures. We launched the ICGC–TCGA (International Cancer Genome Consortium–The Cancer Genome Atlas) DREAM Somatic Mutation Calling Tumor Heterogeneity and Evolution Challenge to benchmark existing subclonal reconstruction algorithms.
Spatiotemporal genomic profiling of intestinal metaplasia reveals clonal dynamics of gastric cancer progression
Highlights • Genomic profiling reveals 26 intestinal metaplasia (IM) driver genes including SOX9 • IM lineage heterogeneity harbors a stem-cell subpopulation linked to malignancy • IM molecular subtypes are associated with inflammation and microbial communities • Genomic-clinical models improve identification of IMs at risk of GC progression Summary Intestinal metaplasia (IM) is a pre-malignant condition of the gastric mucosa associated with increased gastric cancer (GC) risk.
Pan-cancer evolution signatures link clonal expansion to dynamic changes in the tumour immune microenvironment
Abstract Cancer is an evolutionary process characterised by profound intra-tumour heterogeneity. Intra-tumour heterogeneity can be quantified using in silico estimates of cancer cell fractions of tumour-specific somatic mutations. Here we demonstrate a data-driven approach that uses cancer cell fraction distributions to identify 4 robust pan-cancer evolutionary signatures from an analysis of 4,146 individual tumour samples (TCGA) representing 17 distinct cancer types.
Genomic–transcriptomic evolution in lung cancer and metastasis - Nature
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Abstract Intratumour heterogeneity (ITH) fuels lung cancer evolution, which leads to immune evasion and resistance to therapy1. Here, using paired whole-exome and RNA sequencing data, we investigate intratumour transcriptomic diversity in 354 non-small cell lung cancer tumours from 347 out of the first 421 patients prospectively recruited into the TRACERx study2,3.
By Carlos Martinez-Ruiz, Mark Hill, Jonas Demeulemeester, Kerstin Thol, Sophia Ward, Oriol Pich, Takahiro Karasaki, David Moore, Roberto Salgado, Emma Colliver, Michelle Dietzen, Ariana Huebner, Maise Al Bakir, Miljana Tanić, James Clements, Daniel Cook, Alexander Frankell, Philip East, Nicolai J. Birkbak, Allan Hackshaw, Stephan Beck, Peter Van Loo, Mariam Jamal-Hanjani, TRACERx consortium, Charles Swanton, Elizabeth Larose Cadieux, Ali M. Al-Rashed
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Nature
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Evolutionary characterization of lung adenocarcinoma morphology in TRACERx - Nature Medicine
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Abstract Lung adenocarcinomas (LUADs) display a broad histological spectrum from low-grade lepidic tumors through to mid-grade acinar and papillary and high-grade solid, cribriform and micropapillary tumors. How morphology reflects tumor evolution and disease progression is poorly understood.
By Takahiro Karasaki, David Moore, Sophia Ward, Maise Al Bakir, Kristiana Grigoriadis, Ariana Huebner, Mark Hill, Alexander Frankell, Christopher Abbosh, Michelle Dietzen, Oriol Pich, Carlos Martinez-Ruiz, Dhruva Biswas, Claudia Lee, Emma Colliver, Sonya Hessey, Simone Zaccaria, Nicolai J. Birkbak, Jonas Demeulemeester, Peter Van Loo, Prasad S. Adusumilli, Waseem Cheema, Francisco Sanchez-Vega, David Jones, Allan Hackshaw, Roberto Salgado, John Le Quesne, TRACERx consortium, Nicholas McGranahan, Charles Swanton
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Nature
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The evolution of non-small cell lung cancer metastases in TRACERx - Nature
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Abstract Metastatic disease is responsible for the majority of cancer-related deaths1. We report the longitudinal evolutionary analysis of 126 non-small cell lung cancer (NSCLC) tumours from 421 prospectively recruited patients in TRACERx who developed metastatic disease, compared with a control cohort of 144 non-metastatic tumours.
By Maise Al Bakir, Ariana Huebner, Carlos Martinez-Ruiz, Oriol Pich, David Moore, Sophia Ward, Michelle Dietzen, Emma Colliver, Alexander Frankell, Takahiro Karasaki, Christopher Abbosh, Mark Hill, Daniel Cook, Roberto Salgado, Gary Middleton, Neal Navani, Sam M. Janes, Sergio A Quezada, Peter Van Loo, Allan Hackshaw, Nicolai J. Birkbak, Simone Zaccaria, TRACERx consortium, Mariam Jamal-Hanjani, Nicholas McGranahan, Kristiana Grigoriadis, Joanne Laycock, Sonya Hessey, Abigail Bunkum
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Nature
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Author Correction: Pan-cancer analysis of whole genomes identifies driver rearrangements promoted by LINE-1 retrotransposition - Nature Genetics
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Author notes These authors contributed equally: Eva G. Alvarez, Adrian Baez-Ortega, Jorge Zamora, Fran Supek. These authors jointly supervised this work: Peter J. Campbell, Jose M. C. Tubio. A full list of members and their affiliations appears online. Authors and Affiliations Department of Zoology, Genetics and Physical Anthropology, Universidade de Santiago de Compostela, Santiago de Compostela, Spain Bernardo Rodriguez-Martin, Eva G. Alvarez, Jorge Zamora, Martin Santamarina, Javier Temes, Alicia L.
By Bernardo Rodriguez-Martin, Fran Supek, Jonas Demeulemeester, Young Seok Ju, Daniel Garcia-Souto, Miguel Blanco, Daniel Ardeljan, Nicola D. Roberts, Sonia Zumalave, Paul Edwards, Joachim Weischenfeldt, Ken Chen, Keiran Raine, Sebastian M Waszak, Jean Monlong, Guillaume Bourque, Peter J. Park, Jan Korbel, Rebecca Fitzgerald, Peter Van Loo, Kathleen Burns, Peter Campbell, PCAWG Consortium, Javier Temes
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Nature
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A pan-cancer compendium of chromosomal instability - Nature
Abstract Chromosomal instability (CIN) results in the accumulation of large-scale losses, gains and rearrangements of DNA1. The broad genomic complexity caused by CIN is a hallmark of cancer2; however, there is no systematic framework to measure different types of CIN and their effect on clinical phenotypes pan-cancer. Here we evaluate the extent, diversity and origin of CIN across 7,880 tumours representing 33 cancer types.
Signatures of copy number alterations in human cancer - Nature
Abstract Gains and losses of DNA are prevalent in cancer and emerge as a consequence of inter-related processes of replication stress, mitotic errors, spindle multipolarity and breakage–fusion–bridge cycles, among others, which may lead to chromosomal instability and aneuploidy1,2. These copy number alterations contribute to cancer initiation, progression and therapeutic resistance3,4,5.
An integrative analysis of the age-associated multi-omic landscape across cancers
Abstract Age is the most important risk factor for cancer, as cancer incidence and mortality increase with age. However, how molecular alterations in tumours differ among patients of different age remains largely unexplored. Here, using data from The Cancer Genome Atlas, we comprehensively characterise genomic, transcriptomic and epigenetic alterations in relation to patients’ age across cancer types.
Biallelic mutations in cancer genomes reveal local mutational determinants
Abstract The infinite sites model of molecular evolution requires that every position in the genome is mutated at most once. It is a cornerstone of tumour phylogenetic analysis, and is often implied when calling, phasing and interpreting variants or studying the mutational landscape as a whole.
A practical guide to cancer subclonal reconstruction from DNA sequencing
Abstract Subclonal reconstruction from bulk tumor DNA sequencing has become a pillar of cancer evolution studies, providing insight into the clonality and relative ordering of mutations and mutational processes. We provide an outline of the complex computational approaches used for subclonal reconstruction from single and multiple tumor samples. We identify the underlying assumptions and uncertainties in each step and suggest best practices for analysis and quality assessment.
Author Correction: The evolutionary history of lethal metastatic prostate cancer
Correction to: Nature https://doi.org/10.1038/nature14347Published online 1 April 2015 In the Supplementary Information of this Article, some errors were made in compiling the Supplementary Data file called ‘Supplementary Variant Lists’. In the first worksheet (entitled ‘subs’) the clusters to which some single nucleotide variants (SNVs) were assigned were not reported and were replaced with ‘NA’ for ‘not available’. The correct cluster numbers have now been inserted.
Interplay between whole-genome doubling and the accumulation of deleterious alterations in cancer evolution
Abstract Whole-genome doubling (WGD) is a prevalent event in cancer, involving a doubling of the entire chromosome complement. However, despite its prevalence and prognostic relevance, the evolutionary selection pressures for WGD in cancer have not been investigated. Here, we combine evolutionary simulations with an analysis of cancer sequencing data to explore WGD during cancer evolution.
Translating insights into tumor evolution to clinical practice: promises and challenges
Genome Medicine201911:20 https://doi.org/10.1186/s13073-019-0632-z © The Author(s). 2019 Published: 29 March 2019 Abstract Accelerating technological advances have allowed the widespread genomic profiling of tumors. As yet, however, the vast catalogues of mutations that have been identified have made only a modest impact on clinical medicine.
Timing somatic events in the evolution of cancer
Taking multiple samples of a tumor, separated either in space or time, provides the most direct approach for studying tumor evolution. By comparing the cancer genome at different stages of development, one can immediately observe a sequence of events as the cancer progresses. Much information can already be gained from each sample, as sequencing data, both whole genome and exome, contain a detailed catalogue of the somatic mutations that the cancer genome has acquired.
Genomic Characterization of Primary Invasive Lobular Breast Cancer
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Results Besides the high mutation frequency of CDH1 in 65% of tumors, alterations in one of the three key genes of the phosphatidylinositol 3-kinase pathway, PIK3CA, PTEN, and AKT1, were present in more than one-half of the cases. HER2 and HER3 were mutated in 5.1% and 3.6% of the tumors, with most of these mutations having a proven role in activating the human epidermal growth factor receptor/ERBB pathway. Mutations in FOXA1 and ESR1 copy number gains were detected in 9% and 25% of the samples.
By Debora Fumagalli, David Brown, Peter Van Loo, Roberto Salgado, Christine Galant, François Bertucci, Peter Campbell, Gabriele Zoppoli, Gunes Gundem, Giancarlo Pruneri, Denis Larsimont, Marco Fornili, Françoise Rothé, Delphine Vincent, Naima Kheddoumi, Ghizlane Rouas, Samira Majjaj, Sylvain Brohée, Patrick Maisonneuve, Thomas Van Brussel, Diether Lambrechts, Ron Bose, Otto Metzger, Martine Piccart-Gebhart, Giuseppe Viale, Elia Biganzoli
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Journal of Clinical Oncology
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High burden and pervasive positive selection of somatic mutations in normal human skin
Within every tumor, a battle is being waged. As individual tumor cells acquire new mutations that promote their survival and growth, they clonally expand at the expense of tumor cells that are “less fit.” Martincorena et al. sequenced 234 biopsies of sun-exposed but physiologically normal skin from four individuals (see the Perspective by Brash). They found a surprisingly high burden of mutations, higher than that of many tumors.
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