- Head of Computational Biology Research Centre, Computational biology
- Research Group Leader, Sottoriva Group
Andrea Sottoriva is the Head of the Computational Biology Research Centre at Human Technopole.
Andrea’s research focusses on the development of new computational approaches to measure cancer evolution in patients, with the aim of predicting the future course of the disease. Andrea’s lab also integrates patient-derived experimental models and multiomics data, with evolutionary methods to design new treatment strategies that aim at preventing and controlling drug resistance.
After graduating in Computer Science at the University of Bologna in 2006, he obtained a master in Computational Sciences from the University of Amsterdam in 2008. During his studies, he worked in neutrino physics at the Department of Physics of the University of Bologna and at the Institute for Nuclear and High Energy Physics (NIKHEF) in the Netherlands as a research assistant.
In 2012 he completed his PhD in Computational Biology from the University of Cambridge, where he worked at the Cancer Research UK research centre.
After postdoctoral work at the University of Southern California, he started his lab at the Institute of Cancer Research in London in 2013, where in 2018 he became the Deputy Director of the Centre for Evolution and Cancer and then the Director in 2020.
He authored several studies published in prestigious scientific journals, including Science, Nature, Nature Genetics and Cancer Discovery. Among his articles are “The co-evolution of the genome and epigenome in colorectal cancer” (Nature, 2022), “Phenotypic plasticity and genetic control in colorectal cancer evolution” (Nature, 2022), “Subclonal reconstruction of tumors by using machine learning and population genetics” (Nature Genetics, 2020), “Detecting repeated cancer evolution from multi-region tumor sequencing data” (Nature Methods, 2018), “Longitudinal liquid biopsy and mathematical modelling of clonal evolution forecast waiting time to treatment failure in a phase II colorectal cancer clinical trial” (Cancer Discovery, 2018), and “Patient-derived organoids model treatment response of metastatic gastrointestinal cancers” (Science, 2018).
In 2016 he was awarded the Cancer Research UK Future Leaders in Cancer Research prize.
03/2023 - Nature Genetics
In cancer, evolutionary forces select for clones that evade the immune system. Here we analyzed >10,000 primary tumors and 356 immune-checkpoint-treated metastases using immune dN/dS, the ratio of nonsynonymous to synonymous mutations in the immunopeptidome, to measure immune selection in cohorts and individuals. We classified tumors as immune edited when antigenic mutations were removed by […]
10/2022 - Nature
Genetic and epigenetic variation, together with transcriptional plasticity, contribute to intratumour heterogeneity1. The interplay of these biological processes and their respective contributions to tumour evolution remain unknown. Here we show that intratumour genetic ancestry only infrequently affects gene expression traits and subclonal evolution in colorectal cancer (CRC). Using spatially resolved paired whole-genome and transcriptome sequencing, […]
10/2022 - Nature
Colorectal malignancies are a leading cause of cancer-related death1 and have undergone extensive genomic study2,3. However, DNA mutations alone do not fully explain malignant transformation4,5,6,7. Here we investigate the co-evolution of the genome and epigenome of colorectal tumours at single-clone resolution using spatial multi-omic profiling of individual glands. We collected 1,370 samples from 30 primary cancers and […]
08/2022 - Cell Reports
Quantification of spatial subclonal interactions enhancing the invasive phenotype of pediatric glioma
Diffuse midline gliomas (DMGs) are highly aggressive, incurable childhood brain tumors. They present a clinical challenge due to many factors, including heterogeneity and diffuse infiltration, complicating disease management. Recent studies have described the existence of subclonal populations that may co-operate to drive pro-tumorigenic processes such as cellular invasion. However, a precise quantification of subclonal interactions […]
10/2020 - Nature Genetics
Cancers accumulate mutations that lead to neoantigens, novel peptides that elicit an immune response, and consequently undergo evolutionary selection. Here we establish how negative selection shapes the clonality of neoantigens in a growing cancer by constructing a mathematical model of neoantigen evolution. The model predicts that, without immune escape, tumor neoantigens are either clonal or […]