Somatic mutations and clonal dynamics in healthy and cirrhotic human liver

These are mutation calls to support the paper 'Somatic mutations and clonal dynamics in healthy and cirrhotic human liver', which has the following authors and affiliations:
Simon F Brunner (1); Nicola D Roberts (1); Luke A Wylie (1); Luiza Moore (1); Sarah J Aitken (2,3); Susan E Davies (3); Mathijs A Sanders (1,4); Pete Ellis (1); Chris Alder (1); Yvette Hooks (1); Federico Abascal (1); Michael R Stratton (1); Inigo Martincorena (1); Matthew Hoare (2,5) *; Peter J Campbell (1,6) *.

* Co-corresponding authors

Institutes:
(1) Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, CB10 1SA, UK
(2) CRUK Cambridge Institute, Robinson Way, Cambridge, CB2 0RE, UK
(3) Department of Pathology, University of Cambridge, Addenbrooke’s Hospital, Cambridge, CB2 0QQ, UK
(4) Department of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands
(5) Department of Medicine, University of Cambridge, Addenbrooke’s Hospital, Cambridge, CB2 0QQ, UK
(6) Department of Haematology and Stem Cell Institute, University of Cambridge, Hills Rd, Cambridge CB2 0XY, UK

Description of data
The data are SNVs and indels called in 482 microdissections of healthy and cirrhotic liver tissue across 14 subjects, together with 7 matched synchronous hepatocellular carcinomas. The columns in the table are interpreted as follows:
donor: ID for the patient from which the liver biopsy was taken,
sample: ID for the specific microdissection within that donor (multiple microdissections were taken from each liver biopsy),
is_cancer: Indicator variable for whether the sample was a cancer (1) or healthy / cirrhotic hepatocytes (0),
clust_id: Which branch on the phylogenetic tree the mutation was assigned to,
chrom: Chromosome the mutation was located on,
pos: Genomic position on the chromosome for the mutation (genome build GRCh37d5),
ref: The reference base at that position,
alt: The alternate allele created by the mutation,
type: Whether the mutation was a substitution (sub), insertion (ins), deletion (del) or complex indel,
vaf: Variant allele fraction of the mutation,
effect: Predicted consequence of the mutation.