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• SNV and indel calls from 8921 individuals in the British Autozygosity Populations BioResource dataset

  This includes variant calls (single nucleotide variants and small insertions/deletions) from 8086 (mostly British Pakistani/British Bangladeshi) individuals from the following studies: 1. 5236 British Pakistani/British Bangladeshi adults from East London Genes and Health (ELGH) 2. 2624 British South Asian mothers from Born in Bradford (mostly Pakistani) (BiB) 3. 1061 British South Asian adults from Birmingham (mostly Pakistani) (Birm) All of the Birmingham and most of the Born in Bradford samples were previously sequenced as part of PMID: 26940866. In the sample list file, the columns of interest to most people will be: vcf.id - sample ID from the vcf cohort - which cohort they're in sex.assigned - sex inferred from coverage on the X and Y chromosomes. Individuals for whom this did not match their reported sex have been discarded total, chrX and chrY - coverage within bait regions across all chromosomes, chrX and chrY respectively Mapping was done with bwa-mem and variant calling was carried out with GATK HaplotypeCaller. We removed variant sites for which the following was true: SNPs: "QD < 2.0 || FS > 30 || MQ < 40.0 || MQRankSum < -12.5 || ReadPosRankSum < -8.0" Indels: "QD < 2.0 || FS > 30 || ReadPosRankSum < -20.0"

  Dataset EGAD00001005469

• THE GENOMIC LANDSCAPE OF ACTINIC KERATOSIS

  Actinic keratoses (AK) are lesions of epidermal keratinocyte dysplasia and are precursors for invasive cutaneous squamous cell carcinoma (CSCC). Identifying the specific genomic alterations driving progression from normal skin-AK-invasive CSCC is challenging due to the massive ultraviolet radiation-induced mutational burden characteristic at all stages of this progression. Here, we report the largest AK whole exome sequencing study to date and perform mutational signature and candidate driver gene analysis on these lesions. We demonstrate in 37 AK, from both immunosuppressed and immunocompetent patients, that there are significant similarities to CSCC in terms of mutational burden, copy number alterations, mutational signatures and patterns of driver gene mutations. We identify 44 significantly mutated AK driver genes and confirm that these genes are similarly altered in CSCC. We identify the azathioprine mutational signature in all AK from patients exposed to the drug, providing further evidence for its role in keratinocyte carcinogenesis. CSCC differ from AK in having higher levels of intra-sample heterogeneity. Alterations in signaling pathways also differ, with immune-related signaling and TGF-β signaling significantly more mutated in CSCC. Integrating our findings with independent gene expression datasets confirms that dysregulated TGF-β signaling may represent an important event in AK-CSCC progression.

  Dataset EGAD00001006894

• A110632A

  Whole genome sequencing for single cells for library A110632A 1151 cells; filetype=bam

  Dataset EGAD00001007094

• A110632B

  Whole genome sequencing for single cells for library A110632B 892 cells; filetype=bam

  Dataset EGAD00001007095

• A118833A

  Whole genome sequencing for single cells for library A118833A 919 cells; filetype=bam

  Dataset EGAD00001007096

• A118833B

  Whole genome sequencing for single cells for library A118833B 1147 cells; filetype=bam

  Dataset EGAD00001007097

• A118845B

  Whole genome sequencing for single cells for library A118845B 1209 cells; filetype=bam

  Dataset EGAD00001007098

• A118869A

  Whole genome sequencing for single cells for library A118869A 1165 cells; filetype=bam

  Dataset EGAD00001007099

• A118869B

  Whole genome sequencing for single cells for library A118869B 1124 cells; filetype=bam

  Dataset EGAD00001007100

• A95626A

  Whole genome sequencing for single cells for library A95626A 1040 cells; filetype=bam

  Dataset EGAD00001007103