Prostate cancer is a common malignancy with a heterogeneous disease course. Prior studies have identified a paucity of point mutations in protein-coding genes and only a few clinically relevant driver alterations. Here, using the Pan Prostate Cancer Group whole genome sequencing dataset from 1001 men, we perform an int...
D. Pellegrina, Daria Kiriy, Kevin C. L. Cheng et al.· Nature Communications· 1 citation
The inactivation of tumour suppressor genes is a key step in cancer development, and is usually achieved by homozygous loss. In prostate cancer, however, large genomic regions are often hemizygously lost, which complicates the identification of putative tumour suppressors in these regions. Here, we develop Epi2Hit, an...
Daria Kiriy, F. Favero, C. Gerhäuser et al.· Nature Communications· 1 citation
Inflammation accelerates evolutionary dynamics of hematopoietic stem cells (HSCs) in clonal hematopoiesis and myeloid neoplasms. We studied HSCs, progenitors and immune cells from patients with myeloproliferative neoplasms at baseline and following interferon-α (IFNα) treatment, the only therapy to deplete mutated stem...
Prostate cancer follows a long and heterogeneous disease course with incompletely understood aetiology1. Here we dissect the mutational processes shaping the genomes of 959 donors from the Pan Prostate Cancer Group and assess their clinical relevance. By integrating de novo extracted single-base substitution, insertion...
A. Gruber, A. Olsen, Bárbara Hernando et al.· Nature· 2 citations
It is shown that common germline polymorphisms and cancer-associated somatic SNVs recur at identical genomic positions across the human genome, sharing the same nucleotide substitutions more frequently than expected by chance.
Thais Silva Tavares, Daniela Souza Lima Barbosa, R. P. de Souza et al.· bioRxiv· 0 citations
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