User profiles for "author:Steven A Roberts"

Steven A. Roberts

University of Vermont
Verified email at med.uvm.edu
Cited by 20516

Hypermutation in human cancer genomes: footprints and mechanisms

SA Roberts, DA Gordenin - Nature Reviews Cancer, 2014 - nature.com
A role for somatic mutations in carcinogenesis is well accepted, but the degree to which
mutation rates influence cancer initiation and development is under continuous debate …

Mutational heterogeneity in cancer and the search for new cancer-associated genes

MS Lawrence, P Stojanov, P Polak, GV Kryukov… - Nature, 2013 - nature.com
Major international projects are underway that are aimed at creating a comprehensive
catalogue of all the genes responsible for the initiation and progression of cancer …

An APOBEC cytidine deaminase mutagenesis pattern is widespread in human cancers

SA Roberts, MS Lawrence, LJ Klimczak, SA Grimm… - Nature …, 2013 - nature.com
Recent studies indicate that a subclass of APOBEC cytidine deaminases, which convert
cytosine to uracil during RNA editing and retrovirus or retrotransposon restriction, may …

APOBEC-induced mutagenesis in cancer

TM Mertz, CD Collins, M Dennis… - Annual Review of …, 2022 - annualreviews.org
The initiation, progression, and relapse of cancers often result from mutations occurring
within somatic cells. Consequently, processes that elevate mutation rates accelerate …

UV‐induced DNA damage and mutagenesis in chromatin

P Mao, JJ Wyrick, SA Roberts… - Photochemistry and …, 2017 - Wiley Online Library
UV radiation induces photolesions that distort the DNA double helix and, if not repaired, can
cause severe biological consequences, including mutagenesis or cell death. In eukaryotes …

[PDF][PDF] Clustered mutations in yeast and in human cancers can arise from damaged long single-strand DNA regions

SA Roberts, J Sterling, C Thompson, S Harris, D Mav… - Molecular cell, 2012 - cell.com
Mutations are typically perceived as random, independent events. We describe here
nonrandom clustered mutations in yeast and in human cancers. Genome sequencing of …

An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers

K Chan, SA Roberts, LJ Klimczak, JF Sterling, N Saini… - Nature …, 2015 - nature.com
Elucidation of mutagenic processes shaping cancer genomes is a fundamental problem
whose solution promises insights into new treatment, diagnostic and prevention strategies …

[PDF][PDF] Essential roles for polymerase θ-mediated end joining in the repair of chromosome breaks

DW Wyatt, W Feng, MP Conlin, MJ Yousefzadeh… - Molecular cell, 2016 - cell.com
DNA polymerase theta (Pol θ)-mediated end joining (TMEJ) has been implicated in the
repair of chromosome breaks, but its cellular mechanism and role relative to canonical …

Ku is a 5′-dRP/AP lyase that excises nucleotide damage near broken ends

SA Roberts, N Strande, MD Burkhalter, C Strom… - Nature, 2010 - nature.com
Mammalian cells require non-homologous end joining (NHEJ) for the efficient repair of
chromosomal DNA double-strand breaks. A key feature of biological sources of strand …

[PDF][PDF] APOBEC3A and APOBEC3B preferentially deaminate the lagging strand template during DNA replication

JI Hoopes, LM Cortez, TM Mertz, EP Malc… - Cell reports, 2016 - cell.com
APOBEC family cytidine deaminases have recently been implicated as powerful mutators of
cancer genomes. How APOBECs, which are ssDNA-specific enzymes, gain access to …