Results 31 to 40 of about 93,358 (167)
KMT2C-deficient tumors have elevated APOBEC mutagenesis and genomic instability in multiple cancers. [PDF]
Abstract The histone methyltransferase KMT2C is among the most frequently mutated epigenetic modifier genes in cancer and plays an essential role in MRE11-dependent DNA replication fork restart. However, the effects of KMT2C deficiency on genomic instability during tumorigenesis are unclear. Analyzing 9,663 tumors from 30 cancer cohorts,
Hu X, Biswas A, De S.
europepmc +3 more sources
Guardian ubiquitin E3 ligases target cancer-associated APOBEC3 deaminases for degradation to promote human genome integrity [PDF]
APOBEC family members play crucial roles in antiviral restriction. However, certain APOBEC3 (A3) proteins drive harmful hypermutation in humans, contributing to cancer.
Irene Schwartz +14 more
doaj +2 more sources
Spatial genomic diversity associated with APOBEC mutagenesis in squamous cell carcinoma arising from ovarian teratoma. [PDF]
AbstractAlthough the gross and microscopic features of squamous cell carcinoma arising from ovarian mature cystic teratoma (MCT‐SCC) vary from case to case, the spatial spreading of genomic alterations within the tumor remains unclear. To clarify the spatial genomic diversity in MCT‐SCCs, we performed whole‐exome sequencing by collecting 16 samples ...
Tamura R +8 more
europepmc +3 more sources
Whole-genome mapping of APOBEC mutagenesis in metastatic urothelial carcinoma identifies driver hotspot mutations and a novel mutational signature [PDF]
John W Martens +2 more
exaly +2 more sources
Background APOBEC-driven mutagenesis and functional positive selection of mutated genes may synergistically drive the higher frequency of some hotspot driver mutations compared to other mutations within the same gene, as we reported for FGFR3 S249C. Only
Ming-Jun Shi +5 more
doaj +1 more source
PrimPol prevents APOBEC/AID family mediated DNA mutagenesis [PDF]
PrimPol is a DNA damage tolerant polymerase displaying both translesion synthesis (TLS) and (re)-priming properties. This led us to study the consequences of a PrimPol deficiency in tolerating mutagenic lesions induced by members of the APOBEC/AID family of cytosine deaminases.
Pilzecker, Bas +6 more
openaire +2 more sources
BACKGROUND: The rationale for ethnic differences in bladder cancer (BCa) susceptibility is an important open question. In this study, we raised the hypothesis that the APOBEC3-rs1014971 variant associated with BCa risk and APOBEC-mutagenesis probably ...
Xiang-Yu Meng +3 more
doaj +1 more source
Somatic mutations accumulate over time in cancer cells as a consequence of mutational processes. However, the role of mutational processes in carcinogenesis remains poorly understood.
Zedong Jiang +14 more
doaj +1 more source
The Role of APOBECs in Viral Replication
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) proteins are a diverse and evolutionarily conserved family of cytidine deaminases that provide a variety of functions from tissue-specific gene expression and immunoglobulin ...
Wendy Kaichun Xu +2 more
doaj +1 more source
AID/APOBEC–dependent somatic hypermutation and DNA rearrangements of immunoglobulin and non-immunoglobulin genes [PDF]
Editing Ig genes by activation induced deaminase (AID) initiates the antibody diversification process in B lymphocytes. In mammalian B cells, this process includes somatic hypermutation (SHM) and class switch recombination (CSR).
Kolotova T. +3 more
doaj +3 more sources

