Results 31 to 40 of about 93,358 (167)

KMT2C-deficient tumors have elevated APOBEC mutagenesis and genomic instability in multiple cancers. [PDF]

open access: yesNAR Cancer, 2022
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]

open access: yesNature Communications
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]

open access: yesCancer Sci, 2023
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

Identification of new driver and passenger mutations within APOBEC-induced hotspot mutations in bladder cancer

open access: yesGenome Medicine, 2020
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]

open access: yesNucleic Acids Research, 2016
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

Historical Pathogen-Driven Selection May Contribute to Contemporary Ethnic Difference in Bladder Cancer Susceptibility

open access: yesBladder Cancer, 2023
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

Analysis of Mutations and Dysregulated Pathways Unravels Carcinogenic Effect and Clinical Actionability of Mutational Processes

open access: yesFrontiers in Cell and Developmental Biology, 2021
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

open access: yesMicroorganisms, 2020
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]

open access: yesAnnals of Mechnikov's Institute, 2019
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

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