Results 41 to 50 of about 93,358 (167)

APOBEC3A is a prominent cytidine deaminase in breast cancer.

open access: yesPLoS Genetics, 2019
APOBEC cytidine deaminases are the second-most prominent source of mutagenesis in sequenced tumors. Previous studies have proposed that APOBEC3B (A3B) is the major source of mutagenesis in breast cancer (BRCA).
Luis M Cortez   +7 more
doaj   +1 more source

Mutational signatures reveal ternary relationships between homologous recombination repair, APOBEC, and mismatch repair in gynecological cancers

open access: yesJournal of Translational Medicine, 2022
Background Revealing the impacts of endogenous and exogenous mutagenesis processes is essential for understanding the etiology of somatic genomic alterations and designing precise prognostication and treatment strategies for cancer. DNA repair deficiency
Amir Farmanbar   +3 more
doaj   +1 more source

Targeting natural splicing plasticity of APOBEC3B restricts its expression and mutagenic activity

open access: yesCommunications Biology, 2021
A. Rouf Banday et al. report targeting alternative splicing of APOBEC3B as a strategy to modulate APOBEC-mediated mutagenesis in cancers. Higher expression of the mutagenic APOBEC3B isoform predicted shorter progression-free survival in bladder cancer ...
A. Rouf Banday   +12 more
doaj   +1 more source

KMT2C deficiency promotes APOBEC mutagenesis and genomic instability in multiple cancers [PDF]

open access: yes, 2022
Histone methyltransferase KMT2C is among the frequently mutated epigenetic modifier genes in cancer. It has additional roles in DNA replication, but the effects of KMT2C deficiency on genomic instability during tumorigenesis are unclear. Analyzing 9,663 tumors from 30 cohorts, we report that KMT2C mutant tumors have a significant excess of APOBEC ...
Xiaoju Hu, Antara Biswas, Subhajyoti De
openaire   +1 more source

Perspective: APOBEC mutagenesis in drug resistance and immune escape in HIV and cancer evolution

open access: yes, 2021
The apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC) mutational signature has only recently been detected in a multitude of cancers through next-generation sequencing. In contrast, APOBEC has been a focus of virology research for
J Bartek (11283483)   +8 more
core   +1 more source

The Mutation Profile of SARS-CoV-2 Is Primarily Shaped by the Host Antiviral Defense

open access: yesViruses, 2021
Understanding SARS-CoV-2 evolution is a fundamental effort in coping with the COVID-19 pandemic. The virus genomes have been broadly evolving due to the high number of infected hosts world-wide.
Cem Azgari   +4 more
doaj   +1 more source

Mutational signatures and their association with survival and gene expression in urological carcinomas

open access: yesNeoplasia: An International Journal for Oncology Research, 2023
Different sources of mutagenesis cause consistently identifiable patterns of mutations and mutational signatures that mirror the various carcinogenetic processes.
Peeter Karihtala   +2 more
doaj   +1 more source

APOBEC-mediated mutagenesis is a favorable predictor of prognosis and immunotherapy for bladder cancer patients: evidence from pan-cancer analysis and multiple databases

open access: yes, 2022
Background: The APOBEC (apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like) family-mediated mutagenesis is widespread in human cancers.
Shu, Yongqian   +32 more
core   +1 more source

An efficient one-step site-directed deletion, insertion, single and multiple-site plasmid mutagenesis protocol [PDF]

open access: yes, 2012
Background: Mutagenesis plays an essential role in molecular biology and biochemistry. It has also been used in enzymology and protein science to generate proteins which are more tractable for biophysical techniques.
Liu, Huanting, Naismith, James Henderson
core   +2 more sources

Repair of multiple simultaneous double-strand breaks causes bursts of genome-wide clustered hypermutation.

open access: yesPLoS Biology, 2019
A single cancer genome can harbor thousands of clustered mutations. Mutation signature analyses have revealed that the origin of clusters are lesions in long tracts of single-stranded (ss) DNA damaged by apolipoprotein B mRNA editing enzyme, catalytic ...
Cynthia J Sakofsky   +8 more
doaj   +1 more source

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