APOBEC-Induced Mutagenesis in Cancer.

The initiation, progression, and relapse of cancers often result from mutations occurring within somatic cells. Consequently, processes that elevate mutation rates accelerate carcinogenesis and hinder the development of long-lasting therapeutics. Recent sequencing of human cancer genomes has identified patterns of mutations, termed mutation signatures, many of which correspond to specific environmentally induced and endogenous mutation processes.

Single-stranded DNA binding proteins influence APOBEC3A substrate preference.

The cytidine deaminase, APOBEC3A (A3A), is a prominent source of mutations in multiple cancer types. These APOBEC-signature mutations are non-uniformly distributed across cancer genomes, associating with single-stranded (ss) DNA formed during DNA replication and hairpin-forming sequences. The biochemical and cellular factors that influence these specificities are unclear.

APOBEC3A is a prominent cytidine deaminase in breast cancer.

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). We show that APOBEC3A (A3A) is the only APOBEC whose expression correlates with APOBEC-induced mutation load and that A3A expression is responsible for cytidine deamination in multiple BRCA cell lines.

Model intercomparison for the uptake of organic chemicals by plants.

Currently, a variety of models are available for predicting the uptake, translocation, and elimination of organic contaminants by plants. These models range from simple deterministic risk assessment screening tools to more complex models that consider physical, chemical, and biological processes in a mechanistic manner. This study evaluates the performance of a range of such models and model types against experimental data sets.