Clinical and laboratory studies over recent decades have established branched evolution as
a feature of cancer. However, while grounded in somatic selection, several lines of evidence …

Decades of research into the molecular mechanisms of cancer and the development of
novel therapeutics have yielded a number of remarkable successes. However, our ability to …

Tumor mutational burden and heterogeneity has been suggested to fuel resistance to many
targeted therapies. The cytosine deaminase APOBEC proteins have been implicated in the …

APOBEC3 enzymes are cytosine deaminases implicated in cancer. Precisely when
APOBEC3 expression is induced during cancer development remains to be defined. Here …

Mutations in oncogenes such as KRAS and EGFR cause a high proportion of lung cancers.
Drugs targeting these proteins cause tumor regression but ultimately fail to elicit cures. As a …

Abstract Cytotoxic chemo-, radio-, and targeted therapies frequently elicit apoptotic cancer
cell death. Mitochondrial outer membrane permeabilization (MOMP) is a critical, regulated …

Background Studies of targeted therapy resistance in lung cancer have primarily focused on
single-gene alterations. Based on prior work implicating apolipoprotein b mRNA-editing …

Aims Primary head/neck mucosal melanomas (MMs) are rare and exhibit aggressive
biologic behaviour and elevated mutational loads. The molecular mechanisms responsible …

APOBEC mutagenesis is one of the most common endogenous sources of mutations in
human cancer and is a major source of genetic intratumor heterogeneity. High levels of …

The APOBEC3 family of cytidine deaminases is widely speculated to be a major source of
somatic mutations in cancer–. However, causal links between APOBEC3 enzymes and …