DNA replication stress: a source of APOBEC3B expression in breast cancer

David W Cescon; Benjamin Haibe-Kains

doi:10.1186/s13059-016-1069-y

DNA replication stress: a source of APOBEC3B expression in breast cancer

Genome Biol. 2016 Sep 30;17(1):202. doi: 10.1186/s13059-016-1069-y.

Authors

David W Cescon^{1

2

3}, Benjamin Haibe-Kains^{4

5

6

7}

Affiliations

¹ Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. dave.cescon@uhn.ca.
² Campbell Family Institute for Breast Cancer Research, Toronto, Canada. dave.cescon@uhn.ca.
³ Division of Medical Oncology and Hematology, Department of Medicine, University of Toronto, Toronto, Canada. dave.cescon@uhn.ca.
⁴ Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. bhaibeka@uhnresearch.ca.
⁵ Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada. bhaibeka@uhnresearch.ca.
⁶ Department of Computer Science, University of Toronto, Toronto, ON, Canada. bhaibeka@uhnresearch.ca.
⁷ Ontario Institute of Cancer Research, Toronto, ON, Canada. bhaibeka@uhnresearch.ca.

Abstract

APOBEC cytidine deaminases have been implicated as major contributors to the mutation burden in many cancers on the basis of their mutational signature. A new experimental study sheds light on the inciting factors, linking APOBEC3B expression to oncogene- and drug-induced replication stress.

Publication types

Review
Research Support, Non-U.S. Gov't
Comment

MeSH terms

Breast Neoplasms / etiology*
Breast Neoplasms / metabolism*
Cytidine Deaminase / genetics
Cytidine Deaminase / metabolism
DNA Replication*
Female
Gene Expression Regulation, Neoplastic
Genetic Predisposition to Disease
Genome, Human
Genomics
Humans
Minor Histocompatibility Antigens / genetics
Minor Histocompatibility Antigens / metabolism
Multigene Family
Signal Transduction
Stress, Physiological*

Substances

Minor Histocompatibility Antigens
APOBEC3B protein, human
Cytidine Deaminase

Grants and funding

CIHR/Canada