Cytomegalovirus and Epstein-Barr virus in breast cancer

• Published in: PloS one Vol. 10; no. 2; p. e0118989
• Main Authors: Richardson, Ann K, Currie, Margaret J, Robinson, Bridget A, Morrin, Helen, Phung, Yen, Pearson, John F, Anderson, Trevor P, Potter, John D, Walker, Logan C
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 27.02.2015; Public Library of Science (PLoS)
• Subjects: Adult; Aged; Aged, 80 and over; Antibodies, Viral - blood; Breast cancer; Breast Neoplasms - virology; Cancer; Carcinoma - virology; Cytomegalovirus; Cytomegalovirus - immunology; Cytomegalovirus - isolation & purification; Cytomegalovirus infections; Epstein-Barr virus; Female; Health risk assessment; Health risks; Herpesvirus 4, Human - immunology; Herpesvirus 4, Human - isolation & purification; Humans; Immunoglobulin G; Immunoglobulin G - blood; Meta-analysis; Middle Aged; Molecular chains; Polymerase chain reaction; Serology; Tumorigenesis; Tumors; Viruses; Womens health; New Zealand; United States > US
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0118989

Findings of polymerase chain reaction (PCR) studies of cytomegalovirus (CMV) and Epstein-Barr virus (EBV) and breast cancer vary, making it difficult to determine whether either, both, or neither virus is causally associated with breast cancer. We investigated CMV and EBV in paired samples of breast cancer and normal breast tissue from 70 women using quantitative PCR. A serum sample from each woman was tested for CMV and EBV IgG. To place our results in context, we reviewed the existing literature and performed a meta-analysis of our results together with previous PCR studies of EBV, CMV, and breast cancer. Of the serology samples, 67 of 70 (96%) were EBV IgG positive and 49 of 70 (70%) were CMV IgG positive. QPCR detected EBV in 24 (34%) of the tumour and 9 (13%) of the paired normal specimens and CMV in 0 (0%) of the tumour and 2 (3%) of the paired normal specimens. Our findings, together with earlier results summarised in the meta-analysis, suggest several possibilities: variable findings may be due to limitations of molecular analyses; 'hit and run' oncogenesis may lead to inconsistent results; one or both viruses has a role at a later stage in breast cancer development; infection with multiple viruses increases breast cancer risk; or neither virus has a role. Future studies should focus on ways to investigate these possibilities, and should include comparisons of breast cancer tissue samples with appropriate normal tissue samples.