This author interview is by Dr Bernard Friedenson, of University of Illinois. Dr Friedenson's full paper, Many Breast Cancer Mutations Parallel Mutations in Known Viral Cancers, is available for download in Journal of Genomes and Exomes.

Please summarise for readers the content of your article
Infections play a larger role in breast and in other cancers than we previously thought. Gaps in immunity or in infection barriers caused by distinct individual sets of gene mutations make cancer cells more susceptible than normal cells to infections that can exploit cancer mutations. The effect is different in different cancers and explains why it has been so difficult to pin down a specific virus as a cause of breast cancer. The findings can form the basis for a new generation of cancer therapy.

How did you come to be involved in your area of study?
My father died from cancer after a long and terrible struggle.

What was previously known about the topic of your article?
Cancer was thought to develop because of mutations in 2-8 driver genes, with >99.9% of mutations being irrelevant passengers. Immune deficiencies have long been associated with cancer but how this related to the 2-8 driver genes was never clear. The understanding was so poor that immune deficiency models were thought to be weak because people taking antibiotics still got cancer.

How has your work in this area advanced understanding of the topic?
Gaps in immunity or in infection barriers caused by distinct individual sets of mutations make cancer cells more susceptible than normal cells to infections that can exploit the mutations. Some branches of the immune system still function normally. Acquired deficits in immunity may be a lurking variable that explains why some studies find associations between cancer and a given viral infection while other studies do not. The work forms the basis of a new model for cancer based firmly on genomic evidence. Many mutations that were previously discarded as mere passengers in the cancer process actually set the stage for infections that can exploit the mutations. These infections may well cause cancer. The greater ease of infecting cancer cells may be used to specifically destroy them while leaving normal cells intact.

What do you regard as being the most important aspect of the results reported in the article?
In several examples thus far, genomic evidence can be used to suggest effective therapy and predict an individual patient's response. This may foretell new and more rational cancer therapy.

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