October is Breast Cancer Awareness Month in Canada. As part of our commitment to open science, JMIR Publications is highlighting research published in our journals aimed at understanding and combating this disease. Globally, more than 2.3 million women were diagnosed with breast cancer in 2022 1, underscoring the vital need for research into the disease's causes. We hope this research reaches a wide audience, empowering people to learn more about their risk and risk mitigation strategies.
The precise causes of breast cancer remain a central mystery in breast cancer research, making prevention and treatment difficult. A new study highlights an unlikely suspect: the Epstein-Barr virus (EBV).
Dr. Bernie Friedenson, an Associate Professor in the Department of Biochemistry and Molecular Genetics at UIC in Chicago, recently published a paper in JMIRx Med exploring the link between human breast cancer and EBV. This virus, which nearly everyone acquires at some point in their lives, provides no known benefit to the host and is notorious for exploiting weaknesses in the immune system.
While EBV infection is ubiquitous, it’s rarely and inconsistently found in breast tumors. However, previous work suggests that it may cause such severe, permanent damage to human chromosomes that breast cancer develops even if the virus disappears. The question then becomes: can we identify the characteristic genetic damage that EBV leaves behind?
Dr. Friedenson's study tested the hypothesis that EBV infection may predispose someone to breast cancer by causing permanent damage that compromises cells’ natural cancer safeguards. He compared publicly available genome data from approximately 2100 breast cancers and 25 ovarian cancers to cancers with proven EBV associations, such as Burkitt lymphomas and nasopharyngeal cancers.
The findings provided compelling evidence supporting the hypothesis. The study showed that chromosome breakpoints (sites of damage) in breast cancer clustered around the breakpoints found in known EBV-associated cancers. In fact, on some chromosomes, the distribution of breakpoints in breast cancer was statistically indistinguishable from those in EBV-associated cancers.
This damage wasn't random; the breakpoint clusters occurred in high-risk and sporadic breast cancer subgroups and disrupted gene functions essential for cancer protection. The analyses also found evidence of EBV genome fragments regularly interspersed between key genes, acting as "CRISPR-like reminders" of past infection. This damage effectively pushes the cancer toward metastasis and favors the survival of those metastatic cells. By identifying this pathogenic viral damage, this research opens up important new avenues for screening, treatment, and prevention.
Dr. Friedenson described the experience of publishing this work in the JMIRx Med as "absolutely wonderful." He noted that the journal added "a great deal of value and clarity" to the paper, a crucial factor when presenting highly technical, interdisciplinary findings. The positive experience reinforces his plan to submit a follow-up paper to the journal, which he believes will make these conclusions "even stronger and even more robust." The implications are profound: immunizing children against EBV could potentially protect not only against other cancers, but against breast and ovarian cancers, too.
To learn more about the critical link between the Epstein-Barr virus and breast cancer development, watch the video with Dr. Bernie Friedenson and read the full research article to explore the detailed genome analysis.To further explore breast cancer prevention and detection guidelines, please visit the Canadian Cancer Society's official resources.
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