Percentage of Cancers Linked to Viruses Potentially Overestimated
The results of a large-scale analysis of the association between DNA viruses and human malignancies suggest that many of the most common cancers are not associated with DNA viruses. The findings, published in the August issue of the Journal of Virology, challenge earlier studies suggesting that as high as 40% of tumors are caused by viruses.
For years scientists believed viruses played a role in the development of maybe 10% to 20% of cancers. In 2011, scientists at the Karolinska Institute in Sweden identified potential viral links to several cancers not previously associated with viruses, including brain tumors and prostate cancer, suggesting the real number could be as high as 40%. Since then, researchers have been working hard to find more associations, in part because viruses could provide targets for vaccines to prevent or cure these cancers.
Lower Percentage of Tumors Associated With Viruses
To better understand the role of DNA viruses in human cancers, researchers from the The University of Texas MD Anderson Cancer Center in Houston sequenced RNA from 3,775 malignant tumor samples from The Cancer Genome Atlas and then applied a robust bioinformatics algorithm to survey them for the presence of viral transcripts.
Those cancers not associated with DNA viruses included acute myeloid leukemia, cutaneous melanoma, low- and high-grade gliomas of the brain, and adenocarcinomas of the breast, colon, rectum, lung, prostate, ovaries, kidneys, and thyroid.
The findings suggest the estimate that 40% of tumors are virus-related “should be much lower,” said study author Xiaoping Su, PhD, Associate Professor of Bioinformatics and Computational Biology at MD Anderson.
“The search for virus associations in these malignancies has consumed the efforts of many investigators,” said Dr. Su, implying that this large-scale effort will spare researchers fruitless investigations.
Findings May Lead to Targeted Treatments
The study also provides the framework for understanding how viruses integrate into cancer subtypes such as hepatocellular cancer, said Dr. Su. That might make it possible to personalize treatments by targeting genes that are located within known integration sites and that might be drivers of cancer initiation and progression. A key finding was that there are specific sites where viruses integrate into the host genome prior to initiating cancer, and that these sites are frequently located within particular host genes.
“This study highlights the importance of bioinformatics in defining the landscape of virus integration across cancer subtypes,” said Dr. Su.
The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.
