Transposable elements (TEs) make up 50% of the human genome but are referred to as "genomic dark matter" or "junk DNA" and often ignored in genomic medicine - both because they have been presumed to be unimportant and because their high copy number and variability pose unique technical challenges. Neither impediment now seems steadfast. Interest in the human transposable elements and their role in cancer has never been greater, and methods enabling its study are maturing at a fast pace.
Transposable elements directly contribute to cancer through both genetic and epigenetic mechanisms. De novo transposon insertions are known to disrupt important genes and gene regulatory elements and result in tumorigenesis. Epigenetically reactivated transposable elements can become cryptic promoters and enhancers and lead to abnormal gene activities including up-regulating oncogenes. These recent mounting evidences request a full understanding of the contribution of transposable elements to cancer.
On the other hand, transposable elements are a double-edged sword. Recent discoveries reveal that epigenetically reactivated transposable elements can produce cancer specific products including immunogenic antigens and double stranded RNAs, which result in an innate immune response. These findings together with rapid development of immunotherapies open new avenues for cancer treatment.
This meeting will be chaired by Kathleen H. Burns, MD, PhD of Dana-Farber Cancer Institute Ting Wang, PhD of Washington University
register today!Transposable elements (TEs) make up 50% of the human genome but are referred to as "genomic dark matter" or "junk DNA" and often ignored in genomic medicine - both because they have been presumed to be unimportant and because their high copy number and variability pose unique technical challenges. Neither impediment now seems steadfast. Interest in the human transposable elements and their role in cancer has never been greater, and methods enabling its study are maturing at a fast pace.
Transposable elements directly contribute to cancer through both genetic and epigenetic mechanisms. De novo transposon insertions are known to disrupt important genes and gene regulatory elements and result in tumorigenesis. Epigenetically reactivated transposable elements can become cryptic promoters and enhancers and lead to abnormal gene activities including up-regulating oncogenes. These recent mounting evidences request a full understanding of the contribution of transposable elements to cancer.
On the other hand, transposable elements are a double-edged sword. Recent discoveries reveal that epigenetically reactivated transposable elements can produce cancer specific products including immunogenic antigens and double stranded RNAs, which result in an innate immune response. These findings together with rapid development of immunotherapies open new avenues for cancer treatment.
This meeting will be chaired by Kathleen H. Burns, MD, PhD of Dana-Farber Cancer Institute Ting Wang, PhD of Washington University
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