Genetic mutations kick start cancers. Some mutations shuffle the genetic code, others come from the deletion of key genes.
At La Jolla Institute for Immunology (LJI), researchers have made a major breakthrough in understanding how deletion of the genes that encode TET proteins can lead to cancer growth. Their new study, published in Nature Communications, is the first to show the immediate consequences of deleting all three genes from the TET family in mouse embryonic stem cells.
By using this mouse model, the researchers discovered that TET proteins are critical for keeping the process of cell and DNA replication running smoothly. Without TET proteins, important genes go missing, leading to the mutations, or aneuploidies (an-new-ploy-dees).
Aneuploidies are cases where genetic material is added or deleted on a massive scale. Cells with aneuploidies aren’t just missing a gene. Instead, genes go missing across an entire chromosome. “Aneuploidies are a common feature of cancer cells,” says LJI Postdoctoral Researcher Hugo Sepulveda, Ph.D.
Uncovering this direct connection between TET loss of function and aneuploidies is a major discovery in the field of cell biology, and it gives researchers a clue to how to find genes that underpin cancer development. “We can now understand the mechanisms behind aneuploidy development, although we can’t say these changes always happen through the same genes in other cell types,” says LJI Postdoctoral Researcher Hugo Sepulveda, Ph.D.
Sepulveda co-led the research with former LJI postdoctoral researcher Romain Georges, Ph.D., who generated the mouse model and derived the stem cells for the project. LJI Professor Anjana Rao, Ph.D., served as the study’s senior author.
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