Jan Karlseder studies the role of telomeres throughout a cell’s proliferative cycle—from the time the cell starts copying its genetic material to the time it divides into two new cells, as well as throughout the cell’s life—from when a young cell emerges through cell division to when an old cell permanently “retires” (becomes senescent) or dies.
Cell division limits, such as the ones set by telomere shortening, are essential to restrict uncontrolled cell division and thereby to prevent cancer formation. The two fundamental limits preventing primary human cells from becoming cancerous are: replicative senescence, a kind of cellular retirement in which cells stop dividing, and crisis, a state that leads to cell death. While these boundaries had been recognized for decades, it remained unclear how cells become senescent and what happens as cells keep dividing when they should senesce.
By discovering and clearly defining the mechanisms regulating cell division of primary human cells (cells taken from living tissue such as a biopsy), the Karlseder lab has exposed novel pathways during the earliest stages of cancer formation, which may yield potential interventions.