Latest PRC2 Stories
Although doctors have long known that people with Down syndrome have a heightened risk of developing acute lymphoblastic leukemia (ALL) during childhood, they haven't been able to explain why.
A decade ago, gene expression seemed so straightforward: genes were either switched on or off.
Most cancer treatments are blunt. In an attempt to eradicate tumors, oncologists often turn to radiation or chemotherapy, which can damage healthy tissue along with the cancerous growths.
A single embryonic stem cell can develop into more than 200 specialized cell types that make up our body.
The first detailed and complete picture of a protein complex that is tied to human birth defects as well as the progression of many forms of cancer has been obtained by an international team of researchers led by scientists with the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab).
Historically, fly and human Polycomb proteins were considered textbook exemplars of transcriptional repressors, or proteins that silence the process by which DNA gives rise to new proteins.
Scientists at Cold Spring Harbor Laboratory have identified a candidate drug target for treating acute myeloid leukemia (AML), a white blood cell cancer that proliferates out of control in the bone marrow.
A new study published in the journal Nature Medicine by NYU Cancer Institute researchers, shows how the cancer causing gene Notch, in combination with a mutated Polycomb Repressive Complex 2 (PRC2) protein complex, work together to cause T- cell acute lymphoblastic leukemia (T-ALL).
The mechanism by which 'polycomb' proteins critical for embyronic stem cell function and fate are targeted to DNA has been identified by UCL scientists.
Like a child awaiting the arrival of Christmas, embryonic stem cells exist in a state of permanent anticipation.