||May 15, 2009
BIOLOGY: Random Resistance
Researchers led by Peter Sorger have discovered that the genetic
identity of a tumor cell is an incomplete predictor of how it will respond to
treatment. In the case of a new and highly touted cancer therapy, genetically
identical cancer cells responded differently. These variations apparently resulted
from random cell-to-cell differences, such as in the number of protein copies
each cell had at the time of treatment. The study appeared online April 12 in Nature.
CENTRAL: Quick Emergency Response Casts Light on Science of Detection,
Prevention and Control
The local emergence of H1N1 (swine) influenza focuses acute public
attention on the issues and questions that preoccupy many scientists
and public health practitioners in the Harvard community every day.
They work under the pressure of knowing that the world is overdue for
a virulent flu that spreads to every continent. The researchers study
emerging infectious diseases at all levels, from molecules to global
disease patterns, for improving prevention, detection, treatment, and
emergency response strategies.
Covering Your Bases
If genetics deals with the information that cells need to operate,
epigenetics involves the information packaging. Both of these systems
play an essential role in cell behavior; a breakdown in either may
tip a cell toward disease. Understanding the regulation of epigenetic
modifications is a major challenge for biomedical researchers. One
such modification is the addition of methyl groups to the DNA strand.
The enzymes that add the methyl groups are known, but those that remove
them have been elusive. Now research teams in the labs of Anjana Rao
and David Liu, along with other colleagues, have found an enzyme that
modifies methylated DNA. The researchers hope that the findings, published
in the April 16 Science, will provide insight into how the
methyl groups on DNA are removed. In the picture are (clockwise from
left) Rao, Yinghua Shen, Liu, Kian Koh, and Mamta Tahiliani.