NEWS AND MEDIA

April 26, 2018

“Galit Lahav, Harvard Medical School professor of systems biology, will become the new chair of the Department of Systems Biology, effective immediately, Dean George Q. Daley announced in a letter to the HMS community this month.”

Read more from Keven Jiang’s article about Galit’s promotion here.

September 2, 2017

Pulse of Longwood takes you inside one of the nation’s largest hubs of hospitals and biomedical research.

Something unusual just took place at Harvard Medical School: More women than men crossed a stage to join the rank of full professor.

The December ceremony, featuring 22 women, was an anomaly, not a sign of parity. It highlighted how far Harvard has come — and how far it still has to go — as medical schools across the country seek to overcome years of entrenched gender inequality.

Read more

October 8, 2016

Researchers led by members of the Department of Systems Biology at Harvard Medical School had been studying how silencing MDMX, an oncogene, affected the dynamics of p53, a natural tumor suppressor, in cancer cells when they realized those dynamics might affect the cells’ sensitivity to a second, chemotherapy-like treatment.

Live imaging of single cells revealed that time wildly affected cell survival. A short wait between disabling MDMX and administering chemotherapy made the two treatments synergistic, killing cancer cells more effectively than either would have alone, while a longer wait led to treatment resistance, allowing more cancer cells to withstand attack.

“This is the first time someone has shown that timing makes such a big difference in cells’ response to combination therapy,” said Galit Lahav, Professor of Systems Biology at HMS and senior author of the paper, published March 10 in Science. “It’s a first look at how one treatment can change the internal state of individual cells to make them more or less sensitive to a second treatment.”

Read more here

February 2, 2014

For many of people, the concept of mentoring might conjure images of a dyadic, hierarchical relationship between a senior faculty member and a junior faculty member, or between a teacher and student.

When you ask Galit Lahav to contemplate mentoring, she is more likely to envision a collaborative partnership of HMS junior faculty members who provide one another with mutual support and career development guidance.

Such “peer mentoring” has recently gained recognition as a powerful complement to traditional forms of “top-down” mentoring.

Lahav, HMS associate professor of systems biology, was inspired to help create a peer mentoring group as a way of expanding upon positive peer relationships that developed during a two-day leadership workshop offered by the hfp consulting group for HMS quadrangle junior faculty members in 2009.

Read more from the HMS Office of Academic and Clinical Affairs here

November 12, 2013

September 23, 2013

Strike a piano key, and you produce a note. Hit it four times, and you’re playing Beethoven’s Symphony No. 5. Hit it 400 times, and you’re in Philip Glass territory. Cells, too, can play different tunes with the same note, new research suggests, a finding with broad implications for our understanding of biological signaling and potential new therapies.

A damaged cell faces a critical decision: To pause temporarily for DNA repair, or to permanently stop dividing. Research at Harvard Medical School illuminates how the same crucial protein can dynamically trigger either event. The protein, p53, is known as the “guardian of the genome” because it is activated when cells are under stress and prevents damaged cells from growing.

When cells suffer DNA damage, for example (as skin cells do when they are exposed to excessive radiation), the level of p53 is increased. This may cause the cell to delay genetic replication to provide extra time to repair the DNA. Sometimes, however, p53 triggers terminal fates such as cell death or permanent arrest, ending cell division and preventing potentially cancerous growth. The protein is one of the most important natural protections against cancer, and many tumors arise because of mutations in the gene that encodes it.

“Little is known about why some cells recover and grow while others stay arrested,” said Galit Lahav, associate professor of systems biology and senior author on the paper, published June 15 in the journal Science.

Read more from R. Alan Leo’s piece, here

September 2, 2013

January 9, 2013

October 31, 2012

For decades now, the biological community has been focused on the question of how cells transmit information from place to place. It’s a central problem if you want to understand pretty much anything about cell behavior. A signal to grow, for example, might start when a growth factor arrives on the outside of a cell, say in your tissue culture dish when you add fresh medium with growth-factor-containing serum in it. The information that it’s time to grow might be transmitted across the membrane by a membrane-spanning receptor, triggering a series of events such as a cascade of phosphorylations that cause enzymes within the cell to change activity. The final result might be a change of activity of a transcription factor; the presence of a signal outside the cell has thus been converted into a change in the gene expression profile inside the nucleus of the cell. We chiefly think of these processes as linear — a pathway — with a well-defined flow of information from A to B to C. We draw diagrams that show A near the cell membrane, passing information to B (closer to the nucleus) and then to C (closer still). But of course this is just an analogy we use to make it easier for us to think about what’s going on, and like all convenient analogies it has the potential to be seriously misleading. Our so-called “pathways” loop and branch and pass information forward and backward and sideways, losing precision all the way; A, B and C are most often distinguished by the timing of their activation, rather than by their location in the cell; and while it’s easy to tell a general story about how an external stimulus leads to a response inside the cell, it’s still hard to know why the response is the size it is, or happens at the time it does.

One of the most puzzling aspects of signal transduction is what happens when multiple signals impinge on the same mediator — when “paths” cross, or diverge, or merge. In the case of the important anti-oncogene p53, we draw several paths coming in to p53 and several paths going out again. The downstream consequences of p53 activation vary dramatically, from transient cell cycle arrest to senescence and apoptosis. How does this single protein receive and transmit several different types of information?

Read more of Galit’s 2012 piece, here

June 20, 2012