news and media
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Galit Lahav and the Night Science Tuesday
December 10, 2022
Professor Galit Lahav is the Chair of the Systems Biology Department at Harvard Medical School, where she creates an environment that is collaborative, stimulating, and interdisciplinary. In this episode, Galit tells us how her creative process consists of incubation and interaction. She stresses the importance of being vulnerable for creativity to emerge, and also how to use night science to make the tough decision to stop working on a particular project. Thinking about how to normalize incubation at the department level, Galit led us to conclude that Night Science Tuesday should be a part of every scientist’s work week!
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What It’s Like to be a Systems Biologist With Dr. Galit Lahav, Harvard Medical School
April 29, 2021
Galit Lahav is the Chair of the Department of Systems Biology and a professor of systems biology at Harvard Medical School. She is known for identifying a range of behaviors in the tumor suppressor protein p53 and uncovering its significance for killing individual cancer cells. She has been recognized globally for her excellence in teaching and research, receiving awards such as the Vilcek Prize for Creative Promise in Biomedical Science and an Excellence in Mentoring Award. Dr. Lahav received her Ph.D. in 2001 from the Technion, Israel Institute of Technology. She is working to make Harvard a destination of choice for women in science.
WHAT YOU’LL LEARN ABOUT IN THIS EPISODE:
What systems biology is and how it works (3:15)
What Dr. Lahav’s research focuses on (4:40)
Why the P53 protein, the “guardian of the genome,” is so important (5:46)
How taking a systems approach works in researching the P53 protein (9:14)
What Dr. Lahav’s typical workday looks like (13:34)
Why it’s important to give yourself a break from work on a daily basis (16:42)
What the gender breakdown of Galit’s job is like (18:27)
How Dr. Lahav found what she wanted to do post-grad (19:48)
What Dr. Lahav learned from a failure she experienced in New York (22:51)
What advice Galit would give to her former self (27:06)
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Radiation Vulnerability
February 18, 2021
Tumor-suppressor protein dynamics drive cellular radiation survival
Exposure to radiation can wreak indiscriminate havoc on cells, tissues, and organs. Curiously, however, some tissues are more vulnerable to radiation damage than others.
Scientists have known these differences involve the protein p53, a well-studied tumor-suppressor protein that initiates a cell’s auto-destruct programs. Yet, levels of this sentinel protein are often similar in tissues with vastly different sensitivities to radiation, posing the question: How is p53 involved?
A new study by researchers in the Blavatnik Institute at Harvard Medical School, Massachusetts General Hospital, and the Novartis Institutes for BioMedical Research now sheds light on this mystery.
Reporting in Nature Communications on Feb. 9, they describe how cellular survival after radiation exposure depends on behavior of p53 over time. In vulnerable tissues, p53 levels go up and remain high, leading to cell death. In tissues that tend to survive radiation damage, p53 levels oscillate up and down.
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A Switch in p53 Dynamics Marks Cells that Escape from DSB-Induced Cell Cycle Arrest
August 24, 2020
Can you provide a brief overview of your lab’s current research focus?
Our lab’s goal is to determine why individual human cancer cells often show different responses to the same treatment, and to identify new therapies that will increase the efficacy of anti-cancer drugs. To this end, we develop computational and quantitative experimental approaches to study the fate and behavior of human cells in disease and health at the single-cell level. We focus on the tumor suppressor protein p53, perhaps the most important gene protecting human cells against the development of cancer. Most studies on p53 use bulk methods that average the responses of many cells together. We pioneered new approaches for quantifying the behavior of p53 in single living cells. One function of p53 is to detect and respond to DNA damage that may lead to cancer-causing mutations. We found that information about the nature and extent of DNA damage is transmitted through the pattern of p53 over time (p53 dynamics), not the absolute level of the protein, and that the dynamic behavior of p53 determines how each cell responds to radiation and anti-cancer drugs.
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Five Questions: A conversation with Galit Lahav, systems biologist
August 23, 2018
“Your work occurs at the intersection of cancer biology and mathematics. What sparked your interest in this field?
Early on I realized it’s important to me to work on a problem related to human disease, so the work my lab does to understand a gene that suppresses cancer is the type of work that keeps my inner fire burning.”
Read more from Ekaterina Pesheva’s interview with Galit, here
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Keeping Up With Moving Targets: How Do Cancer Cells Switch In And Out Of Therapy-Resistant States?
Science Trends article with Jose Reyes and Galit Lahav
“Tumors result from the expansion of cells that bypass the regulatory mechanisms that otherwise control the birth, death, and elimination of cells within healthy tissues. The overarching goal of cancer therapy is to halt such proliferation and eliminate cancer cells while sparing their non-cancerous counterparts. Although many treatments are successful in eradicating a large fraction of cells within tumors, incomplete elimination and the emergence of a resistant population of tumor cells are major hurdles for the success of cancer therapy.”
Read more here