The Department of Systems Biology is pleased to announce the speakers in its 2016-2017 Seminar Series. The seminar series features leading investigators working in a diverse set of fields, including epigenomics, gene expression regulation, regulatory elements, evolutionary biology, cancer systems biology, and developmental biology, among others. Please save the dates!

All events will be held in the Department of Systems Biology Common Room (ICRC 816), unless indicated otherwise. Additional details about these events will be provided at the links below as they become available.

For a continually updated calendar of all Department of Systems Biology events, and to see an archive of past seminars, visit


In a recent paper published in Molecular Systems Biology, Kam Leong describes a two-compartment microfluidic device that consists of a chamber within which is embedded a "microbial swarmbot" that is isolated by a permeable hydrogel shell. In collaboration with Lingchong You (Duke University), Leong used the device to regulate the dynamics of a population of bacteria containing a genetically engineered switch that reacts to population size. The scale bar in panel 1 represents a length of 250 micrometers.

With a restless curiosity, Kam Leong always seems to be on the lookout for new problems to solve. A versatile biomedical engineer originally trained in chemical engineering, he has developed an impressive array of innovative nanotechnologies that have opened up new opportunities in biomedical research and drug delivery. 

The most widely known of his designs resulted from his work as a postdoc in the laboratory of MIT’s Robert Langer. While there, Leong played a critical role in the development of Gliadel, a controlled-release therapy that uses biodegradable polymer particles to deliver an anticancer drug to a brain tumor site following surgery. Since then his name has appeared on more than 70 patents covering a wide range of inventions — from microfluidics technologies, to scaffolds for growing organic tissues, to nanoscale fluorescent probes, to a method that uses nanoparticles instead of viruses for the oral delivery of gene therapies. These achievements have gained him widespread respect within the engineering community, as evidenced by his 2013 election to both the National Academy of Engineering and the National Academy of Inventors.

Dr. Leong joined Columbia University in 2014. Although his primary affiliation is with the Department of Biomedical Engineering, he was also attracted by the chance to assume an interdisciplinary faculty appointment in the Department of Systems Biology. Since his arrival he has been developing collaborations with several Systems Biology faculty members as well as other scientists at Columbia University Medical Center, and plans are underway for his lab to move into the Lasker Biomedical Research Building to better facilitate interactions with systems biology and clinical investigators. In the following interview, Leong describes why opportunities to interact with scientists in other disciplines is so important to his work, and how the kinds of technologies he has developed could be relevant for systems biology research, as well as for improving treatment of human diseases.

Best Poster Winners
At this year's retreat Alexander Hsieh, Rotem Rubinstein, Jinzhou Yuan, and Jiguang Wang (clockwise from top left) were named winners in the Best Poster Competition.

On September 15, 2016, members of the Columbia University Department of Systems Biology gathered in Tarrytown, New York for the Department’s annual retreat. Although the tranquil setting overlooking the Hudson River was familiar, the event’s timing was new, taking place for the first time at the beginning of the academic year to enable first-year graduate students to become acquainted with the Department as they begin their studies. With a full day of scientific talks, a poster session, and ample time for informal conversation, the retreat provided an up-to-date survey of the diverse research taking place in the Department's laboratories.

September 28, 2016

Can Math Crack Cancer's Code?

An essay coauthored by Andrea Califano (Chair, Department of Systems Biology) and Gideon Bosker and published in the Wall Street Journal asks whether quantitative modeling could reveal the keys for turning cancer off. They write:

  • Disappointed with the slow pace of discovery and inclined to look for elegant, universal explanations for nature’s conundrums, many cancer researchers have increasingly been asking: Is there some sort of “Da Vinci Code” for cancer? And can we crack it using mathematics?

    Quantitative modeling has been extremely successful in disciplines as diverse as astronomy, physics, economics and computer science. Can “cancer quants”—scientists applying quantitative analyses to the landscape of cancer biology—find the answers we seek? And, if so, what would the new paradigm look like? 

The essay goes on to describe how computational methods developed in the Califano Lab are being tested in personalized N of 1 clinical trials to identify essential checkpoints in the molecular regulatory networks that sustain individual patients' tumors — as well as drugs capable of targeting them.

Click here to read the essay. (subscription may be required)

Yufeng Shen
Yufeng Shen's lab is interested in developing better computational methods for identifying rare genetic variants that increase disease risk.

On the surface, birth defects and cancer might not seem to have much in common. For some time, however, scientists have observed increased cancer risk among patients with certain developmental syndromes. One well-known example is seen in children with Noonan syndrome, who have an eightfold increased risk of developing leukemia. Recently, researchers studying the genetics of autism also observed mutations in PTEN, an important tumor suppressor gene. Although such findings have been largely isolated and anecdotal, they raise the tantalizing question of whether cancer and developmental disorders might be fundamentally linked.

According to a paper recently published in the journal Human Mutation, many of these similarities might not be just coincidental, but the result of shared genetic mutations. The study, led by Yufeng Shen, an Assistant Professor in the Columbia University Departments of Systems Biology and Biomedical Informatics, together with Wendy Chung, Kennedy Family Associate Professor of Pediatrics at Columbia University Medical Center, found that cancer-driving genes also make up more than a third of the risk genes for developmental disorders. Moreover, many of these genes appear to function through similar modes of action. The scientists suggest that this could make tumors “natural laboratories” for pinpointing and predicting the damaging effects of rare genetic alterations that cause developmental disorders.

“In comparison with cancer, there are relatively few patients with developmental disorders,” Shen explains, “For geneticists, this makes it hard to identify the risk genes solely based on statistical evidence of mutations from these patients. This study indicates that we should be able to use what we learn from cancer genetics — where much more data are available — to help in the interpretation of genetic data in developmental disorders.”