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Linzixuan (Rhoda) Zhang holding the medal she won in the 2024 Collegiate Inventors Competition

Rhoda Zhang Wins 2024 Collegiate Inventors Competition

MIT News

November 5, 2024

Graduate student Linzixuan (Rhoda) Zhang has won the 2024 Collegiate Inventors Competition in both the Graduate and People's Choice categories. With advisors Robert Langer and Ana Jaklenec, Zhang and KI postdoc Xin Yang are developing metal-organic frameworks and other safe, sustainable nutrient stabilizing materials to address global micronutrient deficiencies. They are also launching MOFe™ Coffee, the first iron-fortified coffee.

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TED Live and Learn

MIT Koch Institute

June 1, 2016

KI engineers Paula Hammond, a David H. Koch Professor of Engineering, and Sangeeta Bhatia, the John J. and Dorothy Wilson Professor of Health Sciences and Technology & Electrical Engineering and Computer Science, made their Broadway debuts at TED Talks Live, in partnership with PBS. Hammond unveiled “a new superweapon in the fight against cancer” (watch now) while Bhatia explored how a “tiny particle could roam your body to find tumors” (watch now). Both presentations were offered as part of the two-day Science & Wonder series within the weeklong event and preceded Bhatia’s appearance at TEDMED, during which she spoke further about her vision for miniaturization of biomedical inventions (watch now).

That's So Ninja

STAT News

May 9, 2016

“Fascinating and daunting” is how KI director Tyler Jacks describes tumors in Episode 10 of STAT’s SIGNAL podcast. Jacks joined former advisor and Nobel Prize winner Harold Varmus and others to talk with STAT’s Luke Timmerman and Meg Tirrell about cancer’s dirty, sneaky ability to evolve, evading both the immune system and treatment, in “Cancer is a low-down, gangster ninja.” Listen online; Jacks makes his first of several appearances around the five-minute mark.

Personalized Drug Device Enters Clinical Trials

American Association for Cancer Research

April 20, 2016

Figuring out which drugs will work best for an individual patient can be challenging and time-consuming, if not impossible. Last spring, however, KI postdoc Oliver Jonas published his development of a microdevice that can be implanted into tumors, using a biopsy needle, to test the efficacy of multiple cancer therapeutics or combinations. At this year's AACR annual meeting, Jonas presented preclinical results on the device, which has also been used to uncover new methods of drug resistance. He described updates to the device, which can now hold up to 100 different drugs or combinations as well as relay results in real-time, and he announced the launch of the first clinical trials of the device.

Jonas is a member of the laboratories of Robert Langer, the David H. Koch Institute Professor, and Michael Cima, a David H. Koch Professor of Engineering. This work was supported in part by the Koch Institute Frontier Research Program.

Timing is of the Essence

Washington Post

March 14, 2016

Cancer patients often endure a battery of different drug treatments to find a therapy that works. Scientists have known for some time that genetics help explain why certain drugs may work on one person and not on another, but new findings by KI members Michael Hemann and Doug Lauffenburger suggest that the timing of these treatments may also be a critical factor. Tumors evolve through various stages, and the team’s study shows that sensitivity to a particular drug can depend on the stage at which it is administered. Their findings indicate that there may be windows of opportunity for drugs that had previously been written off as failures for individual patients. Hemann and Lauffenburger hope that modeling methods will predict tumor evolution and improve targeted therapies to help combat drug resistance. This research was supported in part by the Go Mitch Go Foundation.

Fueling Cancer Growth

MIT News

March 7, 2016

Glucose is the main source of fuel that cancer cells use to divide and reproduce uncontrollably. For some time, this had led scientists to believe that most of the cell mass in new cancer cells comes from glucose. Now new findings from a group including KI members Eisen and Chang Career Development Professor Matt Vander Heiden and Andrew and Erna Viterbi Professor Scott Manalis, suggest that the largest source for new cell material is amino acids, which growing cells consume in considerably smaller quantities than glucose. The paper, published in Developmental Cell, offers a new way to look at cancer metabolism, a process that Vander Heiden mentioned in a recent NPR interview plays an important role in cancer development.

Diet and Cancer

MIT News

March 2, 2016

New research by KI members Omer Yilmaz and David Sabatini sheds light on how a high-fat diet can lead to an increased risk of colon cancer. The team, who published their results in Nature, found that mice fed a high-fat diet exhibit an increased proliferation of both intestinal stem cells and progenitor cells that acquire stemness, both of which increase the risk of tumor formation. If the results hold true for humans, they offer a clue to explain the mechanism by which a high-fat diet contributes to cancer risk. This work was supported in part by the Koch Institute Frontier Research Program through the Kathy and Curt Marble Cancer Research Fund, and by the V Foundation.

Immaculate Suppression

Genes and Development

December 17, 2015

The epigenetic regulator Bmi1 is known to promote cellular proliferation through its control of cell cycle genes. However, researchers in the laboratory of KI faculty member Jacqueline Lees have found an unexpected role for Bmi1 in melanoma, where it does not drive proliferation. Instead, the authors of a recent study published in Genes & Development find that Bmi1 supports melanoma metastasis by turning on genes that help melanoma cells invade tissues and survive new environments. Moreover, they find that melanomas with high Bmi1 levels are resistant to BRAF inhibitors--drugs commonly administered as the BRAF gene is activated in 50% of early-stage melanomas.

SQZ Named Roche's New Squeeze

GEN News

December 7, 2015

SQZ Biotech recently announced a cancer-fighting partnership with pharmaceutical firm Roche. Headed by Koch Institute visiting scientist and former postdoc Armon Sharei, SQZ also counts several Koch Institute members among its Boards of Directors (Robert Langer) and Scientific Advisors (Tyler Jacks, Darrell Irvine, and Christopher Love). SQZ uses a device invented by Sharei, called CellSqueeze, to engineer cell-based therapies for disease, most notably B cell-driven immunotherapies for a broad range of cancers. Earlier this year, SQZ was named one of FierceBiotech's 2015 Fierce 15, and the CellSqueeze device was named one of Scientific American's top ten world-changing ideas of 2014. Development of SQZ's B cells was initially supported by the Koch Institute Frontier Research Program through the Kathy and Curt Marble Cancer Research Fund.

$20 Million Commonwealth Foundation for Cancer Research Challenge Gift to Expand Collaborative Cancer Research

MIT News

October 28, 2015

The Commonwealth Foundation for Cancer Research has pledged $20 million to the Bridge Project, a collaborative research program of the Koch Institute for Integrative Cancer Research at MIT and the Dana-Farber/Harvard Cancer Center, to accelerate the translation of interdisciplinary cancer solutions toward the clinic. The Commonwealth Foundation gift, which will be made over the next five years, will double the number of grants available to fund these multi-investigator teams each year. It also will create two new funding mechanisms that will extend the pipeline of collaboration and catalyze the translation of basic research toward clinical trials. “Footbridge Grants” will enable new teams to form and establish proof of concept. “Expansion Grants” will provide follow-on funding to existing teams that are on the cusp of making significant advances toward clinical implementation.

Yaffe Lab Backs Cancer into a Corner

MIT News

October 22, 2015

Researchers in the laboratory of KI faculty member Michael Yaffe have discovered a drug-resistance mechanism in tumor cells: a backup system that takes over when p53 is disabled. By targeting this backup system, these tumors could be made much more susceptible to chemotherapy.