[News release] Activating genes on demand

In these images, the ability of the new Cas9 approach to differentiate stem cells into brain neuron cells is visible. On the left, a previous attempt to direct stem cells to develop into neuronal cells shows a low level of success, with limited red–colored areas indicating low growth of neuron cells. On the right, the new Cas9 approach shows a 40–fold increase in the number of neuronal cells developed, visible as red-colored areas on the image. Credit: Wyss Institute at Harvard University

 

From the 3 March 2015 Wyss Institute press release

New mechanism for engineering genetic traits governed by multiple genes paves the way for various advances in genomics and regenerative medicine 

When it comes to gene expression – the process by which our DNA provides the recipe used to direct the synthesis of proteins and other molecules that we need for development and survival – scientists have so far studied one single gene at a time. Anew approach developed by Harvard geneticist George Church, Ph.D., can help uncover how tandem gene circuits dictate life processes, such as the healthy development of tissue or the triggering of a particular disease, and can also be used for directing precision stem cell differentiation for regenerative medicine and growing organ transplants.

The findings, reported by Church and his team of researchers at the Wyss Institute for Biologically Inspired Engineering at Harvard University and Harvard Medical School in Nature Methods, show promise that precision gene therapies could be developed to prevent and treat disease on a highly customizable, personalized level, which is crucial given the fact that diseases develop among diverse pathways among genetically–varied individuals. Wyss Core Faculty member Jim Collins, Ph.D. was also a co-author on the paper. Collins is also the Henri Termeer Professor of Medical Engineering & Science and Professor in the Department of Biological Engineering at the Massachusetts Institute of Technology.

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[Press release] New nanodevice defeats drug resistance

New nanodevice defeats drug resistance 

From the 3 March 2015 MIT press release

Tiny particles embedded in gel can turn off drug-resistance genes, then release cancer drugs.

Chemotherapy often shrinks tumors at first, but as cancer cells become resistant to drug treatment, tumors can grow back. A new nanodevice developed by MIT researchers can help overcome that by first blocking the gene that confers drug resistance, then launching a new chemotherapy attack against the disarmed tumors.

The device, which consists of gold nanoparticles embedded in a hydrogel that can be injected or implanted at a tumor site, could also be used more broadly to disrupt any gene involved in cancer.

“You can target any genetic marker and deliver a drug, including those that don’t necessarily involve drug-resistance pathways. It’s a universal platform for dual therapy,” says Natalie Artzi, a research scientist at MIT’s Institute for Medical Engineering and Science (IMES), an assistant professor at Harvard Medical School, and senior author of a paper describing the device in the Proceedings of the National Academy of Sciences the week of March 2.

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[News article] How cancer turns good cells to the dark side

 

From the 28 January 2015 item at Science 360

A new computational study by a team of researchers shows how cancer cells take advantage of the system by which cells communicate with their neighbors as they pass messages to “be like me” or “be not like me.” The team decodes how cancer uses a cell-cell interaction mechanism known as notch signaling to promote metastasis. This mechanism plays a crucial role in embryonic development and wound healing and is activated when a delta or jagged ligand of one cell interacts with the notch receptor on an adjacent one.

Visit Website | Image credit: Marcelo Boareto/Rice University

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• How cancer turns good cells to the dark side
• How cancer turns good cells to the dark side
• How cancer turns good cells to the dark side