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But they don’t. Instead, they are less likely to develop or die of this enigmatic disease. The same is true of elephants and dinosaurs’ living relatives, birds. Marc Tollis, an assistant professor in the School of Informatics, Computing, and Cyber Systems at Northern Arizona University, wants to know why.

Tollis led a team of scientists from Arizona State University, the University of Groningen in the Netherlands, the Center for Coastal Studies in Massachusetts and nine other institutions worldwide to study potential cancer suppression mechanisms in cetaceans, the mammalian group that includes whales, dolphins and porpoises. Their findings, which picked apart the genome of the humpback whale, as well as the genomes of nine other cetaceans, in order to determine how their cancer defenses are so effective, were published today in Molecular Biology and Evolution.

The study is the first major contribution from the newly formed Arizona Cancer and Evolution Center or ACE, directed by Carlo Maley under an $8.5 million award from the National Cancer Institute. Maley, an evolutionary biologist, is a researcher at ASU’s Biodesign Virginia G. Piper Center for Personalized Diagnostics and professor in the School of Life Sciences. He is a senior co-author of the new study.


An all-Princeton research team has identified bacteria that can detect the speed of flowing fluids.

Many kinds of cells can sense , just as our skin cells can feel the difference between a gentle breeze and a strong wind. But we depend on feeling the force involved, the push-back from the air against us. Without that push, we can’t distinguish speed; when the windows are closed, our skin can’t feel any difference in whether we are sitting in an office, a speeding car or a cruising airplane. But now, a team of Princeton researchers has now discovered that some bacteria can in fact detect the speed of flow regardless of the force. Their paper appears in the online journal Nature Microbiology.

“We have engineered bacteria to be speedometers,” said Zemer Gitai, Princeton’s Edwin Grant Conklin Professor of Biology and the senior author on the paper. “There’s an application here: We can actually use these bacteria as flow sensors. If you wanted to know the speed of something in real time, we can tell you.”

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We’re tantalizingly close to growing organs in the lab, but the biggest remaining challenge has been creating the fine networks of blood vessels required to keep them alive. Now researchers have shown that a common food dye could solve the problem.

In the US there are currently more than 100,000 people on organ transplant waiting lists. Even if you’re lucky enough to receive a replacement, you face a lifetime on immunosuppressant drugs. That’s why scientists have long dreamed of growing new organs from patients’ own cells, which could simultaneously tackle the shortage and the risk of organ rejection.

The field of tissue engineering has seen plenty of progress. Lab-grown skin has been medically available for decades, and more recently stem cells have been used to seed scaffolds—either built form synthetic materials or made by stripping cells from natural support structures—to reproduce more complex biological tissue.

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Washington State University researchers have developed an environmentally-friendly, plant-based material that for the first time works better than Styrofoam for insulation.

The is mostly made from nanocrystals of cellulose, the most abundant plant material on earth. The researchers also developed an environmentally friendly and simple manufacturing process to make the foam, using water as a solvent instead of other harmful solvents.

The work, led by Amir Ameli, assistant professor in the School of Mechanical and Materials Engineering, and Xiao Zhang, associate professor in the Gene and Linda School of Chemical Engineering and Bioengineering, is published in the journal Carbohydrate Polymers.

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In an article last May, we covered how Rejuvenate Bio, a startup biotech company led by Professor George Church, was planning to reverse aging in dogs as a step towards bringing these therapies to us. Those plans are now starting to move forward with news of a trial launch in the fall later this year.

Developing anti-aging therapies in dogs is the first step

Back in 2015, the Church lab at Harvard began testing a variety of therapies focused on age reversal using CRISPR, a gene editing system that was much easier and faster to use than older techniques. Since then, Professor Church and his lab have conducted a myriad of experiments and gathered lots of data with which to plan future strategies for tackling aging.

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Here, doctors extract a patient’s own T cells, a type of white blood cell that normally acts as the body’s watcher against cancer and infection. Cancer cells eventually learn to evade T cells or disarm the troops—while turning their own surrounding normal cells into cancerous ones, thus expanding their tumor legion.

CAR-T uses gene therapy to recharge those beaten-down T cells. The UPenn study, for example, relies on a neutered HIV-like virus to deliver an artificial “tracker” protein into those cells. These designer trackers expertly hunt down a protein dubbed NY-ESO-1, which dot certain cancer cells’ surface like a homing beacon.

CRISPR amplifies the CAR-T effect: the team is using the gene editing tool to erase three different “brakes” in T cells. Killing off the first two, TCR α and TCR β, keeps the edited cells in check to prevent friendly autoimmune fire, and allows the added “tracker proteins” to thrive in large numbers. Wiping out the third, PD-1, prevents a phenomenon called T cell exhaustion. It’s aptly named: here, tumor cells secrete molecules that literally shut down T cell activity, zapping away their killing power.

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Targeted genome editing tools, such as meganucleases (MGN), zinc-finger nucleases (ZFN), transcription activator-like effector nucleases (TALENs) and more recently the clustered regularly interspaced short palindromic repeats (CRISPR) have revolutionized most biomedical research fields. Such tools allow to precisely edit the genome of eukaryotic cells by inducing double-stranded DNA (dsDNA) breaks at specific loci. Relying on the cell endogenous repair pathways, dsDNA breaks can then be repaired by non-homologous end-joining (NHEJ) or homology-directed repair (HDR) allowing the removal or insertion of new genetic information at a desired locus.

Among the above-mentioned tools, CRISPR-Cas9 is currently the most simple and versatile method for genome engineering. Indeed, in the two-component system, the bacterial-derived nuclease Cas9 (for CRISPR-associated protein 9) associates with a single-guide RNA (sgRNA) to target a complementary DNA sequence and induce a dsDNA break. Therefore, by the simple modification of the sgRNA sequence, users can specify the genomic locus to be targeted. Consistent with the great promises of CRISPR-Cas9 for genome engineering and gene therapy, considerable efforts have been made in developing efficient tools to deliver the Cas9 and the sgRNA into target cells ex vivo either by transfection of plasmids coding for the nucleases, transduction with viral-derived vectors coding for the nucleases or by direct injection or electroporation of Cas9-sgRNA complexes into cells.

Researchers have designed Nanoblades, a protein-delivery vector based on friend murine leukemia virus (MLV) that allows the transfer of Cas9-sgRNA ribonucleoproteins (RNPs) to cell lines and primary cells in vitro and in vivo. Nanoblades deliver the ribonucleoprotein cargo in a transient and rapid manner without delivering a transgene and can mediate knock-in in cell lines when complexed with a repair template. Nanoblades can also be programmed with modified Cas9 proteins to mediate transient transcriptional activation of targeted genes.

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