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For years, scientists have hoped to use the gene-editing technology CRISPR to help treat all sorts of diseases, including cancer. Now for the first time in the U.S., researchers say they’ve shown that CRISPR-edited immune cells can be safely given to cancer patients and survive for up to nine months—a finding that may signal CRISPR’s future as part of an emerging cancer treatment known as immunotherapy.

The idea that we can boost the human immune system to help it fight off cancer isn’t new. But it’s only recently that researchers have been able to make substantial advances in the field. There are different techniques, but one that’s received lots of attention involves reprogramming our immune system’s shock troops, known as T cells, to attack cancer. T cells are drawn out from a patient’s blood, grown and modified in the lab so that they target tumor cells, and then reintroduced back into the body.

Cancer is a hugely complicated disease, and understanding how it starts and how it can be treated requires an equally enormous effort from scientists. That effort is well underway with the Pan-Cancer Project, an international collaboration dedicated to analyzing thousands of whole cancer genomes. And now, the comprehensive results are being published in 23 separate papers, revealing new details about cancer’s causes and development, and how it can be classified, diagnosed and treated.

Otherwise known as the Pan-Cancer Analysis of Whole Genomes (PCAWG) Project, the collaboration involves over 1,300 scientists from 37 countries. These researchers analyzed over 2,600 whole cancer genomes of 38 different types of tumors, probing deeper than ever into how the disease alters DNA.

One of the most optimistic outlooks from the project is that while the cancer genome is incredibly complex, it’s also finite. That means that it should be technically possible to document every genetic change that cancer can possibly induce. That information can then be used to diagnose which type of tumor a patient has and personalize a treatment plan based on the unique genome of their cancer.

Chronic inflammation, which results when old age, stress or environmental toxins keep the body’s immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer’s and Parkinson’s to diabetes and cancer.

Now, scientists at the University of California, Berkeley, have identified a molecular “switch” that controls the immune machinery responsible for in the body. The finding, which appears online Feb. 6 in the journal Cell Metabolism, could lead to new ways to halt or even reverse many of these age-related conditions.

“My lab is very interested in understanding the reversibility of aging,” said senior author Danica Chen, associate professor of metabolic biology, nutritional sciences and toxicology at UC Berkeley. “In the past, we showed that aged stem cells can be rejuvenated. Now, we are asking: to what extent can aging be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases.”

There is a huge number of living things on Earth, all with their own set of characteristics and unique ways of life. All the way from the smallest ants, up to the huge giraffes and elephants, one thing that everyone has in common is that they are alive! One type of living organism is plants and trees. While they may not walk around like other organisms, or have a kidney and liver, they do actually have their own set of organs, so to speak.

While a tree definitely doesn’t have a heart, the idea that they have their own beat and sense of rhythm isn’t as far fetched as many people think. According to a study which was headed by András Zlinszky, Bence Molnár and Anders S. Barfod from Hungary and Denmark, trees do in fact have a special type of beat within them which resembles that of a heartbeat. Who would have known?

To find this hidden heartbeat, the researchers used advanced monitoring techniques known as terrestrial laser scanning to survey the movement of twenty two different types of trees. The results shocked everyone and revealed that at night, while the trees were sleeping, they often had a beat pulsating throughout their body, just as humans, and other living creatures do too.

One day, we gonna engineer all of these to build better humankind for those capable of surviving in the vas space.


From our free online course, “Cell Biology: Mitochondria”: https://www.edx.org/course/cell-biology-mitochondria-harvard…n=harvardx

Harvard Professor Rob Lue explains how mitochondrial diseases are inherited and discusses the threshold effect and its implications for mitochondrial disease inheritance.

Genomics researchers worldwide are increasingly dealing with vast data sets gathered by consortia spanning many countries. Most are unclear on what to do to protect people’s privacy and to comply with international and national data-protection laws, especially given recent and ongoing changes in legislation.

An international code of conduct for genomic data is now crucial. Built by the genomics community, it could be updated as technologies and knowledge evolve more easily than is possible for national and international legislation.


Efforts to protect people’s privacy in a massive international cancer project offer lessons for data sharing.

In a pair of related studies, a team of Yale researchers has found a way to reverse type-2 diabetes and liver fibrosis in mice, and has shown that the underlying processes are conserved in humans.

The studies appear in the Feb. 4 edition of Cell Reports and in the Jan. 17 edition of Nature Communications.

In the earlier study, researchers found an important connection between how the body responds to fasting and type-2 diabetes. Fasting “switches on” a process in the body in which two particular proteins, TET3 and HNF4α increase in the , driving up production of blood glucose. In type-2 diabetes, this “switch” fails to turn off when fasting ends, as it would in a non-diabetic person.

Researchers at Albany Medical College in New York have discovered that a specific type of immune cell accumulates in older brains, and that activating these cells improves the memory of aged mice. The study, which will be published on February 5, 2020, in the Journal of Experimental Medicine (JEM), suggests that targeting these cells might reduce age-related cognitive decline and combat aging-associated neurodegenerative disease in humans.

The brain is highly susceptible to aging, with cognitive functions, such as learning and memory, gradually declining as we get older. Much of the body’s immune system also deteriorates with age, resulting in increased susceptibility to infection and higher levels of inflammation. In their new JEM study, however, a team of researchers led by Qi Yang and Kristen L. Zuloaga at Albany Medical College reveal that aging-related changes in a class of immune cell known as group 2 innate lymphoid cells (ILC2s) could allow doctors to combat the effects of aging on the brain.

ILC2s reside in specific tissues of the body and help to repair them when they are damaged. Recently, for example, ILC2s in the spinal cord were shown to promote healing after spinal cord injury. “However, whether ILC2s also reside in other parts of the central nervous system, and how they respond to aging, was unknown,” Yang says.

Metarhizium anisopliae infects mosquitoes through the cuticle and proliferates in the hemolymph. To allow M. anisopliae to combat malaria in mosquitoes with advanced malaria infections, we produced recombinant strains expressing molecules that target sporozoites as they travel through the hemolymph to the salivary glands. Eleven days after a Plasmodium-infected blood meal, mosquitoes were treated with M. anisopliae expressing salivary gland and midgut peptide 1 (SM1), which blocks attachment of sporozoites to salivary glands; a single-chain antibody that agglutinates sporozoites; or scorpine, which is an antimicrobial toxin. These reduced sporozoite counts by 71%, 85%, and 90%, respectively. M. anisopliae expressing scorpine and an [SM1]8:scorpine fusion protein reduced sporozoite counts by 98%, suggesting that Metarhizium-mediated inhibition of Plasmodium development could be a powerful weapon for combating malaria.