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Two new therapies—one which uses the gene-editing technology—treat sickle cell anemia.

Significance of the work.

CAR T cells are genetically engineered immune cells tailored to respond to a specific molecule found on the surface of tumor cells. These cells are a form of immunotherapy — an approach that harnesses the native ability of the immune system to fight diseases, particularly cancer. CAR T-cell therapy represents a milestone in cancer treatment. It propels cancer therapies beyond traditional chemotherapy and radiation treatments, which are often highly toxic and non-specific.

The four scientists honored with this year’s Warren Alpert Foundation Prize each played key distinct and complementary roles in developing CAR T cells and making their use in the clinic possible. Today, CAR T-cell therapies offer great hope for patients with various B-cell malignancies who have relapsed or failed to respond to other therapies. CAR T cell-based approaches could eventually be used to treat solid tumors, as well as a variety of autoimmune diseases and other conditions.

A team from the Innovative Genomics Institute at the University of California, Berkeley (UCB) has produced an increase in gene expression in a food crop by changing its upstream regulatory DNA. While other studies have used CRISPR/Cas9 gene-editing to knock out or decrease the expression of genes, new research published in Science Advances is the first unbiased gene-editing approach to increase gene expression and downstream photosynthetic activity.

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Many people have heard of the BRCA1 and BRCA2 genes because of their association with breast cancer. But scientists have now suggested that many of the genetic variants we are born with, in a variety of different genes, can make a powerful prediction about what type of breast cancer an individual could develop, and what the outcome could be. This study has indicated that random genetic variants that are acquired over a lifetimes are far less important to breast cancer risk compared to those a person is born with; the findings have been published in Science.

“Apart from a few highly penetrant genes that confer significant cancer risk, the role of heredity factors remains poorly understood, and most malignancies are assumed to result from random errors during cell division or bad luck,” said senior study author Christina Curtis, PhD, a Professor at Stanford University. While that would make it seem like random events cause the growth of tumors, this is not what’s been observed. Instead, tumor development is influence by immunity and genetics, said Curtis. “This new result unearths a new class of biomarkers to forecast tumor progression and an entirely new way of understanding breast cancer origins.”

WASHINGTON (AP) — The horse transformed human history – and now scientists have a clearer idea of when humans began to transform the horse.

Around 4,200 years ago, one particular lineage of horse quickly became dominant across Eurasia, suggesting that’s when humans started to spread domesticated horses around the world, according to research published Thursday in the journal Nature.

There was something special about this horse: It had a genetic mutation that changed the shape of its back, likely making it easier to ride.

When it comes to development, an epigenetic clock may be responsible for human neurons’ slower maturation.

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In what they believe is a solution to a 30-year biological mystery, neuroscientists at Johns Hopkins Medicine say they have used genetically engineered mice to address how one mutation in the gene for the light-sensing protein rhodopsin results in congenital stationary night blindness.

The condition, present from birth, causes poor vision in low-light settings.

The findings, published May 14 in Proceedings of the National Academy of Sciences, demonstrate that the rhodopsin gene mutation, called G90D, produces an unusual background electrical “noise” that desensitizes the eye’s rods, those cells in the retina at the back of the eye responsible for nighttime vision, thus causing night blindness.