Category Archives: Transhuman News

Scientists from Case Western Reserve University's School of Medicine have discovered a potential treatment that may steer cancer cells toward their own destruction. The study focused on a particular gene that was found to influence levels of a tumor-fighting protein called 53BP1, the heightened presence of which makes cancer cells more vulnerable to existing forms of treatment.

The proposed therapeutic approach centers on the repairing of DNA, a process that sees the body mend molecules damaged by everything from reactive oxygen components to radiation and chemical agents. More specifically, it focuses on a double-strand break, a type of injury that sees both strands of the double helix severed, leading to damaged and dead cells.

One mechanism that the body uses to fix these double-strand breaks is gluing the DNA strands together again, but this isn't ideal as it renders those strands less effective in sending information through to the cell, meaning the cells are often left to die anyway. Another method of repair used by the body is using information from undamaged DNA to mend the broken DNA, a more effective way of repairing the broken double strands.

Through their study, the researchers observed the functions of an important gene in this process called UbcH7, known to help regulate the repair of broken double strands. What they found was that depleting levels of UbcH7 resulted in a significant boosting of the tumor-suppressing 53BP1 protein, which in turn drives the cancer cells toward the first, less effective path of repair: the gluing method. The team says the approach could complement current forms of treatment.

"What we propose is increasing the level of 53BP1 to force cancer cells into the error-prone pathway where they will die," says Youwei Zhang, assistant professor of pharmacology at the university's School of Medicine. "The idea is to suppress deliberately the second accurate repair pathway where cancer cells would prefer to go. It is a strategy that would lead to enhanced effectiveness of cancer therapy drugs.

The team's findings so far are the product of laboratory experiments, but the promising results has them planning on testing the approach in animal models. This would involve introducing the 53BP1 protein in mice and then treating them with radiation therapy and chemotherapy drugs.

The research findings were published in the journal Proceedings of the National Academy of Sciences.

Source: Case Western University

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New approach could lead cancer cells down path of destruction

Researchers have narrowed down the list of genes implicated in autism spectrum disorder, and they appear to point toward a part of the brain that has largely been overlooked.

Most research into the genetic roots of autism, a highly heritable disorder that affects about 1 in 68 children, starts with a kind of inventory of genes. Then, it narrows down this genome-wide survey to prime suspects that appear to be different among those with one or several of the symptoms of autism.

That gene-by-gene approach, however, has unearthed too many suspects, each with somewhat vague relationships to a small sliver of the autism spectrum. That situation has sparked some to abandon the gene-by-gene approach in favor of environmental factors that may alter gene behavior.

Whats special about autism is that it doesnt seem like its a one-gene thing, said Stanford UniversitySchool of Medicinegeneticist Michael Snyder, lead investigator of the study published online Tuesday in the journal Molecular Systems Biology.

Maybe this is a tough way to look at it, Snyder said of the gene-by-gene approach. Maybe a better way to look at it is to see what the normal biological landscape looks like, and see how people who are mutated for autism map onto that.

What followed was a complex computational task that corralled proteins into scores of modules tightly bound by their inter-related functions. Then Snyders team overlaid the map of gene variants implicated in autism.

At first glance, proteins encoded by these 383 suspect genes were scattered among many of these functional modules. But a few of the modules screamed out with autism connections, both from existing data and a genome screening the researchers conducted, Snyder said.

One module involved molecular activity that goes on all over the brain, particularly involving synapses, the tiny spaces where electrochemical signals cross for one neuron to another. This helps explain why so much autism research points toward problems with synapses.

But there was another module just as rich in autism implications, and this one implicated the corpus callosum. That thick band of fibers connects the brains two hemispheres, and its generally smaller among those with autism a disease marked by many anomalies in connectivity.

The corpus callosum is chock full of a different kind of brain cell, oligodendrocytes, which provide a sheath of insulation around the transmission lines of neurons, known as their axons. That greatly aids the propagation of electrochemical signals along the neuron. Defects in this myelin sheathing have been associated with developmentaldisorders.

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Study narrows down genetic suspects in autism