New Cancer Vaccine Eliminates 97 Percent of Tumors in Mice, Clinical Trials On Humans in the Works

Doctors all over the world have been struggling to find the best possible treatment for cancer for decades. The Stanford University School of Medicine is now conducting a study for a new cancer vaccine.

 The study is headed by Dr. Ronald Levy and Idit Sagiv-Barfi. The team has created a vaccine that reduces a person’s chance of getting a tumor by almost 97%. They ran tests on mice by injecting two immune-stimulating agents straight into a malignant tumor.

What happened after that was amazing. They used 90 mice in the trial and they cured 87 successfully. Levy stated that they opted for just one injection of fairly tiny doses of two agents which stimulated the immune cells that already existed inside the tumor. The injection was so effective that even if the animal had other tumors in other parts of the body that weren’t being treated, even those were eliminated completely.

Science Translational Medicine published this study last month and the team is optimistic about the effectiveness of this drug on human patients. If all goes well, no patient will ever have to go through the debilitating side effects of chemotherapy.

According to Levy, the traditional methods of identifying immune targets specially for each tumor, having to activate all of the immune system or even the need for customizing the immune cells of a particular patient for a specific type of cancer, will become unnecessary because the two agents remove tumors from all parts of the body, even if they weren’t meant to treat those.

We might soon be seeing these agents used in cancer therapy. The team has permission to test one agent on humans and the second agent in many other medical trials.

A press release also revealed that the team has already recruited around 15 patients suffering from low-grade lymphoma. If it works on them, Dr. Levy is sure that they can use agents to treat various other tumors that occur.

The body does immediately being to reject any cancerous growths. The immune system and its cells, like T cells, are quick to spot the anomaly and remove it. However, as the tumor develops, it prevents the T cells from working.

This new study focuses on stimulating the T cells already present in the tumor by injecting the vaccine right into it. Dr. Levy is hopeful that as long as the T cells manage to get into the tumor, they can cure almost any variation of cancer using this method.


New Alzheimer’s treatment fully restores memory function.

Of the mice that received the treatment, 75 percent got their memory function back.

Australian researchers have come up with a non-invasive ultrasound technology that clears the brain of neurotoxic amyloid plaques – structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients.

If a person has Alzheimer’s disease, it’s usually the result of a build-up of two types of lesions – amyloid plaques, and neurofibrillary tangles. Amyloid plaques sit between the neurons and end up as dense clusters of beta-amyloid molecules, a sticky type of protein that clumps together and forms plaques.

Neurofibrillary tangles are found inside the neurons of the brain, and they’re caused by defective tau proteins that clump up into a thick, insoluble mass. This causes tiny filaments called microtubules to get all twisted, which disrupts the transportation of essential materials such as nutrients and organelles along them, just like when you twist up the vacuum cleaner tube.

As we don’t have any kind of vaccine or preventative measure for Alzheimer’s – a disease that affects 343,000 people in Australia, and 50 million worldwide – it’s been a race to figure out how best to treat it, starting with how to clear the build-up of defective beta-amyloid and tau proteins from a patient’s brain. Now a team from the Queensland Brain Institute (QBI) at the University of Queensland have come up with a pretty promising solution for removing the former.


Publishing in Science Translational Medicine, the team describes the technique as using a particular type of ultrasound called a focused therapeutic ultrasound, which non-invasively beams sound waves into the brain tissue. By oscillating super-fast, these sound waves are able to gently open up the blood-brain barrier, which is a layer that protects the brain against bacteria, and stimulate the brain’s microglial cells to activate. Microglila cells are basically waste-removal cells, so they’re able to clear out the toxic beta-amyloid clumps that are responsible for the worst symptoms of Alzheimer’s.

The team reports fully restoring the memory function of 75 percent of the mice they tested it on, with zero damage to the surrounding brain tissue. They found that the treated mice displayed improved performance in three memory tasks – a maze, a test to get them to recognise new objects, and one to get them to remember the places they should avoid.

“We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics,” one of the team, Jürgen Götz, said in a press release. “The word ‘breakthrough’ is often misused, but in this case I think this really does fundamentally change our understanding of how to treat this disease, and I foresee a great future for this approach.”

The team says they’re planning on starting trials with higher animal models, such as sheep, and hope to get their human trials underway in 2017.

Prosthetic bladder ‘controls urine’

A device that could one day restore bladder function to patients with a severed spinal cord has been devised by UK researchers and tested in animals.

Nerve damage can leave no sense of when the bladder is full or control over when the contents are released.

A study, published in Science Translational Medicine, showed a device to read the remaining nerves’ signals could be used to control the organ.

The charity Spinal Research said this was “impressive and important” work.

The loss of bladder, bowel and sexual function after spinal cord injury is often rated by patients as having the biggest impact on quality of life.

Blocked signals

When the spinal cord is injured, signals passing up from the bladder cannot tell the brain when the bladder is full. Going the other way, signals from the brain cannot tell the bladder when it is time to go to the toilet.

Researchers at the University of Cambridge have devised a solution that uses the nerves still around the bladder.

Electrodes wrapped around bundles of nerves can interpret signals that say the bladder is full.

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The ultimate aim is to regenerate the spinal cord, what we’re doing is restoring some function.”

Dr Daniel Chew Cambridge University

Stimulating other sets of nerves can get the bladder to contract on demand and prevent it emptying of its own volition.

One of the researchers, Dr Daniel Chew, told the BBC the device had worked on rats.

“It is very effective. The feasibility studies are done, we’re now limited by miniaturisation of the technology,” he said.

While the components that fit inside a rat could be converted for human use, the rest of the technology to process the information recorded currently needs a 6ft (2m) stack of equipment.

This needs to shrunk down to a handheld device that can inform a patient when the bladder is full and a trigger button to contract the bladder.

Bladder x-ray

Dr Chew added: “This device is not the ultimate goal, the ultimate aim is to regenerate the spinal cord. What we’re doing is restoring some function, not curing spinal cord injury.”

Dr Mark Bacon, the director of research at the charity Spinal Research, told the BBC: “Bladder dysfunction blights the life of many with spinal cord injuries and has a very major impact on their health and quality of life.

“This is impressive and important work addressing one of the major limitations found with existing options for electrical stimulation to control bladder emptying, namely the need to surgically destroy the sensory fibres coming from the bladder.

“Sparing and making use of sensory signals from a filling bladder adds a welcome degree of sophistication to elective voiding whilst retaining other functions normally lost such as erectile function – a distressing consequence of current methods.”

Cholera is Altering the Human Genome.

Cholera kills thousands of people a year, but a new study suggests that the human body is fighting back. Researchers have found evidence that the genomes of people in Bangladesh—where the disease is prevalent—have developed ways to combat the disease, a dramatic case of human evolution happening in modern times.


Cholera has hitchhiked around the globe, even entering Haiti with UN peacekeepers in 2010, but the disease’s heartland is the Ganges River Delta of India and Bangladesh. It has been killing people there for more than a thousand years. By the time they are 15 years old, half of the children in Bangladesh have been infected with the cholera-causing bacterium, which spreads in contaminated water and food. The microbe can cause torrential diarrhea, and, without treatment, “it can kill you in a matter of hours,” says Elinor Karlsson, a computationalgeneticist at Harvard and co-author of the new study.

The fact that cholera has been around so long, and that it kills children—thus altering the gene pool of a population—led the researchers to suspect that it was exerting evolutionary pressure on the people in the region, as malaria has been shown to do in Africa. Another hint that the microbe drives human evolution, notes Regina LaRocque, a study co-author and infectious disease specialist at Massachusetts General Hospital, Boston, is that many people suffer mild symptoms or don’t get sick at all, suggesting that they have adaptations to counter the bacterium.

To tease out the disease’s evolutionary impact, Karlsson, LaRocque, and their colleagues, including scientists from the International Centre for Diarrhoeal Disease Research in Bangladesh, used a new statistical technique that pinpoints sections of the genome that are under the influence of natural selection. The researchers analyzed DNA from 36 Bangladeshi families and compared it to the genomes of people from northwestern Europe, West Africa, and eastern Asia. Natural selection has left its mark on 305 regions in the genome of the subjects from Bangladesh, the team reveals online today in Science Translational Medicine.

The researchers bolstered the case that cholera was the driving force behind the genomic changes by contrasting DNA from Bangladeshi cholera patients with DNA from other residents of the country who remained healthy despite living in the same house as someone who fell ill with the disease. Individuals who were susceptible to cholera typically carried DNA variants that lie within the region that shows the strongest effect from natural selection.

One category of genes that is evolving in response to cholera, the researchers found, encodes potassium channels that release chloride ions into the intestines. Their involvement makes sense because the toxin spilled by the cholera bacterium spurs such channels to discharge large amounts of chloride, leading to the severe diarrhea that’s characteristic of the disease.

A second category of selected genes helps manage the protein NF- kB, the master controller of inflammation, which is one of the body’s responses to the cholera bacterium. A third category involves genes that adjust the activity of the inflammasome, a protein aggregation inside our cells that detects pathogens and fires up inflammation. However, the researchers don’t know what changes natural selection promotes in these genes to strengthen defenses against the cholera bacterium.

Researchers have identified other examples of infectious diseases driving human evolution, such as malaria in Africa favoring the sickle cell allele, a gene variant that provides resistance to the illness. But they are just starting to search the entire genome for signs of disease effects, and this study is the first to use such methods for cholera.

“I think it’s a great example of the impact infectious diseases have had on human evolution,” says infectious disease specialist William Petri of the University of Virginia School of Medicine in Charlottesville, who wasn’t involved with the study. “It’s ambitious, fairly extensive, and very well done,” adds medical microbiologist Jan Holmgren of the University of Gothenburg in Sweden. One strength of the work is that it flags genes, such as those involved with the inflammasome, that researchers have implicated in other intestinal illnesses such as inflammatory bowel disease, says genetic epidemiologist Priya Duggal of the Johns Hopkins Center for Global Health in Baltimore, Maryland. “Overall, they make a very nice case.”

The findings probably won’t lead to new cholera treatments, says LaRocque, because current measures—which rapidly replace the water and electrolytes patients lose—work very well. “The real issue with cholera,” she says, “is how do we prevent it,” a difficult problem in areas without clean water supplies. But understanding how humans have evolved in response to cholera might help researchers devise more potent vaccines that would provide better protection against this killer, she says.