The Cancer “Vaccine” That Eliminated Tumors in Mice is Now Beginning Human Trials

What could be one of the most promising scientific advances of the 21st century thus far has just entered a new stage.

An injectable “vaccine” delivered directly to tumours in mice has been found to eliminate all traces of those tumours, cancer researchers have found – and it works on many different kinds of cancers, including untreated metastases in the same animal.

Scientists at Stanford University School of Medicine have developed the potential treatment using two agents that boost the body’s immune system, and a human clinical trial in lymphoma patients is currently underway.

“When we use these two agents together, we see the elimination of tumours all over the body,” said senior researcher, oncologist Ronald Levy.

“This approach bypasses the need to identify tumour-specific immune targets and doesn’t require wholesale activation of the immune system or customisation of a patient’s immune cells.”

Cancer immunotherapy is tricky. Because cancer cells are produced by the body, the immune system doesn’t see them as a threat the same way it sees invaders like viruses.

That’s why some cancer immunotherapy treatments focus on training the immune system to recognise cancer cells as a problem.

It’s an effective area of treatment, but one that often involves removing the patient’s immune cells from their body, genetically engineering them to attack cancer, and injecting them back in – a process that is both expensive and time-consuming.

The Stanford vaccine could be much cheaper and easier.

It doesn’t work like the vaccines you might be familiar with. Instead of a prophylactic administered prior to infection, the researchers gave it to mice that already had tumours, injecting directly into one of the affected sites.

“Our approach uses a one-time application of very small amounts of two agents to stimulate the immune cells only within the tumour itself,” Levy said.

“In the mice, we saw amazing, bodywide effects, including the elimination of tumours all over the animal.”

The vaccine exploits a peculiarity of the immune system. As a tumour grows, the immune system’s cells, including T cells, recognise the cancer cells’ abnormal proteins and move in to take care of business.

But cancer cells can accumulate mutations to avoid destruction by the immune system, and suppress the T cells, which attack abnormal cells.

The new vaccine works by reactivating these T cells.

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Of the 90 mice with lymphoma, 87 were completely cured – the treatment was injected into one tumour, and both were destroyed. The remaining 3 had a recurrence of the lymphoma, which cleared up after a second treatment.

The treatment was also effective on the mice genetically engineered to develop breast cancer. Treating the first tumour often, but not always, prevented the recurrence of tumours, and increased the animals’ lifespan, the researchers said.

The team then tested mice with both lymphoma and colon cancer, injecting only the lymphoma. The lymphoma was destroyed, but the colon cancer was not. This demonstrates that T cells in tumours are specific to that kind of tumour – so the treatment isn’t without limitations.

But it does mean that immunotherapy is possible without genetically engineering cells outside the body; or, as is the case with a previous vaccine, extracting cancer RNA, treating it, injecting it into the body, and applying an electric charge to deliver it to immune cells.

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Its efficacy is about to be tested, though. The clinical trial currently underway is expected to recruit 15 patients with low-grade lymphoma to see if the treatment works on humans.

If it’s effective, the treatment may be used in the future on tumours before they’re surgically extracted to help prevent metastases, or even prevent recurrences of the cancer.

“I don’t think there’s a limit to the type of tumour we could potentially treat, as long as it has been infiltrated by the immune system,” Levy said.

The research has been published in the journal Science Translational Medicine.

Obesity May Dull the Sense of Taste

The study here found that obese mice had about 25 percent fewer taste buds than mice of a healthy weight. As some similar effect is likely found in humans, this research should provide an increased motivation (that is, enjoyment of food) for reducing the obesity epidemic, which I have written about at more length before.

Previous studies have indicated that weight gain can reduce one’s sensitivity to the taste of food, and that this effect can be reversed when the weight is lost again, but it’s been unclear as to how this phenomenon arises. Now a study publishing March 20 in the open-access journal PLOS Biology by Andrew Kaufman, Robin Dando, and colleagues at Cornell University shows that inflammation, driven by obesity, actually reduces the number of taste buds on the tongues of mice.

A taste bud comprises of approximately 50 to 100 cells of three major types, each with different roles in sensing the five primary tastes (salt, sweet, bitter, sour, and umami). Taste bud cells turn over quickly, with an average lifespan of just 10 days. To explore changes in taste buds in obesity, the authors fed mice either a normal diet made up of 14% fat, or an obesogenic diet containing 58% fat. Perhaps unsurprisingly, after 8 weeks, the mice fed the obesogenic diet weigh about one-third more than those receiving normal chow. But strikingly, the obese mice had about 25% fewer taste buds than the lean mice, with no change in the average size or the distribution of the three cell types within individual buds.

Diabetes Drug Significantly Reverses Alzheimer’s Memory Loss in Mice

It looks as though this may be a promising development in Alzheimer’s research.

A drug developed for diabetes could be used to treat Alzheimer’s after scientists found it “significantly reversed memory loss” in mice through a triple method of action.

The research, published in Brain Research, could bring substantial improvements in the treatment of Alzheimer’s disease through the use of a drug originally created to treat type 2 diabetes.

Lead researcher Professor Christian Holscher of Lancaster University in the UK said the novel treatment “holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer’s disease.”

Scientists Find Where Nicotine Addiction Can be Blocked in the Mouse Brain, Providing an Advance to Blocking It in the Human Brain

Humans and mice have some similar enough brain structures that make this a relevant advance in giving people increased control to stop the scourge of nicotine addiction.

Brain researchers have pinpointed a small group of brain cells that are especially responsive to nicotine, and which might be the main culprits in driving addiction to the substance.

By tweaking these neurons in mouse brains, scientists were able to curb nicotine addiction in the animals. Not only have their results solved an important piece of the nicotine addiction puzzle, but they could also lead us towards new treatments for the problem.

Nicotine is one of humanity’s most popular drugs – it’s considered to be the third most addictive substance we know. And because it holds such a sway on our brains, it’s extremely difficult to quit.

According to the US Centres for Disease Control and Prevention, smoking is a leading cause of preventable death, with about 1,300 people in the US dying every day due to cigarette smoking or smoke exposure.

Which is why a team led by researchers from The Rockefeller University has been digging around brain chemistry to identify potential new drug targets that could help curb the addiction.

They focussed on two small brain regions located in the midbrain – the evolutionary older part of vertebrate brains, and one of the many brain features we share with mice.

These two interconnected regions – the medial habenula and the interpeduncular nucleus (IPN) – are known to be involved in drug dependence, and also contain the receptors that nicotine binds to once it enters the bloodstream and crosses into the brain.

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Even though so far we only have seen these results in mice, we do share similar brain structures with these animals, so the researchers are confident we can learn something about human addiction here.

“What all of this tells us is that the habenula-IPN pathway is important for smoking in humans,” says Ibanez-Tallon.

Now that the researchers know where to look, they’ll be further investigating how to manipulate the Amigo1 neurons in order to discover new ways to target nicotine addiction.

The study has been published in PNAS.