Nanorobots Successfully Programmed to Seek and Eliminate Tumors in Major Nanomedicine Study

This is a significant nanotechnology advance, although there’s still progress needed for it in further trials. These nanorobots have yet to be tested on humans, which makes them another advance worth looking for the human trial results on when they’re available.

In a major advancement in nanomedicine, Arizona State University (ASU) scientists, in collaboration with researchers from the National Center for Nanoscience and Technology (NCNST), of the Chinese Academy of Sciences, have successfully programmed nanorobots to shrink tumors by cutting off their blood supply.

“We have developed the first fully autonomous, DNA robotic system for a very precise drug design and targeted cancer therapy,” said Hao Yan, director of the ASU Biodesign Institute’s Center for Molecular Design and Biomimetics and the Milton Glick Professor in the School of Molecular Sciences.

“Moreover, this technology is a strategy that can be used for many types of cancer, since all solid tumor-feeding blood vessels are essentially the same,” said Yan.

The successful demonstration of the technology, the first-of-its-kind study in mammals utilizing breast cancer, melanoma, ovarian and lung cancer mouse models, was published in the journal Nature Biotechnology.

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First and foremost, the team showed that the nanorobots were safe and effective in shrinking tumors.

“The nanorobot proved to be safe and immunologically inert for use in normal mice and, also in Bama miniature pigs, showing no detectable changes in normal blood coagulation or cell morphology,” said Yuliang Zhao, also a professor at NCNST and lead scientist of the international collaborative team.

Most importantly, there was no evidence of the nanorobots spreading into the brain where it could cause unwanted side effects, such as a stroke.

“The nanorobots are decidedly safe in the normal tissues of mice and large animals,” said Guangjun Nie, another professor at the NCNST and a key member of the collaborative team.

The treatment blocked tumor blood supply and generated tumor tissue damage within 24 hours while having no effect on healthy tissues. After attacking tumors, most of the nanorobots were cleared and degraded from the body after 24 hours.

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Yan and his collaborators are now actively pursuing clinical partners to further develop this technology.

“I think we are much closer to real, practical medical applications of the technology,” said Yan. “Combinations of different rationally designed nanorobots carrying various agents may help to accomplish the ultimate goal of cancer research: the eradication of solid tumors and vascularized metastases. Furthermore, the current strategy may be developed as a drug delivery platform for the treatment of other diseases by modification of the geometry of the nanostructures, the targeting groups and the loaded cargoes.”

Cancer Immunotherapy Eliminates Tumors in Mice

It’s notable research due to the similarities humans share with mice, but it’s unclear just how relevant this improvement in immunotherapy will be.

Injecting minute amounts of two immune-stimulating agents directly into solid tumors in mice can eliminate all traces of cancer in the animals, including distant, untreated metastases, according to a study by researchers at the Stanford University School of Medicine.

The approach works for many different types of cancers, including those that arise spontaneously, the study found.

The researchers believe the local application of very small amounts of the agents could serve as a rapid and relatively inexpensive therapy that is unlikely to cause the adverse side effects often seen with bodywide immune stimulation.

“When we use these two agents together, we see the elimination of tumors all over the body,” said Ronald Levy, MD, professor of oncology. “This approach bypasses the need to identify tumor-specific immune targets and doesn’t require wholesale activation of the immune system or customization of a patient’s immune .”

One agent is currently already approved for use in humans; the other has been tested for human use in several unrelated clinical trials. A clinical trial was launched in January to test the effect of the treatment in patients with lymphoma.

Significant Step Forward With Basic Cancer Detection Blood Test

Encouraging work, although there is still much that needs done for progress.

A team of researchers has taken a major step toward one of the hottest goals in cancer research: a blood test that can detect tumors early. Their new test, which examines cancer-related DNA and proteins in the blood, yielded a positive result about 70% of the time across eight common cancer types in more than 1000 patients whose tumors had not yet spread—among the best performances yet for a universal cancer blood test. It also narrowed down the form of cancer, which previously published pan-cancer blood tests have not.

The work, reported online today in Sciencecould one day lead to a tool for routinely screening people and catching tumors before they cause symptoms, when chances are best for a cure. Other groups, among them startups with more than $1 billion in funding, are already pursuing that prospect. The new result could put the team, led by Nickolas Papadopoulos, Bert Vogelstein, and others at Johns Hopkins University in Baltimore, Maryland, among the front-runners.

Article in the British press:

Tumours release tiny traces of their mutated DNA and proteins they make into the bloodstream.

The CancerSEEK test looks for mutations in 16 genes that regularly arise in cancer and eight proteins that are often released.

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Dr Cristian Tomasetti, from Johns Hopkins University School of Medicine, told the BBC: “This field of early detection is critical.

“I think this can have an enormous impact on cancer mortality.”

The earlier a cancer is found, the greater the chance of being able to treat it.

Amazing Virus Attacks Brain Cancer and Boosts Immune System

This virus-based approach is at the forefront of the new ways medicine is tackling cancer.

A study attempting to show that viruses could be delivered to brain tumours has delivered that and more.

Not only did the virus in question reach its target, it also stimulated the patient’s own immune system – which then also attacked the tumour.

Preclinical experiments in mice, followed by window-of-opportunity trials in nine human patients, showed that the naturally occurring virus offers potential for a new type of cancer therapy that could be used alongside other treatments.

The virus they used is one that has previously shown potential for cancer treatment – what is known as an oncolytic virus.

It’s called mammalian orthoreovirus type 3, from the reovirus family, and it has previously been shown to kill tumour cells, but leave healthy cells alone.

Previous experiments have demonstrated this mechanism, but researchers from the University of Leeds are the first to successfully direct it at brain tumours.

This is because, until now, it was thought unlikely that the reovirus would be able to cross the blood-brain barrier, a membrane that protects the brain from pathogens.

“This is the first time it has been shown that a therapeutic virus is able to pass through the brain-blood barrier, and that opens up the possibility this type of immunotherapy could be used to treat more people with aggressive brain cancers,” co-lead author Adel Samson said.

Nine patients were selected to be injected with the virus via a single-dose intravenous drip. All either had brain tumours that had spread to other parts of the body, or fast-growing gliomas – a type of brain tumour that is difficult to treat and has a poor prognosis.

All were scheduled to have their brain tumours surgically removed in a matter of days following the reovirus experiment.

The researchers took samples from their tumours after they had been removed, and compared to the tumours of patients who had had brain surgery, but not the reovirus treatment beforehand.

The researchers found the virus in the tumour samples of the trial patients, clearly showing that the virus has been able to reach the cancer.

But they also found an elevated level of interferons, the proteins that activate our immune system. The team says that these interferons were attracting white blood cells to the site to fight the tumour.

“Our immune systems aren’t very good at ‘seeing’ cancers – partly because cancer cells look like our body’s own cells, and partly because cancers are good at telling immune cells to turn a blind eye. But the immune system is very good at seeing viruses,” said co-lead author Alan Melcher.

“In our study, we were able to show that reovirus could infect cancer cells in the brain. And, importantly, brain tumours infected with reovirus became much more visible to the immune system.”

These findings are already being applied in a clinical trial, where patients are being given the reovirus treatment in addition to chemotherapy and radiotherapy. One patient’s treatment is already underway – he is being given 16 doses of the reovirus to treat his glioblastoma.

The reason he is being given multiple doses is because of the way the virus activates the immune system. This clinical trial will determine how well cancer patients can tolerate the treatment, since the virus creates flu-like side effects, and whether it makes the standard treatments more effective.

“The presence of cancer in the brain dampens the body’s own immune system. The presence of the reovirus counteracts this and stimulates the defence system into action,” said one of the researchers, oncologist Susan Short, who is also leading the clinical trial.

“Our hope is that the additional effect of the virus on enhancing the body’s immune response to the tumour will increase the amount of tumour cells that are killed by the standard treatment, radiotherapy and chemotherapy.”

Research: Strong Evidence for Alcohol Causing DNA Damage

It relates to alcohol’s property as a carcinogen.

Scientists have shown how alcohol damages DNA in stem cells, helping to explain why drinking increases your risk of cancer, according to research part-funded by Cancer Research UK and published in Nature today (Wednesday).

Much previous research looking at the precise ways in which alcohol causes cancer has been done in cell cultures. But in this study, researchers have used mice to show how alcohol exposure leads to permanent genetic damage.

Scientists at the MRC Laboratory of Molecular Biology, Cambridge, gave diluted alcohol, chemically known as ethanol, to mice. They then used chromosome analysis and DNA sequencing to examine the genetic damage caused by acetaldehyde, a harmful chemical produced when the body processes alcohol.

They found that acetaldehyde can break and damage DNA within blood stem cells leading to rearranged chromosomes and permanently altering the DNA sequences within these cells.

It is important to understand how the DNA blueprint within stem cells is damaged because when healthy stem cells become faulty, they can give rise to cancer.

These new findings therefore help us to understand how drinking alcohol increases the risk of developing 7 types of cancer including common types like breast and bowel.

Professor Ketan Patel, lead author of the study and scientist, part funded by Cancer Research UK, at the MRC Laboratory of Molecular Biology, said: “Some cancers develop due to DNA damage in stem cells. While some damage occurs by chance, our findings suggest that drinking alcohol can increase the risk of this damage.”

The study also examined how the body tries to protect itself against damage caused by alcohol. The first line of defence is a family of enzymes called aldehyde dehydrogenases (ALDH). These enzymes break down harmful acetaldehyde into acetate, which our cells can use as a source of energy.

Worldwide, millions of people, particularly those from South East Asia, either lack these enzymes or carry faulty versions of them. So, when they drink, acetaldehyde builds up which causes a flushed complexion, and also leads to them feeling unwell.

In the study, when mice lacking the critical ALDH enzyme — ALDH2 — were given alcohol, it resulted in four times as much DNA damage in their cells compared to mice with the fully functioning ALDH2 enzyme.

The second line of defence used by cells is a variety of DNA repair systems which, most of the time, allow them to fix and reverse different types of DNA damage. But they don’t always work and some people carry mutations which mean their cells aren’t able to carry out these repairs effectively.

Professor Patel added: “Our study highlights that not being able to process alcohol effectively can lead to an even higher risk of alcohol-related DNA damage and therefore certain cancers. But it’s important to remember that alcohol clearance and DNA repair systems are not perfect and alcohol can still cause cancer in different ways, even in people whose defence mechanisms are intact.”

This research was funded by Cancer Research UK, Wellcome and the Medical Research Council (MRC).

Professor Linda Bauld, Cancer Research UK’s expert on cancer prevention, said: “This thought-provoking research highlights the damage alcohol can do to our cells, costing some people more than just a hangover.

“We know that alcohol contributes to over 12,000 cancer cases in the UK each year, so it’s a good idea to think about cutting down on the amount you drink.”