Scientists have developed a new way of treating cancer with iron nanoparticles, which were able to kickstart the immune system into attacking tumours in groups of mice.
In the study, macrophages (white blood cells) fought back against spreading tumours after a dose of iron nanoparticles, stopping the cancer from taking hold.
In addition to shrinking existing tumours in mice, the treatment stopped cancer tumours from spreading through the body, according to researchers from Stanford University and Oregon Health & Science University.
“It was really surprising to us that the nanoparticles activated macrophages so that they started to attack cancer cells in mice,” said researcher Heike Daldrup-Link from Stanford. “We think this concept should hold in human patients, too.”
The researchers used ferumoxytol for their tests, an iron supplement already available commercially for the treatment of anaemia, where the body doesn’t have enough iron naturally.
Originally the idea was to use the iron nanoparticles as a kind of Trojan horse, sneaking chemotherapy into tumours. As it turned out, though, the control group of mice – which were given iron without chemo drugs – showed the best results in terms of tumour suppression.
Follow-up tests conducted in cells in a dish determined that it was the macrophages that were battling the cancer after receiving the iron – ordinarily, these macrophages stop attacking tumours and start helping their growth, once the tumours reach a certain size.
The researchers think the iron and macrophages were able to somehow restart cell apoptosis (natural programmed cell death) inside tumours. While the treatment isn’t strong enough to remove cancer on its own, it could be if used in combination with existing drugs.
The dose of ferumoxytol used in the tests was similar to a safe dose given in the treatment of anaemia, with the anti-cancer effect from each dose seeming to last for around three weeks.
In subsequent tests, the team noticed iron nanoparticles having a suppressive effect on cancer metastasis – where tumours spread to nearby tissues and organs – and found the treatment reduced tumour size when given before the cancers were introduced
Now the researchers want to work out ways in which this could benefit humans as a complement to existing chemotherapy.
While the results have only been seen so far in mice, the team hopes the iron nanoparticles might be able help while patients recover between doses of chemo – or perhaps clean up remaining tumour cells after surgery.
“In many studies, researchers just consider nanoparticles as drug vehicles,” added Daldrup-Link. “But they may have hidden intrinsic effects that we won’t appreciate unless we look at the nanoparticles themselves.”
The findings have been published in Nature Nanotechnology.
The first new asthma pill in two decades has just completed its third phase of clinical trials, and not only did patients report instant relief – the pill actually started to repair the lining of their airways.
Taken twice daily, the pill was shown to reduce inflammation by 80 percent in people with moderate-to-severe asthma.
“This research shows massive promise and should be greeted with cautious optimism,” said Samantha Walker from charity organisation Asthma UK, which was not involved in the research. “The possibility of taking a pill instead of using an inhaler will be a very welcome one among the 5.4 million people in the UK with asthma.”
Researchers from Leicester University in the UK just finished testing the drug, called Fevipiprant, in a phase-III trial. This means it’s already passed phase-I and phase-II trials, which assess safety and severe side effects, and also short-term results on a small group of patients.
The trial involved 61 participants, split into two groups. One group was given 225 mg of the drug twice a day for 12 weeks, and the other were assigned a placebo. Both the Fevipiprant and placebos were taken with existing asthma medications, rather than replacing them.
The effects were tested via a series of breathing tests, airway tissue samples, and CT scans of the chest, but one of the main aims of the trial was to observe the effect of Fevipiprant on the patients’ airway inflammation – typically measured via something called sputum eosinophil count.
As the researchers explain, the sputum eosinophil count measures inflammation by detecting levels of a specific type of white blood cell that’s associated with asthma, and is found in higher levels the more severe the condition.
As a baseline, people who don’t have asthma will have less than 1 percent sputum eosinophil count, while those with moderate-to-severe asthma usually have a reading of about 5 percent.
“The rate in people with moderate-to-severe asthma taking [Fevipiprant] was reduced from an average of 5.4 percent to 1.1 percent over 12 weeks,” the researchers report in a press release.
The researchers say that this progressive effect, plus indications that the drug was actually repairing damaged airway tissue, could allow patients with severe asthma to stop taking strong medications to deal with their disease.
“I’m really excited by this because this is the first treatment that I’m aware of that has been able to show effects across the board,” lead researcher Chris Brightling told Denis Campbell at The Guardian.
“I’m excited by how effective it’s likely to be and also about its potential to reduce the need for patients to take oral steroids. Those people would be able to stop taking those drugs, which would make a huge difference to them.”
Of course, there’s still a long way to go before we’ll see the drug on the market – if it even makes it. Brightling told The Guardian, “more than two but less than three years’ time”, if everything goes to plan.
He’s now preparing for another clinical trial involving 850 patients, and results are expected some time in 2018. Other studies are also reportedly in the planning stages.
Let’s hope this drug continues to live up to its promise to give asthmatics a better option – or at least sparks more research in an area that’s been dormant for too long.
The results of the trial have been published in Lancet Respiratory Medicine.
The U.S. Food and Drug Administration approved the first intraocular lens (IOL) that provides cataract patients with an extended depth-of-focus, which helps improve their sharpness of vision (visual acuity) at near, intermediate and far distances.
Cataracts are a common eye condition where the natural lens becomes clouded, impairing a patient’s vision. According to the National Eye Institute, more than 20 percent of Americans will have cataracts by the age of 65, and the prevalence increases with age. In cataract surgery, the clouded natural lens is removed and replaced with an IOL.
“While IOLs have been the mainstay of cataract treatment for many years, we continue to see advances in the technology,” said Malvina Eydelman, M.D., director of the Division of Ophthalmic and Ear, Nose and Throat Devices in the FDA’s Center for Devices and Radiological Health. “The Tecnis Symfony Extended Range of Vision IOL provides a new option for patients that may result in better vision across a broader range of distances.”
Traditional monofocal IOLs have been limited to improving distance vision. The Tecnis Symfony IOL improves visual acuity at close, intermediate and far ranges and, therefore, may reduce the need for patients to wear contact lenses or glasses after cataract surgery.
The approval is based on a review of results from a randomized clinical trial comparing 148 cataract patients implanted with the Tecnis Symfony IOL to 151 cataract patients implanted with a monofocal IOL. The study evaluated visual acuity at near, intermediate and far ranges; contrast sensitivity (the ability to distinguish small differences between light and dark); and adverse events for six months after implantation. Of the patients implanted with the Tecnis Symfony IOL, 77 percent had good vision (20/25), without glasses at intermediate distances, compared to 34 percent of those with the monofocal IOL. For near distances, patients with the Tecnis Symfony IOL were able to read two additional, progressively smaller lines on a standard eye chart than those with the monofocal IOL. Both sets of patients had comparable results for good distance vision.
Patients implanted with the Tecnis Symfony IOL may experience worsening of or blurred vision, bleeding or infection. The device may cause reduced contrast sensitivity that becomes worse under poor visibility conditions such as dim light or fog. Some patients may experience visual halos, glare or starbursts. The device is not intended for use on patients who have had previous trauma to their eye.
The Tecnis Symfony IOL is also available in four toric models, which are indicated for the reduction of residual refractive astigmatism or imperfections in the curvature of the eye.
The Tecnis Symfony Extended Range of Vision IOL is manufactured by Abbott Medical Optics, Inc. of Santa Ana, California.
Scientists in the UK have developed a new material that can be inserted into teeth to repair and regenerate dentin – the hard, bone-like tissue that makes up the bulk of all teeth.
Just like regular fillings, which are inserted into a tooth to block off spaces where bacteria could colonise, the new material is injected into the tooth and hardened with UV light. But once inside the pulp of the tooth, it actually encourages stem cells to proliferate and grow into dentin.
“We have designed synthetic biomaterials that can be used similarly to dental fillings but can be placed in direct contact with pulp tissue to stimulate the native stem cell population for repair and regeneration of pulp tissue and the surrounding dentin,” says lead researcher Adam Celiz, a therapeutic biomaterials researcher from the University of Nottingham.
The technique just won second prize in the materials category of the UK Royal Society of Chemistry’s Emerging Technologies Competition 2016, and while there’s not a whole lot of information available about how it actually works, it appears to be a new form of ‘pulp capping’.
Pulp capping is a technique dentists use to try and stop dental pulp from dying. Pulp is one of the four major components of teeth, along with enamel, dentin, and cementum.
The surface enamel is the hardest layer, and under that is the second hardest layer, dentin. Dentin is important because it surrounds and connects to the pulp of the tooth, which is made up of living connective tissue and cells called odontoblasts, and found in the middle of your tooth.
The pulp is where your blood vessels, nerves, and connective tissue are found, so you really don’t want to mess that up.
Problems start when you get a cavity that eats away your enamel, dentin and cementum – a calcified substance covering the root of a tooth – and exposes the pulp. If dentists don’t get in there fast enough with a protective pulp-capping substance (or if the procedure fails), you’re looking at an expensive and painful root canal treatment.
Right now, pulp capping materials are usually made of materials such as calcium hydroxide or Mineral trioxide aggregate (MTA), and they don’t do anything other than protect, and around 10 to 15 percent of these fillings fail.
That’s where the University of Nottingham’s invention comes in. Their new pulp capping material is designed to stop pulp capping failure by encouraging the growth of more natural dentin to protect it.
“In in vitro testing, the fillings stimulated the proliferation and differentiation of stem cells into dentin, the bony tissue that forms the bulk of the tooth under the white enamel.
The researchers believe that if used in a damaged tooth, those stem cells can repair the kind of damage that often comes from the installation of a filling. In essence, the biomaterial filling would allow the tooth to heal itself.”
As mentioned earlier, the team hasn’t released a lot of information about their new material, and have yet to publish it in a peer-reviewed journal, so we’ll have to be cautiously optimistic about it for now until we can see more information about exactly how it works, and how expensive it will be.
Cancer stem cells can take cover and evade chemotherapy by hiding in fatty tissue, according to new research.
A team of scientists in the US looked at the behaviour of leukaemia stem cells in mice and found they were building their own hideout in the fat – a bolt-hole that then increased their resistance to chemo treatments.
Not only that, but the cancer cells apparently use the fatty deposits to generate extra energy for themselves. The researchers say this activity could help explain why some cancers prove harder to treat, and are more likely to recur.
The fatty tissue acts as a kind of “robber’s cave” for the cancer cells, according to the team from the University of Colorado Cancer Centre.
“The basic biology was fascinating: the tumour adapted the local environment to suit itself,” said researcher Craig Jordan.
When analysing a mouse model of leukaemia, the researchers noted the fatty (or adipose) tissue had a higher concentration of cancer stem cells to regular cancer cells.
Like healthy stem cells, cancer stem cells are capable of developing into several cell types, and are thought to form new tumours and cause relapses.
These cancer stem cells were also found to be triggering a process called lipolysis, where fatty acids are released from tissue to produce energy: in essence, the cells were creating a new energy source for themselves.
When a chemotherapy treatment was introduced, the cancer stem cells hiding in the fatty tissue and living off its acids were noted to be more resistant than the other cancer stem cells outside the tissue. The same effects were found in samples of human leukaemia.
Three clues prompted the scientists to carry out their research: obesity is already linked to a poorer recovery rate for leukaemia patients; cancer stem cells drive growth and can cause relapses in leukaemia; and they rely heavily on the tumour micro-environment they’re in.
With those factors in mind, the researchers wondered – could cancer stem cells in fatty tissue be causing poorer prognosis in obese patients? From the new findings, it seems the answer could be yes, although this is still just a hypothesis for now.
The researchers intend to follow up their study by testing mouse models of different obesity levels, to see if extra fat provides more space for cancer stem cells to hide away in (or more energy for them to live off).
Obesity increases the risk of several cancer types, although scientists haven’t yet pinned down the reason why.
Although this new study doesn’t solve the problem, it means we’re getting closer, giving us new understanding into why leukaemia in overweight patients is harder to fight and more likely to come back.
The findings are published in Cell Stem Cell.