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Guess what the killer of dreaded cancer could be.

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Scientists probing the reason why cancer is far less common in individuals with Huntington’s disease have revealed that the gene responsible for the fatal brain condition produces a molecule that is deadly to cancer cells.

In a recent paper published in the journal EMBO Reports, scientists from Northwestern University in Chicago, IL, note exactly how they tested the molecule in human and mouse cancer cells, as well as in mice with ovarian cancer.

“This molecule,” explains senior study author Marcus E. Peter, who’s a professor of cancer metabolism, “is a super assassin against all tumor cells. We’ve never seen anything this powerful.”

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He and his colleagues hope that the discovery will lead to a short-lived treatment that can target and destroy cancer cells without triggering the progressive brain damage that occurs alongside Huntington’s disease.

Huntington’s disease is a fatal and inherited disorder that destroys nerve cells in the brain, causing a progressive decline in mental and physical ability. Symptoms will typically emerge between age 30 and 50 and progress over a period that lasts 10–25 years.

There are currently 30,000 people in the United States living with Huntington’s disease, as well as another 200,000 who are at risk of inheriting it.

There is currently no cure for Huntington’s disease, which arises from a fault in the huntingtin gene. The gene is passed from parent to child. Children with a parent who has the disease have a 50 percent chance of carrying the gene.

The faulty huntingtin gene contains more than a normal number of repeats of a certain sequence of nucleotides in its DNA code. Nucleotides are the “alphabet”of DNA and RNA and there are five of them: A, G, C, T, and U.

In Huntington’s disease, the huntingtin gene contains too many repeated sequences of CAG. The more repeated sequences of CAG in the gene, the earlier the disease develops.

The repeated sequences give rise to molecules called small interfering RNAs that attack genes that are important for cell survival, and they trigger a type of cell death that brain cells are susceptible to.

However, it seems that cancer cells are much more vulnerable to this type of cell death, which opens up the possibility of using the process to eliminate cancer cells in a way that does not damage healthy cells.

The cell death mechanism that is activated by small interfering RNAs was first identified in previous research by Prof. Peter and first study author Dr. Andrea E Murmann, who is a research assistant professor in medicine.

Explaining the reason for the new study, Dr. Murmann says that the researchers wondered whether there might be situations in which the cell death mechanism is “overactive in certain people, and where it could cause loss of tissues.”

“These patients,” she adds, “would not only have a disease with an RNA component, but they also had to have less cancer.”

In a search for diseases with this combination of features — high tissue loss, lower incidence of cancer, and involving RNAs — Huntington’s stood out the most.

Closer examination of the faulty huntingtin gene revealed a similar pattern of repeated sequences of DNA code to that found in the cell death mechanism identified in the earlier study: both were high in C and G nucleotides.

“Toxicity,” Dr. Murmann notes, “goes together with C and G richness. Those similarities triggered our curiosity.”

The team tested the effects of the small interfering RNAs produced by the repeated sequences in human and mouse cancer cells grown from laboratory cell lines.

They tested them in brain, breast, colon, liver, lung, ovarian, and skin cancer cells. The “assassin molecules” killed all the cancer cells from both human and mouse cell lines.

They also tested the molecules’ effects on live mice with human ovarian cancer. The molecules were delivered in nanoparticles that released their cargo when they reached the tumors.

The results showed that the molecules slowed down tumor growth “with no signs of toxicity to the mice,” and also with no evidence that the tumors developed resistance to the treatment.

The team is now working on improving the method so that the nanoparticles can reach the tumors more effectively. The scientists also want to find a way to keep them stable during storage.

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Health & Lifestyle

Quick rise in young people with Type 2 diabetes is alarming

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Hundreds of young people are being treated for Type 2 diabetes, a 41% rise in just four years.

The condition occurs when the body cannot make enough insulin to regulate blood sugar levels.

It is often linked to obesity and is most commonly seen in adults, where it can lead to a range of health problems such as heart disease and strokes.

Some 715 people under the age of 25 received treatment for the disease in England and Wales during 2016/17 and 78.6% of them were obese.

The number of cases is up from the 507 registered in 2013/14, according to the Royal College of Paediatrics and Child Health.

But the true number may be much higher, as the RCPCH recorded only those young people being treated in paediatric units, not by a GP.

Professor Russell Viner, president of the RCPCH, said: “A rise in Type 2 diabetes of this magnitude is alarming and shows that the childhood obesity epidemic is starting to bite.

“It’s also concerning that we might not be seeing the full picture.”

The Local Government Association, which represents 370 councils in England and Wales, said more support was needed, especially for obese children and ethnic minorities, as almost half of those treated in 2016/17 were black or Asian.

Izzi Seccombe, chairwoman of the LGA’s community wellbeing board, said: “These figures are a sad indictment of how we have collectively failed as a society to tackle childhood obesity, one of the biggest health challenges we face.”

She called for “urgent action”, saying: “Type 2 diabetes can be a lifelong debilitating illness and these figures will only multiply if we delay.

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Health & Lifestyle

A new way to ‘freeze’ water

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In an experiment, the researchers demonstrated that it is possible to more than double the amount of time, from the clinical standard approach, that red blood cells can be stored. At present, red blood cells can be stored for a maximum of 42 days. Using this new approach, it was possible to extend this up to 100 days.

Alongside the immediate practical applications, the researchers also believe that this discovery could enable fundamental scientific research by making it possible to study liquid phase reactions at a much lower temperature than is currently possible.

Heck, who knows — although this approach studiously avoids actual freezing, maybe it could prompt advances in the kind of long-term cryogenic preservation process that scientists, sci-fi authors, and, allegedly, Walt Disney have speculated about for years.

“We are now focused on increasing the volume of the preserved liquid phase from the 1-100 milliliter range to 500 milliliters to enable mass preservation of samples,” Usta continued. “[We also want to translate] our approach to the preservation of exotic cell types and organs, such as the liver, since our center already has a very active cell and organ preservation research thrust. Through collaborations, we are also looking into further understanding our observations by conducting [additional] computational and laboratory experiments.”

A paper describing the work was recently published in the journal Nature Communications.

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