Scientists discover new compound that could help treat ovarian cancer

A new research now finds scientists  discover a compound that could be more effective in treating a few types of cancers than standard chemotherapy.

While chemotherapy is still the first line of defense for most cancer tumours and is often highly effective, many cancers are naturally resistant, or develop resistance, to commonly used first-line chemotherapy drugs like cisplatin.

Researchers identified new drug-candidates that would work against these types of treatment resistant cancers.

In the study, scientists screened new compounds made in the lab against a “panel” of cancers that were sensitive and resistant to standard cancer therapy. They further tested the compounds with non-malignant cells to see how toxic they were to normal cells.

They found two lead compounds that had low toxicity to non-malignant cells but were highly active against cancer cells sensitive or resistant to standard treatment.

Speaking about it, a Prof. said, “Many cancer cells – about 20 per cent – become resistant to common treatments by learning to ignore the internal signals that tell them to undergo programmed cell death, known as apoptosis.

He further added, “We have identified a compound that kills cancer cells that avoids the need for apoptosis, and so the usual resistance mechanism doesn’t work against our compound.”

According to the Prof., the compound is as potent as common current chemotherapeutics, but crucially retains its potency against treatment-resistant cancers.

By looking at the cellular response from the cancers the researchers found the new drug lead works by two different mechanisms simultaneously, making it much more difficult for cancers to develop resistance toward them during treatment.

“We think this compound could be particularly effective against ovarian cancer,” he added.
The team used a technique called “proteomics” to determine how thousands of proteins in the cells responded to exposure to the drug lead.

Professor said, “Proteomics is a remarkably powerful approach we have  to identify how living things respond to new drug candidates. The multiple mechanisms of action of the new molecules was an unexpected and exciting result.”

Researchers now want to carry out further studies to find out if the compound can be used in combination with current treatments to improve their performance.

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New compound shows promise in treatment of Alzheimer’s

Some researchers have identified a drinkable cocktail of designer molecules that interferes with a crucial first step of Alzheimer’s and even restores memories in mice.

The binding of amyloid beta peptides to prion proteins triggers a cascade of devasting events in the progression of Alzheimer’s — accumulation of plaques, a destructive immune system response, and damage to synapses.

“We wanted to find molecules that might have a therapeutic effect on this network,” said senior author.

Researchers screened tens of thousands of compounds looking for molecules that might interfere with the damaging prion protein interaction with amyloid beta. They found that an old antibiotic looked like a promising candidate but was only active after decomposing to form a polymer. Related small polymers retained the benefit and also managed to pass through the blood-brain barrier.

They then dissolved the optimized polymeric compound and fed it to mice engineered to have a condition that mimics Alzheimer’s. They found that synapses in the brains were repaired and mice recovered lost memory.

A collaborating team  reported a positive response when they delivered the same cocktail to cells modeled to have Creutzfeldt-Jakob Disease, a devasting neurological condition caused by infection with misfolded prion protein.

The next step is to verify the compounds aren’t toxic in preparation for translation to clinical trials for Alzheimer’s disease.

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New compound heals diabetic wound faster

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Researchers have discovered a compound that accelerates diabetic wound healing, which may open the door to new treatment strategies.

Non-healing chronic wounds are a major complication of diabetes, but the reasons why diabetic wounds are resistant to healing are not fully understood, and there are limited therapeutic agents that could accelerate or facilitate their repair.

A team of researchers from University of Notre Dame in Indiana, US previously identified two enzymes called matrix metalloproteinases (MMPs), MMP-8 and MMP-9, in the wounds of diabetic mice.

The researchers used the MMP-9 inhibitor referred to as ND-322, which accelerated wound healing in diabetic mice.

In this new study, the researchers report the discovery of a better MMP-9 inhibitor referred to as ND-336.

"ND-336 is a six-fold more potent inhibitor than ND-322 and has 50-fold selectivity towards inhibition of MMP-9 than MMP-8," said lead researcher Mayland Chang.

"The compound ND-336 has potential as a therapeutic to accelerate or facilitate wound healing in diabetic patients," Chang pointed out.

The researchers said they are currently recruiting diabetic patients to ascertain the levels of MMP-8 and MMP-9 in their wounds.

The study appeared in the journal Proceedings of the National Academy of Sciences (PNAS)

New compound shrinks pancreatic cancer tumours

Scientists have designed a new chemical compound that has reduced the growth of pancreatic cancer tumours by 80% in treated mice.

The compound, called MM41, was designed to block faulty genes by targeting little knots in the DNA, called quadruplexes, which are very different from normal DNA and which are especially found in faulty genes. The findings showed that MM41 had a strong inhibiting effect on two genes - k-RAS and BCL-2 - both of which are found in the majority of pancreatic cancers.

Researchers at the University College London (UCL), led by professor Stephen Neidle, conducted a small-scale trial, treating two groups of eight mice with pancreatic tumours with different doses of MM41 twice a week for 40 days (12 doses). A further control group received no treatment.

The tumours in the group given the larger dose decreased by an average of 80% during the treatment period, and after 30 days, tumour regrowth stopped in all the mice. For two of the mice in this group, the tumour disappeared completely with no signs of regrowth after treatment ended for a further 239 days (the approximate equivalent to the rest of their natural life span).
Analysis of the mice tumours showed that the MM41 compound had been taken up into the nucleus of the cancer cells showing that it was able to effectively target the pancreatic cancer tumour. The team also saw no significant side effects on the mice during the study: there was no damage to other tissue or organs, and none of the mice showed any significant weight loss.

"This research provides a potentially very powerful alternative approach to the way that conventional drugs tackle pancreatic cancer, by targeting a very specific area of the DNA of faulty genes," said Neidle. "One of the genes that MM41 blocks - the BCL-2 gene - is involved in regulating apoptosis, the body's natural process which forces cells to die if they become too damaged or unhealthy to be repaired.

"BCL-2 is present in high amounts in many tumours and helps cancer cells to survive, but when the BCL-2 gene is blocked by MM41 in mice, the cancer cells succumb to apoptosis and die," said Neidle. Neidle stressed that although these results are exciting, MM41 is not ideal for trialling in humans and further refinements are needed.

The study was published in the journal Nature Scientific Reports.

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