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Researchers employ a genetically modified bacteria to eliminate tumors in mice.
The report published in February issue of the Science Translational Medicine discloses an immunological mechanism that contributes to bacteria-driven, cancer–killing activity claiming that a genetically altered Salmonella typhimurium a gastroenteritis-causing bacteria, is an effective destroyer of mouse tumors.
The reasoning behind most bacteria-driven cancer therapies is the fact that oxygen-starved and necrotic cores of tumors are attractive environments for anaerobic bacteria such as Salmonella, Clostridium, and Listeria, and an infection can lead to tumor colonization by these bugs. By means of active multiplication, the bacteria can directly kill the cancer cells and also attract the attention of the body’s immune system (which is generally suppressed within tumors), leading to further tumor destruction.
Things are not so easy and there are safety issues in implementation for patients. In a recent trial, researchers found attenuated Salmonella bacteria to be safe, but they were unable to create a strong response. To overcome the issue researchers tried to boost the potency of the Salmonella by engineering the bacteria to overexpress a protein proven to induce a strong immune response—flagellin B. As per the new report, intravenous injections of the flagellin expressing Salmonella eliminated the experimental tumors in 55 percent of mice, which then remained healthy until the end of the four-month observation period. Without overexpression of flagellin, the tumors in the mice tended to regrow after initial shrinking by the Salmonella.
Some scientist agrees that current study extends our understanding of bacterial-based cancer therapy at a molecular level but one of the problems with developing bacterial cancer treatments has been that “these bacteria are almost a black box.” They promote cancer destruction, but no one is exactly sure how.
Source: J.H. Zheng et al., “Two-step enhanced cancer immunotherapy with engineered Salmonella typhimurium secreting heterologous flagellin,” Science Translational Medicine, 9, eaak9537, 2017.
Cambridge, UK (Scicasts) — A gene essential to the production of pain-sensing neurons in humans has been identified by an international team of researchers co-led by the University of Cambridge.
The discovery, reported May 25 in the journal Nature Genetics, could have implications for the development of new methods of pain relief.
Pain perception is an evolutionarily-conserved warning mechanism that alerts us to dangers in the environment and to potential tissue damage. However, rare individuals – around one in a million people in the UK – are born unable to feel pain. These people accumulate numerous self-inflicted injuries, often leading to reduced lifespan.
Using detailed genome mapping, two teams of researchers collaborated to analyse the genetic make-up of 11 families across Europe and Asia affected by an inherited condition known as congenital insensitivity to pain (CIP). This enabled them to pinpoint the cause of the condition to variants of the gene PRDM12. Family members affected by CIP carried two copies of the variant; however, if they had only inherited one copy from their parents, they were unaffected.
The team looked at nerve biopsies taken from the patients to see what had gone wrong and found that particular pain-sensing neurons were absent. From these clinical features of the disease, the team predicted that there would be a block to the production of pain-sensing neurons during the development of the embryo – they confirmed this using a combination of studies in mouse and frog models, and in human induced pluripotent stem cells (skin cells that had been reset to their ‘master state’, which enables them to develop into almost any type of cell in the body).
PRDM12 had previously been implicated in the modification of chromatin, a small molecule that attaches to our DNA and acts like a switch to turn genes on and off (an effect known as epigenetics). The researchers showed that all the genetic variants of PRDM12 in the CIP patients blocked the gene’s function. As chromatin is particularly important during formation of particular specialised cell types such as neurons, this provides a possible explanation for why pain-sensing neurons do not form properly in the CIP patients.
“The ability to sense pain is essential to our self-preservation, yet we understand far more about excessive pain than we do about lack of pain perception,” says Professor Geoff Woods from the Cambridge Institute for Medical Research at the University of Cambridge, who co-led the study. “Both are equally important to the development of new pain treatments – if we know the mechanisms that underlie pain sensation, we can then potentially control and reduce unnecessary pain.”
PRDM12 is only the fifth gene related to lack of pain perception to have been identified to date. However, two of the previously-discovered genes have already led to the development of new pain killers that are currently been tested in clinical trials.
“We are very hopeful that this new gene could be an excellent candidate for drug development, particularly given recent successes with drugs targeting chromatin regulators in human disease,” adds Dr. Ya-Chun Chen from the University of Cambridge, the study’s first author. “This could potentially benefit those who are at danger from lack of pain perception and help in the development of new treatments for pain relief.”
Article adapted from a University of Cambridge news release. The original article is licensed under a Creative Commons Licence.
Publication: Transcriptional regulator PRDM12 is essential for human pain perception. Chen, Y-C et al. Nature Genetics; (May 25, 2015)
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