As AIBN researcher and study researcher Dr. Abu Sina explains: “Because cancer is an extremely complicated and variable disease, it has been difficult to find a simple signature common to all cancers, yet distinct from a healthy cell” . Patients with a few rare blood cancers can be treated with engineered white blood cells – the immune system’s T-cells – that go directly to the tumors and kill them.
But researchers now say they have a found a way to use electrical fields, not viruses, to deliver both gene-editing tools and new genetic material into the cell. Previously, researchers found that tracking ctDNA can predict lung cancer recurrence weeks or months before a patient has clinical symptoms. For the first time, scientists have found a way to efficiently and precisely remove genes from white blood cells of the immune system and to insert beneficial replacements, all in far less time than it normally takes to edit genes.
The Bedford, MA, is building a new type of gene-editing tool based on the research of its founder, Saswati Chatterjee, a professor of Virology at Beckman Research Institute. Since 2011, the researchers have been trying to develop a drug that controls the spread of cancer. By bindings to these proteins, the substance inhibits their mobility without any side effects – an unusual mechanism that the scientists have spent years trying to understand.
A new study by Brown University researchers is the first to reveal key physical properties of these “giant” cancer cells.
I think these polyploidal giant cancer cells ( PGCCs ) are the missing link for why tumors become so complex and heterogeneous so quickly, said Dr. Michelle Dawson, an Assistant Professor of Molecular Pharmacology, Physiology and Biotechnology at Brown and the study’s corresponding author.
The researchers are also going to look for polyploidal giant cancer cells in samples from patients. The Belmonte lab in California, USA developed a modified technique using the CRISPR Cas9 system and published their results in Cell. That is something that is going to stay with us with CRISPR or any other tool we develop that cuts DNA. Belmonte believes the technique could be used to potentially treat neurological disorders like Parkinson’s and Alzheimer’s disease. He envisions a future for rejuvenating groups of neurons – just as they restored muscle, kidney, and insulin-producing function in mice – and possibly even applying this new technology to human patients one day.
Scientists have for the first time used gene-editing to treat Duchenne muscular dystrophy in a large mammal, a significant step towards effective treatment for people with the disorder. But this was the first time the technique was carried out in a large mammal.
Using the CRISPR gene-editing tool, scientists were able to restore dystrophin in four dogs that had the most common genetic mutation seen in DMD patients, by making a single strategic cut in the faulty DNA. Children born with the degenerative disease have a genetic mutation that stops them producing dystrophin, a protein that is vital for muscle strength and function. And while dystrophin production was increased, what impact this might have had on improvements in muscle function was not measured. This was done by injecting the dogs, who were one month old, with two harmless viruses that edited the genome of the dog in the cells of the muscles and heart. The dogs were given CRISPR – via a harmless virus that makes its home in heart and muscle tissue – at one month old.
The study was a collaboration between the Royal Veterinary College, in London, and the UT Southwestern Medical Center, in the US. The technique used in the study was for a genetic fault that affects about 13 % of people with DMD. Dr Eric Olson, Director of UT Southwestern’s Hamon Center for Regenerative Science and Medicine, hopes the next step beyond dogs is a clinical trial in humans.
Our strategy is different from other therapeutic approaches for DMD because it edits the mutation that causes the disease and restores normal expression of the repaired dystrophin, said Dr Leonela Amoasii, lead author of the study.
“Our strategy is different from other therapeutic approaches for DMD because it edits the mutation that causes the disease and restores normal expression of the repaired dystrophin”, said lead author Leonela Amoasii, a researcher at the University of Texas Southwestern Medical Center, in a statement. “But we have more to do before we can use this clinically”.
More research is needed before the program could be used clinically. Independent experts said the study was “promising” and might one day be seen as “ground-breaking” but pointed out that there were some limitations, including the small group of dogs used. Two companies – one local and another foreign – have already shown interest in investing in the upcoming phases of the research. Although a study published last month raised the possibility that the technology might also cause cancer in human cells, experts think this problem is probably only a speed bump on the road to a medical revolution. These “immature” stem cells haven’t learned bad behavior yet, and replace the destructive cells that previously were attacking the patients insulin producing cells.
The authors studied a small group of aged male and female marmosets, non-human primates whose brains are much like humans’ and which exhibit “complex behavior”, senior author Lacreuse explains. To investigate that risk requires a completely different type of research”.
Research using APMCC will help to identify novel therapeutic targets and pinpoint the potential for re-purposing existing cancer drugs.
In fact, more than half of all human cancers are associated with malfunctions that disrupt p53 function. Also contributing were Charles Danko, assistant professor at the Baker Institute for Animal Health in the College of Veterinary Medicine, and John Parker, associate professor of virology in the Baker Institute. But you will also want to understand the long-term effects of cancer therapy. Previous studies have linked the methylation at specific MEs to the development of obesity and cancers. Recent research suggests that MMPs are involved in breast cancer initiation, invasion and metastasis.
The advent of the CRISPR Cas system, a relatively cheap and easy gene-editing method, has only further raised that hope. The researchers bred four beagles with DMD, then used CRISPR to edit exon 51, riddling it with errors. These errors, it was theorized, would cause the body’s affected cells to skip exon 51 altogether.
Now, for the first time, a research team in Lund has succeeded in obtaining dendritic cells by a process called direct reprogramming. Particularly, they found that DNA methylation in senescent cells was highly programmed, and had uniform epigenetic patterns among the different senescent groups. They have also confirmed that the same protein cocktail reprograms human skin-derived cells to dendritic cells. The findings of the UAE research team regarding WWP2 gene is a break through for cancer patients. The exact role of Aβ is still not fully understood; however, scientists are gradually closing in on the answers – which could mean that effective treatments are not far behind.
This finding opens up future possibilities to develop new strategies for immunotherapy against solid tumours and blood cancers, beyond the treatments currently available. Because the forces that twist how science is communicated are elaborate, systemic and interrelated, correcting for science hoopla will not be easy. The key role of adult stem cells is to keep up nutritious tissue and initiate the therapeutic of weakened tissue by replenishing dying or damaged cells. However, researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have shown for the first time that neural stem cells, the cells that give rise to neurons, maintain high levels of ROS to help regulate normal self-renewal and differentiation. UW bioengineering professor Henry C. Lai has focused much of his research on trying to understand the way electromagnetic radiation emitted from these wireless devices affects the human body.
