And, depending on how further studies progress, it could be implemented via gene therapy.
Early-stage pancreatic cancer has a ‘reset button’
Continue reading “A Biological ‘Time Machine’ With Human Cells Can Help Reverse Cancer” »
Brains aren’t the easiest of organs to study, what with their delicate wiring and subtle whispering of neurotransmitter messages. Now, this research could be made a little easier, as we’ve learned we can swap some critical chemical systems with the host animal being none the wiser.
In a proof-of-concept study run by a team of US researchers, the microscopic worm Caenorhabditis elegans was genetically gifted pieces of a nervous system taken from a radically different creature – a curious freshwater organism known as Hydra.
The swap wasn’t unlike teaching a specific brain circuit a foreign language, and finding it performs its job just as well as before.
Genetic information can be messy. Mapping proteins could offer a clearer view of what’s driving cancer.
Scientists have unveiled new maps of the protein networks underlying different types of cancer, offering a potentially clearer way to see what’s driving the disease and to find therapeutic targets.
Sequencing the genetic information of tumors can provide a trove of data about the mutations contained in those cancer cells. Some of those mutations help doctors figure out the best way to treat a patient, but others remain more of a mystery than a clear instruction manual. Many are exceedingly rare, or there are so many mutations it’s not clear what’s fueling the cancer.
Continue reading “Mapping proteins could offer a clearer view of what’s driving cancer” »
A new resource profiles gene expression and the accessibility of DNA in single cells across the developing human cerebral cortex and may help scientists decipher the effects of noncoding mutations linked to autism.
DNA extracted from ancient Egyptian mummies is offering an intriguing glimpse at what three men might’ve looked like when they hung out in the Fertile Crescent more than 2,000 years ago.
The genetic sleuthing led to highly detailed 3D constructions of a trio from an ancient Nile community known as the Abusir el-Meleq who are estimated to have lived between 2,023 and 2,797 years ago.
The images result from DNA phenotyping, which predicts a person’s physical characteristics based on genetic data. The re-creations mark the first time comprehensive DNA phenotyping has been performed on human DNA this old, according to Virginia-based Parabon NanoLabs, the company behind the images. Parabon typically taps DNA phenotyping to help solve criminal cases.
New research exploring theories of aging has found that small mutations accumulating in DNA are unlikely to be fully responsible for this process.
The research, a collaboration between the Wellcome Sanger Institute, University of Birmingham, University of Edinburgh and others, found that human cells and tissues can accumulate many more mutations than are normally present, without the body showing the features associated with aging.
The new study, published today (30 September) in Nature Genetics, compared DNA taken from individuals with inherited mutations in genes involved in DNA replication with DNA from individuals who have normal versions of these genes. The researchers aimed to understand the impact of defective DNA replication on cancer risk and features associated with aging. The results suggest that build-up of mutations in normal cells is unlikely to be the only factor in the development of age-related disease, adding to the ongoing debate about the causes of aging.
Genetic diseases are a compelling target for viral gene therapy. One condition that scientists are investigating to see if they can treat with gene therapy is a rare genetic disease called Leber congenital amaurosis, or LCA is a progressive condition that disables critical cells within the retina. The damage begins at birth: it eventually robs patients of central vision and color perception, often rendering them legally blind. But there may be another way. On Wednesday, researchers presented evidence from a breakthrough gene-editing experiment that restored some color vision to patients with LCA vision loss.
CRISPR is already under investigation as a gene therapy for blood disorders like sickle cell disease and beta-thalassemia. It may well have other uses, such as treating cancer by editing mutated DNA. But the process is not without its hurdles. Treatments for blood disorders like these involve taking cells from the patient’s body, changing them in vitro in the lab, and then re-infusing them back into the patient’s body. That works great for blood, which you can take out, filter, and put back in with relatively few consequences.
But because LCA is a disease of the retina, you can’t just take out cells and then infuse them back in. The retina is a delicate, multilayered membrane that resents any disturbance. The eye also has a system of physical defenses not unlike the blood-brain barrier. Furthermore, the immune system sometimes responds with extreme prejudice to eye injuries or infections, to the point of causing an actual autoimmune disease where the body attacks its own eyes. How, then, could researchers get the CRISPR treatment into the retina, past the body’s ferocious defenses and without further damage?
(https://www.linkedin.com/in/evelyne-yehudit-bischof/) is an expert in internal medicine and oncology, with a focus on preventative and precision medicine, bio-gerontology, and geronto-oncology.
Dr. Bischof is deeply passionate about next-generation medical technology, and the applications of artificial intelligence for biomedical research and practice.
Fixing breaks in genes with speed and perfection can be a matter of life and death for most organisms. Even the simplest changes in a sequence risk catastrophe, especially if the altered code is responsible for a critical function.
Over the past half a century, biologists have studied the mechanisms involved to piece together most of the major steps involved in making faithful repairs in DNA. Yet, one part of the process has remained frustratingly unclear.
By marking key enzymes and DNA with fluorescent tags and watching the repair process unfold in real-time in an Escherichia coli model, researchers from Uppsala University in Sweden have filled in missing details on how bacteria find the templates they rely on to keep genetic repairs error-free.
New #preprint from JAX’s Nadia Rosenthal and researchers at Rocky Mountain Laboratories: “Genetically diverse mouse models of SARS-CoV-2 infection recapitulate clinical variation and cytokine responses in COVID-19”
The preprint, which has yet to be peer reviewed, shows that mice with different genetic backgrounds exhibit highly variable responses to SARS-CoV-2 infection, mirroring the large differences in #COVID19 disease severity seen in humans:
Since the advent of the COVID-19 pandemic, tremendous progress has been made in developing effective vaccines against SARS-CoV-2, the coronavirus that causes COVID-19, and in treating ill patients. Nonetheless, much more needs to be learned about SARS-CoV-2 infectivity and COVID-19 progression to lessen the continuing threat of infection, as the recent emergence and rapid spread of the delta variant has emphasized.
