Pediatrics researchers at The Children’s Hospital of Philadelphia and McGill University in Montreal have identified a gene variant that raises a child’s risk for type 1 diabetes, formerly called juvenile diabetes. As investigators continue to pinpoint genes contributing to diabetes, they have their eyes on providing a scientific basis for designing better treatments and preventive measures for the disease.
The research adds a new gene and new knowledge to the four genes previously discovered for type 1 diabetes, in which the immune system destroys insulin-producing beta cells in the pancreas and makes patients dependent on frequent insulin injections to keep the body’s blood sugar under control.
A tumor paint developed by researchers will help surgeons see where a tumor begins and ends more precisely by illuminating the cancerous cells.
The study shows that the tumor paint can help surgeons distinguish between cancer cells and normal brain tissue in the operating room. The paint is a scorpion-derived peptide called chlorotoxin that is linked to the molecular beacon Cy5.5.Until now there has been no way to allow surgeons to see tumors “live” during surgery.
When a cell is seriously stressed, say by a heart attack, stroke or cancer, a protein called Bak just may set it up for suicide, researchers have found.
In a deadly double whammy, Bak helps chop the finger-like filament shape of the cell’s powerhouse, or mitochondrion, into vulnerable little spheres. Another protein Bax then pokes countless holes in those spheres, spilling their pro-death contents into the cell.
“We found out Bak has a distinct function in regulation of the mitochondrial morphology,” says Dr. Zheng Dong, cell biologist at the Medical College of Georgia and the Veterans Affairs Medical Center in Augusta .
By bypassing a well-known gene implicated in almost one-third of all cancers and instead focusing on the protein activated by the gene, Dr. Christopher Counter and colleagues at the Duke University Medical Center have identified IL6 as a new target in the battle against Ras-induced cancers.
The ras gene, known as an oncogene when it is in this mutated state, has been implicated in several different cancers, including those of the pancreas and lungs. To date, efforts at blocking or turning off ras have proven ineffective.
Contrary to textbook models, many genes that should be 'off' in embryonic stem cells and specialized adult cells remain primed to produce master regulatory proteins, leaving those cells vulnerable to identity changes
Biologists have long thought that a simple on/off switch controls most genes in human cells. Flip the switch and a cell starts or stops producing a particular protein. But new evidence suggests that this model is too simple and that our genes are more ready for action than previously thought.
Scientists in the lab of Whitehead Member Richard Young have discovered that many human genes hover between “on” and “off” in any given cell. According to the study, these genes begin making RNA templates for proteins—a process termed transcription—but fail to finish.
When a strand of DNA breaks in the body's cells, it normally does not take long until it has been repaired. Now researchers at the Swedish medical university Karolinska Institutet have discovered a new mechanism that helps to explain how the cell performs these repairs.
The new results examine a phenomenon called 'cohesion', whereby two copies of a chromosome in the cell nucleus are held tightly together by a protein complex called cohesin. Cohesion fulfils an important function during cell division as the newly copied chromosomes, the sister chromatids, have to stay together until the right moment of separation. If the chromatids come apart too early, there is a risk of the daughter cells getting the wrong number of chromosomes, something that is often observed in tumor cells.
For the first time, it can now be shown what enzyme copies the genetic make-up of cells. The discovery is being published in the journal Science by researchers at Umeå University in Sweden in collaboration with a team in the U.S. led by Thomas A. Kunkel.
The human genome has already been mapped, as have the genomes of several other organisms. On the other hand, little has been known how genes are copied and repaired so efficiently and precisely.
These processes always involve a so-called DNA polymerase, an enzyme that performs the actual new growth of genes. The genes consist of two DNA strands, but scientists have not known what polymerase copies the two DNA strands.
One of the major issues associated with longer life expectancy in man and his best friend is an increase in the incidence of cancer.
Dr Ali Mobasheri, an Associate Professor from the School of Veterinary Medicine and Science at The University of Nottingham, says that studying tumors in dogs and humans could give us a better understanding of their shared pathogenesis.
Cancer is the single biggest cause of death in dogs over the age of 2. The incidence of bone cancers, skin cancers, and lymphomas is increasing in humans and dogs and there are significant similarities between certain types of human and canine cancer – such as breast and prostate cancer.
A startling discovery on the development of human embryonic stem cells by scientists at McMaster University will change how future research in the area is done.
A study this week reports on a new understanding of the growth of human stem cells. It had been thought previously that stem cells are directly influenced by cells in the local environment or ‘niche’, but the situation may be more complex. Human embryonic stem cells are perpetual machines that generate fuel for life.
Not all fat is bad. Brown fat is a type of adipose tissue that generates heat and counters obesity caused by overeating.
Researchers at Dana-Farber Cancer Institute have identified a long-sought "master switch" in mice for the production of brown fat and they say that turning up the equivalent switch in people might be a new strategy for treating overweight and obesity. The investigators said their next step is to rev up the control in mice and overfeed them to see if they are resistant to becoming obese.