In the past ten years, researchers in genome stability have observed that many kinds of cancer are associated with areas where human chromosomes break. They have hypothesized – but never proven – that slow or altered replication led to the chromosomes breaking.
In a Tufts University study, two molecular biologists have used yeast artificial chromosomes to prove the hypothesis. They have found a highly flexible DNA sequence that increases fragility and stalls replication, which then causes the chromosome to break.
Catherine Freudenreich, associate professor of biology at Tufts University, and doctoral student Haihua Zhang focused on one particular human common fragile site – an area that is a normal part of chromosome structure but is prone to breaking.
Cancer causing mutations occur in our bodies every day – but luckily, we have specific genes that recognize these malignant events and keep cells from growing out of control. Only a few of these genes – called tumor suppressors – are currently known.
Now scientists at the University of North Carolina at Chapel Hill School of Medicine and Harvard Medical School have added to the list another powerful tumor suppressor, a gene called LKB1. Their research indicates that this gene is mutated in almost a quarter of all human lung cancers. In mice, these mutations result in tumors that are more aggressive and more likely to spread throughout the body.
Scientists at the Institute for Stem Cell Research, of the University of Edinburgh show that mouse embryonic stem cells need the protein FGF4 to become competent to be converted into specialized cell types, such as brain or muscle cells.
These findings add to the growing body of knowledge that researchers all over the world are using to direct embryonic stem cells to become specific specialised cells – a fundamental requirement for using lab-grown cells to model disease, test the effects of new drugs and, potentially, treat disease and injury.
Embryonic stem cells have the unique ability to divide to produce both copies of themselves and other, more specialised, cell types. The process whereby embryonic stem cells commit to become specialised cells is still obscure.
A new UC Davis study that explains the actions of a gene mutation that causes early onset cancer provides a fundamental insight into the mechanism of DNA-break repair.
People with Bloom's syndrome, a rare genetic disease, typically develop cancer in their twenties. The underlying cause is a mutation in a gene called Blm, which encodes a member of the RecQ family of DNA-unwinding enzymes, or helicases, that are involved in repairing DNA.
Neil Hunter, assistant professor of microbiology at UC Davis, and his colleagues studied the equivalent protein in yeast, SGS1.
There are a number of things which can damage DNA - toxic chemicals are the primary concern on earth but, in space, ionized radiation is the worry. Unrepaired DNA can lead to mutations, which in turn can lead to diseases like cancer. Intricate DNA repair mechanisms in the cells' nuclei are constantly working to fix what's broken, but whether the repair work happens "on the road" — right where the damage occurs — or "in the shop" — at specific regions of the nucleus — is an unanswered question.
NASA scientists are working on understanding where and how DNA is repaired so they can be prepared for long distance space travel.
In 2004, Korean investigators announced the creation of the world's first human embryonic stem cells through somatic cell nuclear transfer, entailing transfer of genetic material from a cell in the body into an egg.
Research led by Kitai Kim, PhD, and George Q. Daley, MD, PhD, of the Children's Hospital Boston Stem Cell Program demonstrates that the Koreans created something entirely different – the world's first human embryonic stem cell to be derived by parthenogenesis, a process that creates an embryo containing genetic material only from the donor egg.
The report sheds new light on a now-discredited Korean embryonic stem cell line, setting the historical record straight and also establishing a much-needed set of standards for characterizing human embryonic stem cells.
Low-intensity electric fields can disrupt the division of cancer cells and slow the growth of brain tumors, suggest laboratory experiments and a small human trial, raising hopes that electric fields will become a new weapon for stalling the progression of cancer.
In the studies, the research team uses alternating electric fields that jiggle electrically charged particles in cells back and forth hundreds of thousands of times per second. The electric fields have an intensity of only one or two volts per centimeter. Such low-intensity alternating electric fields were once believed to do nothing significant other than heat cells.
Engineering pliable, new vocal cord tissue to replace scarred, rigid tissue in these petite, yet powerful organs is the goal of a new University of Delaware research project.
Xinqiao Jia, UD assistant professor of materials science and engineering, is leading the project. Jia's research focuses on developing intelligent biomaterials that closely mimic the molecular composition, mechanical responsiveness and nanoscale organization of natural extracellular matrices--the structural materials that serve as scaffolding for cells. These novel biomaterials, combined with defined biophysical cues and biological factors, are being used for functional tissue regeneration.
After lung and stomach cancer, liver cancer is the third largest cause of cancer deaths in the world. A new study on the relationship between coffee drinking and the risk of hepatocellular carcinoma (HCC) confirmed that there is an inverse association between coffee consumption and HCC.
At least eleven studies conducted in southern Europe and Japan have examined the relationship between coffee drinking and the risk of primary liver cancer. The current study, led by Francesca Bravi of the Istituto di Ricerche Farmacologiche Mario Negri in Milan, Italy, was a meta-analysis of published studies on HCC that included how much coffee patients had consumed.
The major active component of marijuana could enhance the ability of the virus that causes Kaposi’s sarcoma to infect cells and multiply, according to a team of researchers at Harvard Medical School. According to the researchers, low doses of Ä-9 tetrahydrocannabinol (THC), equivalent to that in the bloodstream of an average marijuana smoker, could be enough to facilitate infection of skin cells and could even coax these cells into malignancy.
While most people are not at risk from Kaposi’s sarcoma herpes virus (KSHV), researchers say those with lowered immune systems, such as AIDS patients or transplant recipients, are more susceptible to developing the sarcoma as a result of infection.