In today’s online edition of Genome Research, a husband-and-wife research team from Thomas Jefferson University report the discovery of a gene that, when mutated, may suppress colorectal cancer. To conduct the study, the researchers used a strain of mice that develop polyps, or small growths of tissue, in the digestive tract—the harbingers of cancer. When these mice possessed one copy of the mutated gene, the incidence of small intestinal and colon polyps were reduced by about 90%.
“This gene may give us a novel target to aid in the diagnosis, prevention, and/or treatment of cancer,” says Dr. Arthur Buchberg, one of the co-senior authors on the report.
A small molecule derived from the spacer domain of the tumor-suppressor gene Rb2/p130 has demonstrated the ability to inhibit tumor growth in vivo and could be developed into an anti-cancer therapeutic, according to researchers at Temple University's Sbarro Institute for Cancer Research and Molecular Medicine.
The researchers reported their findings, "A small molecule based on the pRb2/p130 spacer domain leads to inhibition of cdk2 activity, cell cycle arrest and tumor growth reduction in vivo," in the March 22 issue of the journal Oncogene (http://www.nature.com/onc
Ever since 1887, when Norwegian mathematician Sophus Lie discovered the mathematical group called E8, researchers have been trying to understand the extraordinarily complex object described by a numerical matrix of more than 400,000 rows and columns.
Now, an international team of experts using powerful computers and programming techniques has mapped E8--a feat numerically akin to the mapping of the human genome--allowing for breakthroughs in a wide range of problems in geometry, number theory and the physics of string theory.
In 2002, when astronomers first detected cosmic gamma rays – the most energetic form of light known – coming from the constellation Cygnus they were surprised and perplexed. The region lacked the extreme electromagnetic fields that they thought were required to produce such energetic rays. But now a team of theoretical physicists propose a mechanism that can explain this mystery and may also help account for another type of cosmic ray, the high-energy nuclei that rain down on Earth in the billions.
A new study suggests how a notorious cancer gene may contribute to tumor growth.
The insight emerged from a long-running study of a protein called PMR1, the key player in an unusual mechanism that cells use to quickly stop production of certain important proteins.
Researchers discovered that PMR1 is activated – or “turned on – by another molecule, an energy-packing protein called Src (pronounced “sark”).
New non-toxic and targeted therapies for metastatic breast and ovarian cancers may now be possible, thanks to a discovery by a team of researchers at the University of British Columbia.
In a collaboration between UBC stem cell and cancer scientists, it was found that a protein called podocalyxin – which the researchers had previously shown to be a predictor of metastatic breast cancer – changes the shape and adhesive quality of tumour cells, affecting their ability to grow and metastasize. Metastatic cancer is invasive cancer that spreads from the original site to other sites in the body.
The discovery demonstrated that the protein not only predicted the spread of breast cancer cells, it likely helped to cause it.
"Build a better mousetrap," the saying goes, "and the world will beat a path to your door." In the complex field of organic chemistry, that path leads to Florida State University, where a newly developed substance could make the jobs of scientists throughout the world a little easier as they work to develop new drugs and other chemicals that benefit humanity.
Researchers from the Dudley Laboratory at FSU have invented a reagent — a substance used in a chemical reaction to detect, measure, examine or produce other substances — that can trap specific regions of complex molecules in such a way that those molecules can be released at a later time.
New research from the University of North Carolina at Chapel Hill School of Medicine has identified two proteins that may help protect against skin cancer.
The study, which appears in the advance online edition of the journal Molecular and Cellular Biology, indicates that two proteins, named Timeless and Tipin, form a complex that regulates the rate at which DNA is replicated after exposure to ultraviolet radiation.
Ultraviolet radiation in sunlight damages the DNA in skin cells. If left unrepaired by the cell, this damage can turn into mutations that lead to cancer. Before cells divide, they must replicate, or copy, their DNA to form new daughter cells.
The cause of one notorious childhood disease, poliovirus, could be used to treat the ongoing threat of another childhood disease, neuroblastoma. In the March 15 issue of Cancer Research, researchers from Stony Brook University report that an attenuated -- or non-virulent -- form of poliovirus is effective in obliterating neuroblastoma tumors in mice, even when the mice had been previously vaccinated against the virus.
By its nature, poliovirus destroys the cells it infects in an attempt to replicate copies of itself. When released from the cells it kills, the replicated particles then attack surrounding cells.
The problem of efficiently delivering drugs, especially those that are hydrophobic or water-repellant, to tumors or other disease sites has long challenged scientists to develop innovative delivery systems that keep these drugs intact until reaching their targets.
Now scientists in the University at Buffalo’s Institute for Lasers, Photonics and Biophotonics and Roswell Park Cancer Institute have developed an innovative solution in which the delivery system is the drug itself.