UCLA Pockets $1M for Novel Pharmacogenetics Project
UCLA’s Johnson Cancer Center and its School of Public Health last week received a $1 million gift to create an environmental genomics program at the school, the university said last week.
Robert Schiestl, a professor of pathology, environmental health, and radiation oncology at UCLA, will lead the program, which will study SNPs and other genetic factors that predispose people to cancer after exposure to certain environmental toxins.
"We’ll investigate the molecular mechanism by which environmental agents such as air pollution, pesticides, and radiation cause cancer and why a certain sub-population of people are more sensitive to these environmental exposures than the general population,” Schiestl said in a statement. “It’s our goal to develop improved biomarkers of exposure, to identify people at increased risk, and to design nutritional and chemical interventions to counteract the development of cancer, especially in those with increased sensitivity."
Specific projects will look at the impact of air pollution on DNA-induced changes in cellular metabolism; examine the relationship between environmental pollutants, genetics, and a non-smoker’s susceptibility to lung cancer; study proteins that inhibit carcinogenesis following exposure to smog, cigarette smoke, and certain cooked foods; and others.
The program is being funded with a $1 million donation by a local resident, Art Alper, whose wife died from lung cancer last year. The Kenneth Jonsson Family Foundation and UCLA’s Jonsson Cancer Center Foundation contributed to the fund.
Some experts remained skeptical. Tatyana Zhukov, an assistant professor at H. Lee Moffitt Cancer Center’s molecular screening lab, questioned the project’s stated goal to “identify the specific protein” that prevents an oncogenetic enzyme from activating “potent carcinogens” found in smog, certain cooked foods, and cigarette smoke.
“I’m absolutely sure they will find something, but they will not find one protein,” said Zhukov, whose research for more than 10 years has focused on early lung-cancer detection.
“I don’t believe that only one causes something. I think they may find different mechanisms and groups for different types of cancers and environmental agents: They may find … groups of biomarkers that could [have] several proteins or profiles,” she added.
British Team Uses Oligos to Reverse Mutations in a Single-Gene Disease
A team of British scientists said it has devised a way to use oligonucleotides to correct genetic mutations that encourage abnormal splicing.
“Although oligos have previously been developed to block expression of genes, this research indicates that we can also use them to restore the proper expression of defective genes,” said Ian Eperon, a professor from the University of Leicester and a member of the research team.
Researchers from the University of Leicester, Imper-ial College London, and Hammersmith Hospital said they were able to manipulate the splicing reaction in cells provided by a patient with spinal muscular atrophy by using oligonucleotides to adhere the correct gene sequences onto exons.
“By putting these oligos into the cells, much of the protein required for the splicing process could be produced, allowing normal development of the cells,” the scientists said in a joint statement.
The research was carried out at Imperial College London and the University of Leicester as a collaboration between Eperon and Francesco Muntoni. The team’s study is published in this month’s Proceedings of the National Academy of Science.
“Many genetic diseases are caused by the mutation of just one or two … base pairs of DNA,” Muntoni said in a statement released last week. “The technique we have developed … allows us to correct genetic mutations which result in abnormal splicing.”
Spinal muscular atrophy, which occurs in one in 10,000 births in the United States, is caused by a mutation in the SMN1 gene. About one in 50 people are believed to have a mutated version of the gene, the researchers pointed out.
However, the fact that individuals carry a second copy of the SMN1 gene, called SMN2, “does not compensate for the problem [because] a difference in a single base pair from SMN1 in just one exon prevents proper splicing,” the researchers said.
The researchers have applications into other disease states, the authors explained:
“We are aware that other conditions such as inflammation or cancer involve changes in the splicing of normal genes and our method might allow us to reverse these and facilitate treatment of the illness,” Eperon said in the statement.
He did not return a telephone call seeking comment.