In one area at the Salk Institute for Biological Studies, for instance, they have determined how a pesky cold virus can be a valuable ally in the fight against cancer. In another, they have put together findings that might encourage inroads in dealing with Parkinson’s disease.
Of course, most of the discoveries are meshed from research and language adaptable only to laboratory conversation and arrived at with major input from colleagues in other countries. These things take teamwork.
According to a study recently released in Cell, adenovirus, a type of cold virus, has developed molecular tools or proteins that allow it to hijack a cell’s molecular machinery, including large cellular machines involved in growth, replication and cancer suppression. Researchers identified the construction of these molecular weapons and found they form a three-dimensional web inside cells that traps and overpowers cellular sentries involved in growth and cancer suppression.
Findings suggest a new avenue for developing cancer therapies by mimicking strategies employed by the viruses.
“Cancer was once a black box,” said Clodagh O’Shea, an assistant professor in Salk’s Molecular and Cell Biology Laboratory, who led the study. “The key that opened that box was revealing the interactions between small DNA tumor virus proteins and cellular tumor suppressor complexes.”
The suggestions may help scientists develop small molecules — the basis for the vast majority of current drugs — capable of destroying tumors by binding and disrupting large and complex cellular components that allow cancer cells to grow and spread.
The work was supported by the National Institutes of Health, American Cancer Society, Sontag Foundation, the Arnold and Mabel Beckman Foundation and the Anna Fuller Foundation.
By reprogramming skin cells from Parkinson’s disease patients with a known genetic mutation, researchers have identified damage to neural stem cells as a powerful player in the disease. The findings, reported in Nature, may lead to new ways to diagnose and treat the disease.
The research team, which included scientists from China and Spain, as well as the University of California, San Diego, and Scripps Research Institute, made discoveries using human-induced pluripotent stem cells.
They found that a common mutation to a gene that produces an enzyme responsible for both familial and sporadic cases of Parkinson’s disease deforms the membrane surrounding the nucleus of a neural stem cell.
Damaging the nuclear architecture leads to destruction of these powerful cells, as well as their decreased ability to spawn functional neurons, like the ones that respond to dopamine.
The researchers checked their laboratory findings with brain samples from Parkinson’s disease patients and found the same nuclear envelope impairment.
“This discovery helps explain how Parkinson’s disease, which has been traditionally associated with loss of neurons that produce dopamine and subsequent motor impairment, could lead to locomotor dysfunction and other common non-motor manifestations, such as depression and anxiety,” said Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory, who led the research team.
Although researchers say they don’t yet know whether these nuclear aberrations cause Parkinson’s disease or are a consequence of it, they say the discovery could offer clues about potential new therapeutic approaches.
— Johnny McDonald is a longtime writer and columnist for the San Diego Community Newspaper Group. He can be reached at firstname.lastname@example.org.