Advancing cancer drug delivery
Therapeutic drugs generally have a difficult time penetrating cancer tumor tissue. The result of delivering a less-than-optimal dose to a tumor is an increased risk of cancer recurrence and drug resistance.
Researchers at the Sanford-Burnham Medical Research Institute have shown that a particular peptide can be used to make tumors more porous, allowing medicines (including small molecules, nanoparticles and antibodies) to penetrate the entire tumor. This makes treatment more effective at a lower dose. The peptide has been shown to substantially increase treatment effectiveness against human breast, prostate cancer and pancreatic cancers in mice models.
The paper is published in the online edition of the journal Science. News release:
Mapping heart disease
Very little is understood about the genetic underpinnings of heart disease. Recently, an international research team, which includes the Sanford-Burnham Medical Research Institute, identified a number of genes associated with heart disease. This was accomplished by studying Drosophila (fruit flies). The team investigated 7,061 Drosophila genes from which it built a detailed map that shows how a portion of these genes contribute to heart function and disease.
Using technology that selectively knocks out genes, researchers studied their function one by one and found nearly 500 genes that, when inhibited, caused fruit flies to experience heart problems while under stress. A significant percentage of known human disease genes have a recognizable match in the genetic code of fruit flies.
The research appears as the cover story in the journal Cell. News release:
When Alzheimer’s drugs cause harm
Some current therapies being investigated for Alzheimer’s disease may cause further neural degeneration and cell death, according to a discovery by UCSD researchers.
By combining 3-D computer simulations with high-resolution imaging, electrical recording and cellular assays, researchers investigated the structure and function of truncated peptides, known as nonamyloidgenic peptides, formed by some Alzheimer’s drug candidates. They found that the nonamyloidgenic peptides formed active ion channels that caused cells to take in very high levels of calcium ions, which damaged synaptic efficiency and eventually killed neurons — two actions linked to memory loss in the human brain.
The findings appear in the Proceedings of the National Academy of Sciences. News release:
Lynne Friedmann is a science writer based in Solana Beach.