The researchers, from the Washington University School of Medicine in St. Louis, said that when they transplanted the beta cells into mice that could not make insulin, the new cells began secreting insulin within a few days, and they continued to control blood sugar in the animals for months.
‘We’ve been able to overcome a major weakness in the way these cells previously had been developed. The new insulin-producing cells react more quickly and appropriately when they encounter glucose,’ said lead author Jeffrey R. Millman, PhD, Assistant Professor.
‘The cells behave much more like beta cells in people who don’t have diabetes,’ he said.
For the study, published in the journal Stem Cell Reports, the team grew beta cells from human stem cells, but they made numerous changes to the ‘recipe’ for producing insulin-producing beta cells, treating the cells with different factors at different times as they grew and developed to help the cells mature and function more effectively.
After that process was complete, the researchers transplanted the beta cells into diabetic mice with suppressed immune systems so that they wouldn’t reject the human cells.
Those transplanted cells produced insulin at levels that effectively controlled blood sugar in the mice, functionally curing their diabetes for several months, which, for most of the mice in the study, was about the length of their lives.
The researcher said he can’t predict exactly when such cells may be ready for human trials but believes there are at least two ways that stem cell-derived beta cells could be tested in human patients.
Drugs for diabetes, inflammation, alcoholism — and even for treating arthritis in dogs — can also kill cancer cells in the lab, according to a new health news and study.
The researchers systematically analysed thousands of already developed drug compounds and found nearly 50 that have previously unrecognised anti-cancer activity.
The findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.
“We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said study researcher Todd Golub from Harvard University in the US.
The study, published in the journal Nature Cancer, yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs).
Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits.
“We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, from Dana-Farber Cancer Institute and founder of the Drug Repurposing Hub.
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad’s Cancer Cell Line Encyclopedia (CCLE).
Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment.
The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.
They found nearly 50 non-cancer drugs — including those initially developed to lower cholesterol or reduce inflammation — that killed some cancer cells while leaving others alone.
Some of the compounds killed cancer cells in unexpected ways.
“Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello.
Some of the four-dozen drugs researchers identified appear to act not by inhibiting a protein but by activating a protein or stabilising a protein-protein interaction.
For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilising the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs.
These unexpected drug mechanisms were easier to find using the study’s cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target.
For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. (IANS)