NEW YORK (CBSNewYork) — Researchers have a found a surprising potential ally in the search for a cure for Type-1 diabetes.
It’s a rare tumor that produces a lot of what diabetics are missing — insulin.
Type-1 diabetics have two problems. Their own immune system destroys the beta-cells that make insulin. To cure diabetes, you have to stop that autoimmune attack and then replace the destroyed beta-cells.
That’s where the tumor comes in.
CBS2’s Dr. Max Gomez first met diabetic Alecia Wesner shortly after she was diagnosed with Type-1 diabetes at age 6. Her continuous glucose monitor and a small insulin pump have made managing her blood sugar easier, but not easy.
“There’s no break from Type-1 diabetes, there’s no vacation,” she said. “Trying to manage all of this with a lot of things that beep to wake me up if something has gone too high or two low is a tremendous amount of work.”
What gives Alecia a lot of hope for the future is what’s being done in the lab of Dr. Andrew Stewart at the Icahn School of Medicine at Mount Sinai. He explains that even though Alecia has had diabetes for almost four decades, she still has a few beta-cells left.
The key to getting them to replicate Alecia’s destroyed beta-cells, says Dr. Stewart, may lie in the DNA of rare benign tumors called beta-cell insulinomas.
“Those small insulinoma tumors in the pancreas have the genomic recipe, if you will,” Dr. Stewart said. “They now have the genomic wiring diagram or roadmap for knowing how to make beta-cells replicate.”
By sequencing every gene in these tumors, Dr. Stewart found the ones that put the brakes on beta-cell regeneration. As it turns out, certain drugs can take the brakes off the genes in normal beta-cells so they can start to divide.
“We found lots of candidates and we’re in the process now of screening drugs that take off these other brakes and we’re making progress there,” Dr. Stewart said.
It’s not about implanting tumors in diabetics. Rather, it’s using the abnormal genetic information in the tumors to find drugs that will get normal beta-cells to divide. The rest is stopping the autoimmune destruction of beta-cells, something other researchers are also getting close to doing.