Two new breakthroughs offer novel ways for preventing cancerous tumor cells from flourishing.
Killing tumor cells is the core of treating cancer and two new studies have unique approaches that cause those deadly cells to self-destruct.
The two unrelated findings are potential avenues for cancer treatments that would alter the lifeline of a cancer cell.
The two therapies target leukemia — the most common childhood cancer — and lung cancer, the type that kills more Americans than any other.
But researchers believe their methods may have greater impact, someday giving cancer a fatal blow.
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Researchers from the Dana-Farber Cancer Institute in Boston published a paper in Science today that highlights a new cancer therapy that pits a cancer cell’s growth proteins against itself.
A major hurdle in current cancer treatments that target these proteins is how they become ineffective as the cancer develops resistance to drugs aimed at shortening the cell’s lifespans. Essentially, a therapy works for a while until the cancer cells get wise and learn to beat the drugs and continue to grow.
“Conventional drugs allow the targeted protein to adapt to the drug and the cell finds alternate routes for its growth signals,” Dr. James Bradner, the paper’s senior author and an oncologist and chemist at Dana-Farber said in a press release. “We began designing approaches that cause the target protein to disintegrate, rather than merely be inhibited.”
Typically, unusable proteins in a cancer cell are tagged with ubiquitin — a protein signaled by enzymes — for removal, the same way you take your trash out to the curb. In cancer cells, the dump is called proteasome, the place where proteins are ground up and recycled.
Bradner and his team designed a method they describe as working like a trailer hitch that allows targeted drugs to tow the cell’s protein-recycling mechanism directly to the desired protein. Once that occurs, it’s game over for cancer.
This technology is still new, and it has only been tested on laboratory samples of leukemia cells and mice with a widespread and aggressive form of human leukemia. Still, these tests revealed the method rapidly degraded BRD4 — a protein that signals cancer cells to grow — with few noticeable side effects.
“We’re very excited that this chemical technology may offer a way to improve many cancer drug molecules, and of course this strategy has implications beyond cancer for the treatment of other life-threatening diseases,” Bradner said.
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Another method of killing cancer cells was discovered by researchers at the Winship Cancer Institute of Emory University in Atlanta. It has different methods but achieves the same result: cancer cell death.
Their method exploits a form of programmed cell death, apoptosis, in lung cancer cells. It targets a protein Bcl-2, an already known target for cancer treatment. It’s an effective target because this specific protein helps cancer cells avoid an untimely death.
But lead study author Dr. Xingming Deng, a Winship cancer biologist, and his colleagues, have found a way to tell cancer the clock is ticking.
The Winship team discovered a new class of compounds that prevent Bcl-2 from functioning, essentially breaking down a cancer cell’s defenses and opening it up to invasion by cancer-killing drugs.
In a paper published in the journal
“This potential drug identified by Dr. Deng and our Winship team may accelerate our success against lung and other cancers. We are now testing this molecule further in preparation for future testing among eligible patients,” Dr. Walter J. Curran, Jr., the study’s co-author and Winship’s executive director, said in a press release.
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