Cancer-battling Einsteins sing “executioner’s” song

BAX a real punch: Researchers believe they have found a way to direct cancer cells to self-destruct, by chemically reviving overwhelmed "executioner proteins."

Clinical researchers are trumpeting a novel compound that causes cancer cells to self-destruct – without affecting healthy cells.

A team of biochemistry-focused scientists at the Albert Einstein College of Medicine announced its discovery in Monday’s issue of Cancer Cell, a peer-reviewed medical journal.

According to the article, “Direct Activation of BAX by BTSA1 Overcomes Apoptosis Resistance in Acute Myeloid Leukemia,” their novel compounds essentially cause cancer cells to commit suicide by triggering apoptosis, a chemical process that rids the body of unwanted or malfunctioning cells.

Apoptosis involves activation of the “executioner protein” BAX, which is very good at punching lethal holes in mitochondria, the organelles that generate a cell’s energy. Cancer cells usually fend off BAX by producing copious amounts of “anti-apoptotic” proteins, which basically overwhelm BAX – a self-generated, cellular-level stay of execution.

But the Albert Einstein College of Medicine researchers, led by associate biochemistry Professor Evripidis Gavathotis, formulated a compound that “revives suppressed BAX molecules,” Gavathotis said Monday, allowing the executioner protein to “swing into action, killing cancer cells while leaving healthy cells unscathed.”

Gavathotis’ team successfully tested the compounds against acute myeloid leukemia grafted into laboratory mice. According to their report, test subjects treated with the novel formula BTSA1 – for BAX Trigger Site Activator 1 – survived longer than untreated mice, with 43 percent of treated mice “showing no signs of AML” after 60 days.

The researchers are optimistic about the possibility of also convincing other types of cancers to fall on their cellular swords.

“We’re hopeful that the targeted compounds we’re developing will prove more effective than current anti-cancer therapies by directly causing cancer cells to self-destruct,” noted Gavathotis, also an associate professor of medicine and the lead author of a study that included 13 other biochemists, oncology experts and assorted researchers.

Ultimately, the team hopes to create novel compounds that work in concert with existing cancer treatments, both increasing efficiency and reducing negative side-effects.

“Ideally, our compounds would be combined with other treatments to kill cancer cells faster and more efficiently and with fewer adverse effects, which are an all-too-common problem with standard chemotherapies,” Gavathotis said.

The Albert Einstein School of Medicine is an affiliate, but not member, of the New Hyde Park-based Northwell Health System, through Northwell’s strategic alliance with the college’s parent organization, the Bronx-based Montefiore Health System.

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