Researchers Develop New Drug Combo To Fight Cancer Deaths

Researchers at the Albert Einstein College of Medicine have developed a new and highly efficient approach for bringing down the number of deaths caused due to cancer. They have devised a strategy to overcome the serious problem of the ability of cancer cells to survive the onslaught of chemotherapy drugs, which are meant to destroy them.

The researchers made use of a two-drug combination to achieve the results secured from chemotherapy; i.e. to make cancer cells self-destruct through the biological process known as apoptosis, commonly known as programmed cell death. The treatment worked against human cancer cell lines, which fought against apoptosis despite being exposed to various types of chemotherapy, and also against apoptosis-resistant human tumors implanted in mouse models.

Commenting on the research findings, Evripidis Gavathiotis, corresponding author on the paper, said, "Targeted therapies that home in on specific genetic vulnerabilities of cancers have vastly improved treatment in recent years, but not everyone has benefited. We need new, broadly active therapies that can attack a range of cancers while causing fewer side effects than current treatments, and we hope our new therapeutic strategy will prove to be a viable option."

The human body uses apoptosis for getting rid of unwanted cells like extra cells pruned during embryological development and damaged cells, which need to be removed so they don't survive to become cancer cells. Both the commonly used forms of cancer treatment namely, chemotherapy and radiation, work by damaging cancer cells severely enough that they'll undergo apoptosis, which in certain cases does not happen.
The new drug combination discovered by Gavathiotis and colleagues kills apoptosis-resistant cancer cells by boosting the active form of one pro-apoptotic protein in particular: BAX, dubbed the "executioner protein."

In 2012, Gavathiotis discovered the first small, human-made molecule capable of directly activating BAX. In their new study, he and his team evaluated whether BTSA1.2 - their third-generation BAX activator - would be effective against a wide group of 46 human blood and solid tumor cell lines, including different cancer cell lines. Most of these cell lines had survived all pro-apoptotic drugs developed so far.

The combination of BTSA1.2 and Navitoclax proved to be a game-changer. When Gavathiotis and colleagues, led by co-first author Andrea Lopez tested the drug duo against the 46 cell lines, it had two effects with BTSA1.2 improving active BAX to toxic levels in cancer cells, and Navitoclax acting as BAX's bodyguard by preventing BCL-XL from neutralizing BAX.

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