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Why Some Cancer Cells Die With Treatment & Others Don’t
A question – Several cancer drugs work by promoting “apoptosis,” or programmed cell death, some cancer cells readily undergo apoptosis in response to these therapies, but others don’t. Why?
Researchers at the Mount Sinai School of Medicine teamed up with IBM Research have come up with an answer to the above question – they have found a clue in the mitochondria, the components of cells which produce energy. In short, cells with fewer mitochondria were more likely to react to drugs that promote apoptosis.
With a mathematical model developed by IBM, the team started their examination by exposing several kinds of cells, including breast and pancreatic cancer cells into six different doses of an apoptosis-promoting drug, then they also measured how differences in cell survival changed according to the abundance of mitochondria.
They concluded that 30 percent of the variability in responses to pro-apoptosis drugs could result from mitochondria. The Researchers discovered that Cancer cells with identical genes but different quantities of mitochondria could react differently to medication treatments. Their detailed study was published in the journal Nature Communications.
In an announcement, co-author Pablo Meyer, Ph.D., team leader
of Translational Systems Biology at IBM Research and an adjunct professor at Mount Sinai stated that- Enhancing our knowledge of the relationship between mitochondria variability and drug response may lead to more effective targeted cancer therapies, allowing us to find new ways to attack the issue of drug resistance. The potential role of cancer cells energy facilities in drug resistance has been of interest in the oncology community. Last year, scientists at the University of Cincinnati found that genetic abnormalities in mitochondria can affect “autophagy,” the process by which cells recycle elements and use them as energy resources. Those abnormalities may interfere with some cancer therapies.
Other researchers are exploring a range of options for controlling mitochondria in cancer cells, including targeting an enzyme that repairs damaged mitochondrial DNA and inhibiting mitochondria that are key to cell metabolism working with the diabetes medication metformin.
The Researchers from Mount Sinai and IBM believe their findings will have broad utility in cancer research going forward.
They Mentioned in their study that- let say For example higher mitochondria abundance can be a non-genetic mechanism of immunity to pro-apoptotic therapeutics. Incorporating such knowledge may be an important consideration in developing therapeutic strategies such as combination therapies.
