In a surprise study from MIT and Harvard comes a ground-breaking study that shows dozens of non-oncology drugs can kill cancer cells. Who would have thought it!
Researchers tested approximately 4,518 drug compounds on 578 human cancer cell lines and found nearly 50 that have previously unrecognized anti-cancer activity. These varied drugs have been used to treat conditions such as diabetes, inflammation, alcoholism, and even arthritis in dogs. The findings suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.
Almost anything has to be better than the wave of toxic and brutal oncology drugs, which don’t really work when you consider the topic of healing in its greater sense. Mind you, I have been saying for over a decade, that good doctors exist who are looking for viable ways out of the current toxic oncology trap. Not everyone is in the pay of Big Pharma!
“We thought we’d be lucky if we found even a single compound with anti-cancer properties,” said Todd Golub, chief scientific officer and director of the Cancer Program at MIT, Charles A. Dana Investigator in Human Cancer Genetics at Dana-Farber, and professor of pediatrics at Harvard Medical School. “But we were surprised to find so many,”
The new work appears in the journal Nature Cancer, which I had never heard of. The drug directory that was used comprised 4,518 drugs at the time that are either FDA-approved or have been proven safe in clinical trials (the list has grown since). The researchers screened the entire collection of mostly non-cancer drugs for their anti-cancer capabilities!
Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits or Viagra’s erectile effect. “We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, an oncologist at Dana-Farber, a member of the Golub lab, and founder of the Drug Repurposing Hub.
Not sure what he means by deliberate serendipity, but this isn’t a grammar lesson!
Stephen Corsello MD. I am reminded of the old, trenchant observation that you know you are growing old when the policemen start to look very young!
The researchers tested all the compounds on 578 human cancer cell lines. Using a molecular barcoding method known as PRISM, the researchers tagged each cell line with a kind of DNA “barcode”, allowing them to pool batches of several cell lines together in each dish and more quickly conduct a larger experiment. The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.
This ambitious “batching” approach enabled them to test a large number of possible compounds quickly.
They found nearly 50 non-cancer drugs—including those initially developed to lower cholesterol or reduce inflammation—that killed some cancer cells while leaving others alone. This is the gold standard of chemotherapy! Nobody would have a problem with it, if it were not for the fact that most chemo agents also kill healthy cells, with disastrous results.
Some of the compounds killed cancer cells in unexpected ways. “Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello. Some of the four-dozen drugs he and his colleagues identified appear to act not by inhibiting a protein but by activating a protein or stabilizing a protein- interaction. For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilizing the interaction between PDE3A and another protein called SLFN12—a previously unknown mechanism for some of these drugs.
Not Just The Killer Effect
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs.
That’s ironic!
The researchers were also able to predict whether certain drugs could kill each cell line by looking at the cell line’s genomic features, such as mutations and methylation levels. This suggests that these features could one day be used as biomarkers to identify patients who will most likely benefit from certain drugs. For example, the alcohol dependence drug disulfiram (Antabuse) killed cell lines carrying mutations that cause depletion of metallothionein proteins.
“The genomic features gave us some initial hypotheses about how the drugs could be acting, which we can then take back to study in the lab,” said Corsello. “Our understanding of how these drugs kill cancer cells gives us a starting point for developing new therapies.”
The next step is to study the library compounds in more cancer cell lines and try to include more compounds that have been tested in humans. The team will also continue to analyze the trove of data from this study, which have been shared openly with the scientific community, to better understand what’s driving the compounds’ selective activity.
“This is a great initial dataset, but certainly there will be a great benefit to expanding this approach in the future,” said Corsello.
I agree. What’s more this was an exploration of substances that are safe and proven, not vile and destructive chemicals that trash bone marrow, intestinal linings and hair roots (it’s ironic that most chemo agents target fast growing cells in the body, which is what produces these specific symptoms.
Read my further thoughts on cancer alternative therapies, which includes using holistic measures to counteract the destructive powers of chemotherapy, without blocking any possible beneficial effects. It’s the most comprehensive guide to alternatives you can get!
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To your good health,
Prof. Keith Scott-Mumby
The work was funded in part by SIGMA (Slim Initiative in Genomic Medicine for the Americas), the National Institutes of Health, and an anonymous donor (never had to report that last before—not Bill Gates, I hope!)
SOURCE:
ScienceDaily. www.sciencedaily.com/releases/2020/01/200120113130.htm