Non-Cancerous Medicines
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Several Non-Cancerous Medicines Inhibit the Growth of Cancerous Cells 

A new study conducted by the research team from the Broad Institute (MIT) and Harvard and Dana-Farber Cancer Institute shows that the non-cancerous medicines such as those which are used for inflammation, alcoholism, diabetes, and fo arthritis especially may also destroy cancer cells. The new study also suggests the feasible ways for the development of new drugs for cancer and also for accessible drugs to treat cancer. Thousands of drug compounds that are already developed and more than 50 compounds that had unrecognized anti-cancer action in the past are analyzed by the scientists.

Charles A. Dana, the lead investigator along with Todd Golub came to an end explaining that getting many anti-cancer compounds is a big success as the scientists were thinking that discovering only one anti-cancer compound will be their great achievement. This study was published in Nature Cancer and it is currently available online to read.

The researchers screened several non-cancer drugs first time for cancer treatment. About six thousand accessible drugs and FDA-approved drugs and the drugs that are safe for clinical trials are analyzed by the researchers for anti-cancer capabilities.

In the Drug Repurposing Hub, all the existing and new drug compounds were experienced in the Broad Cancer Cell Line Encyclopedia on about 578 human cancer cell lines. With the help of the molecular barcoding method also called PRISM, each one of these cell line was tagged using a unique DNA barcode so that it may pool many cell lines together and perform a larger experiment more quickly.

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Each pool of the cells was exposed to only one compound from the repurposing collection and then the survival rate of each cancer cell was measured. The non-cancer drugs were developed to minimize the inflammation or to reduce cholesterol that destroyed cancer cells while left the others alone.

Corsello finds that several existing drugs of cancer show functions by blocking proteins but the researchers want the compounds that can proceed through some other mechanisms. Corsello and his colleagues identified about four dozen drugs that can stabilize the protein-protein interaction or activates the protein but do not act to inhibit a protein.

The mechanism of the drugs that were found unexpectedly was easy to find by the study’s cell-based approach than the non-cell-based high-throughput screening methods. The study shows that several non-cancer drugs that destroyed the cancer cells did this by interacting with the highly unidentified molecular target in the past as the drug tepoxalin was developed for people but later was approved for the treatment of osteoarthritis in dogs.

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Now the researchers can also predict some drugs whether these drugs can destroy each cell line by just looking at the genomic features of cell lines like methylation levels and mutations that were also included in the Cancer Cell Line Encyclopedia (CCLE) database.

This study suggests that these genomic features will be helpful in the feature as biomarkers to identify which drug will most benefit the patient. The understanding of the researchers with the mechanism of cancer cells killing drugs provides a starting point to establish more new therapies.