September 24, 2017 |
Long-Sought Drug Candidate Can Halt Tumor Growth
August 13, 2014  | 
La Jolla, CA - It’s a trick any cat burglar knows: to open a locked door, slide a credit card past the latch.

Scientists at The Scripps Research Institute (TSRI) tried a similar strategy when they attempted to disrupt the function of MYC, a cancer regulator thought to be “undruggable.” The researchers found that a credit card-like molecule they developed somehow moves in and disrupts the critical interactions between MYC and its binding partner.

The research, published the week of August 11 in the journalProceedings of the National Academy of Sciences, also shows the drug candidate can stop tumor growth in animal models.

“We finally hit a home run with this—maybe a grand slam,” said Kim Janda, co-author of the new study and Ely R. Callaway, Jr. Professor of Chemistry, director of the Worm Institute for Research and Medicine, and Skaggs Scholar and member of the Skaggs Institute for Chemical Biology at TSRI.

MYC is a transcriptional factor, meaning it controls gene expression. When MYC is overexpressed or amplified, the unregulated expression of genes involved in cell proliferation, a key step in cancer growth, follows. MYC is involved in a majority of cancers, including Burkitt’s lymphoma, a fast-growing cancer that tends to strike children.

For years, MYC had challenged researchers who sought to disrupt its activity in cancer cells. Researchers often design drugs by determining the structure of a disease-related molecule then finding weak points to attack to interfere with the molecule’s function. Continue>

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