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Amanda Corbel

Manager, Communications Office

Email amanda.corbel@nih.gov or call 301-228-4489 for all media related questions.

Artistic rendition of gene editing using CRISPR-Cas9 technology
Genome Modification Core

New CRISPR screening platform could drive development of next-generation drugs

Scientists at the Frederick National Laboratory for Cancer Research (FNL) and their National Cancer Institute colleagues have developed a method that enhances the capacity to identify interactions between proteins and molecules that are critical to drug targeting. The study reported in Science Advances includes libraries to aid other researchers. A bedrock of drug discovery is identifying interaction between cell surface proteins (receptors) and molecules that bind to them (ligands) to deliver signals. However, there are still many receptors for which there is no known binding partner, which limits the drug discovery progress. While high-throughput screening, a method to rapidly test a large drug library against a receptor, investigates for these binding partners, it is complex and costly. To address these challenges, scientists developed a highly efficient screening platform to identify previously unknown interactions between receptors and ligands. This screening platform uses CRISPR/Cas9technology, a powerful, accurate and relatively simple method for POSTED: 5/2/2024
FIB-SEM reconstructions of nuclear morphology and centriolar structures

CDK2 inhibition may have potential for treating lung and other cancers

Many cancer cells–and lung cancers in particular–have an abnormal number of chromosomes, a feature that can help shield them from therapeutic attack. But now scientists are exploring ways to turn the tables and use this abnormality as a weapon against cancer. In a recent example of this, scientists at the Frederick National Laboratory for Cancer Research (FNL) found that by inhibiting the cell-cycle regulator CDK2 (cyclin-dependent kinase 2) it is possible to force a chromosomally abnormal cancer cell to divide in such a way that its progeny cannot survive. The daughter cells die in what is called anaphase catastrophe. The original experiments were conducted in mice. Since then, many CDK2 inhibitors have been shown to cause anaphase catastrophe, and several of these are in clinical testing as potential treatments for human cancers. In marked contrast, this death program was not observed in CDK2-inhibited normal human alveolar epithelial cells that line POSTED: 4/23/2024
cartoon structure shows binding site of BBO inhibitor (L) to G12C KRAS-GppNHp

RAS Initiative partnership identifies novel therapeutic, improves predominant drug discovery model

 A team from the National Cancer Institute RAS Initiative and collaborators at Lawrence Livermore National Laboratory and BridgeBio TheRas Pharma have made a dual discovery involving the much-studied protein KRAS, identifying a better model and a highly potent anticancer compound. Their findings, the product of a long-term partnership, appear in the Journal of Biological Chemistry and focus on targeting mutated versions of KRAS in human cancer cell lines. The anticancer compound, BBO-8956, is one of the first dual inhibitors of the cancer-causing KRAS G12C mutant, said Anna Maciag, Ph.D., senior principal scientist at Frederick National Laboratory’s Cancer Research Technology Program, where the RAS Initiative is headquartered. In the team’s laboratory models, it potently blocked cancer cells from proliferating. BBO-8956 is an experimental compound used for laboratory studies but is closely related to a compound that’s being evaluated as a potential treatment. As with all new therapeutics, studies in humans will POSTED: 4/22/2024
Illustration of mitochondria on sticks in a row
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