While at Sanford-Burnham in the 1990s, Dr. Steven Frisch (now at West Virginia University) discovered a cellular process he called “anoikis”. Anoikis (which means “homelessness” in ancient Greek) describes how cells from a particular organ or tissue are programmed to self-destruct if they ever stray from home base. When functioning properly, anoikis prevents cells from reattaching and proliferating at inappropriate locations. Metastatic tumor cells have become resistant to anoikis, permitting them to survive and proliferate elsewhere.

At the same time Dr. Frisch was trying to publish his discovery of anoikis, a laboratory across the street at The Scripps Research Institute was about to issue the same finding. A recent article in The Scientist describes how the two labs simultaneously – but independently – discovered anoikis in 1993, and the separate paths they took to publishing that data.

“We could see each other’s buildings,” says Steven Frisch, then at the La Jolla Cancer Research Foundation, now called the Sanford-Burnham Medical Research Institute. “And neither of us knew what the other was doing.”

(Read more in “Breakthroughs from the Second Tier”.)

Understanding why anoikis does or does not take place is critical to understanding metastasis. In collaboration with Dr. Kristiina Vuori, Dr. Frisch’s laboratory reported a role for focal adhesion kinase (FAK), a protein that is overproduced in many human cancers. These days, Dr. Vuori and Dr. Nicholas Cosford are working with the Conrad Prebys Center for Chemical Genomics to identify FAK inhibitors that may lead to future cancer therapies. Several additional Sanford-Burnham laboratories are studying other proteins that talk to FAK, providing a framework for novel drug discovery efforts focused to restore anoikis sensitivity in tumor cells.