Sanford Burnham Prebys scientist receives NIH grant to continue research on cellular signaling in cancer

Brooke Emerling from Sanford Burnham Prebys has been awarded a new grant from the National Institutes of Health (NIH) to continue her work on cellular signaling in cancer. The four-year, $2.3 million project could accelerate the development of new therapies for a range of cancers, particularly metastatic breast cancer. It also offers an answer to a longstanding mystery in cancer metabolism.

We're helping piece together how cancer works at the molecular level. The pathways we're working on have been poorly understood so far, and investigating them could possibly provide new therapeutic strategies for cancer."

Brooke Emerling from Sanford Burnham Prebys

The project focuses on a signaling system called the hippo pathway, which helps our organs grow and controls their size. One of the key characteristics of cancer is uninhibited growth, and the hippo pathway is known to contribute to cancer growth when it's not functioning correctly.

"There's no single mutation we can pin this effect on or target, so it's been a mystery for years as to why and how hippo is activated in cancer," says Emerling. "We're just now beginning to piece that together."

The researcher's key breakthrough was the discovery that a specific family of proteins called PI5P4Ks, which are known to be activated in breast cancer cells, also directly interact with parts of the hippo pathway.

"It was a pretty serendipitous discovery," says Emerling. "We've found a connection between these seemingly unrelated elements of cancer metabolism, and this gives us a whole new angle we can use to tackle cancer."

Because the hippo pathway plays a role in many parts of our biology, targeting this pathway with drugs could have implications for a wide range of cancers and other diseases.

"This work has great potential to help people, and we're grateful that this new funding will help us do the research we need to do so we can make that happen," adds Emerling.

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