I wish we could tell you it was complicated—some mysterious algorithm favoring high-risk research, East coast labs, and Volvo drivers, perhaps, or something equally facetious—but it just isn’t. The Damon Runyon Cancer Research Foundation is an open book, priorities-wise, and when it gives away millions, it doesn’t play games.
Peeking at this latest crop of Damon Runyon Fellows, it’s easy to see what caught the foundation’s eye. It’s widely known that the DRCRF favors high-risk, high-reward ventures and routinely gives its fellows enough support in the form of these four-year awards to guarantee investigative independence. (This year, basic scientists received $208,000 apiece; physician-scientists received $248,000.) And though all of these latest awardees are undertaking high-risk science, and all of them are from prominent labs at huge research institutions, most of them have something else in common, too.
It’s proteins. Seven of the sixteen newly minted fellows are seeking to answer questions about the roles of specific proteins in different cancers: there’s mediator and its connection to mixed-lineage leukemia; histones and their link to chondroblastoma; Sonic Hedgehog, BET-bromodomain, and MeCP2, and their connections to multiple cancers.
At the Gladstone Institutes in San Francisco (the sole outlier in this crop of scientists from big research institutions), Casey A. Gifford, PhD, will use her research into DNA-binding proteins to understand how the lack or erroneous expression of said proteins can lead to cancer. At Harvard University, Sungwook Woo, PhD, aims to delve deeply into the mechanistic and structural nature of proteins, using his findings to help inform the development of tailored therapies for cancer.
Gifford and Woo’s work is representative in its high-risk nature: It isn’t about developing a drug to solve a problem, it’s about the basic research that could, over time, lead to the discovery of a whole new line of treatments for cancers. It’s the bold stuff DRCRF likes, and it’s surely found plenty of that with this batch.
Also well-represented in this group of young scientists are projects seeking to better understand signaling pathways—including the bacterial signaling that can implicate colon cancer—signaling enzymes like Cas9, and genetic factors and their links to cancer.
At Brigham and Women’s Hospital in Boston, Timothy D. Martin, PhD, is examining “genomic instability,” the sorts of changes that foreshadow genetic mutations and shifts in chromosome count that can lead to cancers down the line. Martin’s goal involves simulating a variety of genomic alterations and determining how each contributes to the development of cancer.