A patient is taking a chemotherapy drug that may stop the progression of their cancer, but they develop painful blisters and swelling on their hands and feet, which affects their daily life, another challenge on an already arduous journey navigating a cancer diagnosis. This condition, palmar-plantar erythrodysesthesia (PPE), causes inflammation and damage to the palms and soles of the feet as a side effect of certain anticancer treatments, limiting these drugs’ effectiveness. Drug developers and researchers have struggled to identify new drugs’ potential for PPE because of a lack of reliable animal and laboratory models. Being able to identify this potential side effect earlier in the process could prevent researchers from expending effort developing treatments that’d cause it. In partnership with outside collaborators, the Nanotechnology Characterization Laboratory (NCL) at the Frederick National Laboratory for Cancer Research (FNL) worked backwards from drugs known to cause the toxicity to develop an assay that could identify it.

After nearly eight years of meticulous collaborative effort, the HPV Serology Laboratory at the Frederick National Laboratory for Cancer Research has achieved a major milestone in advancing global human papillomavirus (HPV) research. They and their research network have developed and established International Standards for antibodies to seven types of HPV—HPV6, HPV11, HPV31, HPV33, HPV45, HPV52, and HPV58. These are the first-ever serology International Standards for these HPV types.

CRPV has long served as a stand-in for studying HPV. However, researchers at NCI Frederick and Pennsylvania State University Cancer Institute have only recently decoded its transcriptome—the complete map of its active RNA—revealing how CRPV’s RNA toggles genes on and off in host cells, allowing the virus to replicate and  modulating the cells’ functions.

A mutated, cancer-causing protein twisted and bent across the computer screen. As Ruth Nussinov, Ph.D., and her team watched the simulation, two things quickly became evident. First, it was clear how the mutation paved the way for cancers to form. Second, the twisting and bending created a pocket—a gap in the protein’s proverbial armor—no one had seen before. Nussinov’s team at Frederick National Laboratory for Cancer Research has illuminated through computational simulations how mutated versions of that protein, mTOR, contribute to cancer at a molecular level.

Imagine you’re building a dresser. You find all the wood and hardware you need and have the instructions, the right tools, and a team of professionals to help. As you and your team put it together, you realize that while the frame is solid, the drawers don’t open and close correctly. You might be tempted to feel discouraged by the results. But a group of scientists from the National Cancer Institute (NCI), Frederick National Laboratory for Cancer Research (FNL), and other collaborating institutions share a different perspective in their recent work published in PNAS. They weren’t trying to assemble furniture but rather generate a new, better mouse model of the most common kidney cancer, clear cell renal cell carcinoma (ccRCC).