This is a recurring column on early stage research in animals or other laboratory models that has not entered the clinic yet but could have implications for future research and development of human medicines.
New cancer drug stops cancer from spreading
Scientists have developed a drug that targets tumors forming in other parts of the body in late-stage cancer, according to a study published in the Science Translational Medicine.
The drug, called metarrestin, appears to work by killing cells with a structure in their nuclei called perinucleolar compartment, or PNC, said Sui Huang, a lead investigator from Northwestern University's Feinberg School of Medicine.
PNCs develop almost exclusively in cancer cells, especially the ones in metastasized tumors, Huang said.
Metastatic tumors refer to cancer growth that has spread to other parts of the body from the original cancer site.
The identification of metarrestin as a potential cancer-targeting compound began nearly a decade ago through a collaboration between Huang's lab and researchers from the University of Kansas and the National Institute of Health.
After initial experiments using cancer cell cultures showed that it can reduce PNC prevalence and kill tumor cells, researchers began studying the drug in mouse models.
In mice with pancreatic cancer, metarrestin treatment reduced PNC prevalence in metastatic tumor cells and more than doubled how long they survived.
Compared with untreated mice that had tumors developing in the liver and lung, mice treated with metarrestin were free of tumors at these sites.
The drug also shrank metastatic tumors in breast cancer and prostate cancer, studies showed.
"Our results show metarrestin is a very promising agent that we should continue to investigate against metastasis," said Juan Marugan, a co-lead investigator of the study who led a team at the University of Kansas and the National Center for Advancing Translational Sciences.
Based on the results from the animal studies, researchers are collecting laboratory data to submit an investigational new drug application to the U.S. Food and Drug Administration so that they can test metarrestin in human studies.
If all goes as planned, the application should be filed by the fall of 2018 or early 2019, said Udo Rudloff, one of the study's lead investigators working at the National Cancer Institute's Center for Cancer Research.
Human trials would begin soon after, first in patients with any type of metastatic solid cancer, and later focusing on pancreatic cancer, Rudloff said.
Toe infection drug kills sleeping cancer cells
Itraconazole, an antifungal medicine, could help fight dormant cancer cells in the gut, researchers at the Cancer Research UK Cambridge Institute said.
Published in the Journal of Experiment Medicine, the study tested the drug on mice and found that it effectively stopped cancer growth and progression in certain types of bowel cancer in the rodent subjects.
According to the Cambridge team, these "sleeping" cells are resistant to drugs. Even after using chemotherapy — which target cells that are actively growing — dormant cells can reawaken and lead to tumor regrowth.
"One of the biggest challenges in treating any cancer is the diversity of different cells within the same tumor. We've targeted a type of cell that lies asleep within bowel tumors, remaining unresponsive to treatment and putting the patient at risk of their cancer coming back," said Simon Buczacki, a clinical scientist at the research institute.
The team found that itraconazole blocked two cell signaling pathways involved in cell dormancy. Blocking one of these pathways, known as Wnt, led to tumors collapsing and dormant cells disappearing in mice.
"This drug seems to kick both dormant and non-dormant cells into action," said Buczacki.
"It forces cells back into a short cycle of growth before slamming on an irreversible 'stop' button," he said.
Bowel cancer is the fourth most common cancer in the U.K., with approximately 41,300 people diagnosed each year, according to the Cancer Research UK Cambridge Institute.
Brain's emotion center may hold key to new eating disorder treatments
The brain's desire for sweets and aversion to bitter taste can be switched on or off, according to new research published in the journal Nature.
Normally, the recognition of a food and the pleasure derived from eating it are intertwined. But the study's results suggest that these components can be isolated from each other and manipulated separately, a discovery that could lead to new strategies in understanding and treating eating disorders such as obesity and anorexia.
Scientists at Columbia University's Mortimer B. Zuckerman Mind Brain Behavior Institute performed a series of experiments on mice to artificially switch on or off sweet or bitter taste connections at the amygdala, the emotion center of the brain.
When the connections were turned on, the mice responded to water as if it was sugar.
When researchers switched off the connections but left the taste cortex untouched, the mice could still distinguish between sweet and bitter tastes, though they did not show any emotional preference.
"It would be like taking a bite of your favorite chocolate cake but not deriving any enjoyment from doing so," said Li Wang, a research scientist from the institute.
"After a few bites, you may stop eating, whereas otherwise you would have scarfed it down."
The next step is to study other brain regions that are also connected to the taste system.
"Our goal is to piece together how those regions add meaning and context to taste," said Wang.
"We hope our investigations will help to decipher how the brain processes sensory information and brings richness to our sensory experiences."
