When it spreads, it becomes more difficult to treat. Understanding metastatic cancer presents significant challenges to doctors and scientists in part because the disease is different in the liver than it is in the lungs.
Lloyd Trotman, an associate professor at Cold Spring Harbor Laboratory, has created a mouse model of prostate cancer that becomes metastatic. By exploring what happens to cells in different areas, Trotman hopes to get a better understanding of cancer as it spreads.
“New technology allows us to tag cells when they are at the metastatic site,” he said. He can look at “how they differ from where they started.”
When prostate cancer becomes metastatic, the cells “forget about their identity,” Trotman said. They become more like cells that are developing, which means they are not as dependent on male hormones for their survival. This change in their identity makes them difficult to treat with hormone therapy.
By developing these metastatic models of prostate cancer, Trotman has been able to do preclinical studies of drugs designed to treat the original disease and its metastatic form. He has worked with scientists from Cornell University, the Dana-Farber Cancer Institute, and the Memorial Sloan Kettering Cancer Center.
“We can ask if a drug specifically is beneficial against metastatic cancer and especially against the hormone-refractory kind,” he said.
Trotman’s research also explores how cancers that were in remission become active again. “Most [treatments] will not be curative,” he said. “Why? If it works, but then the disease comes back, what is driving the disease? What is it that the drug is doing wrong at the point that it was looking good? What limit does the drug need to push to be curative?”
With his model of the disease, he can track the changes in a living animal. He can see how the cancerous cells are glowing in areas including the liver, lymph nodes, lungs, and bone. “Our hope is that by making these things visible at a very primitive level, we can see it first, then harvest it, and read the sequencing,” he said.
Trotman’s approach has won him the admiration of other scientists. “For an early career scientist, his work stands out as particularly innovative,” said Scott Lowe, a cancer biologist and chairman of the Geoffrey Beene Cancer Research Center at Memorial Sloan Kettering.
Lowe was deputy director of the cancer center at Cold Spring Harbor Laboratory, where he was involved in recruiting Trotman to join CSHL. “His research on an important cancer gene caught our attention,” Lowe said. He described Trotman as an “enthusiastic scientist who strives to address the most important questions in his field.”
Trotman explained that his goal isn’t just to understand how the genome works to cause cancer, but to figure out how to cure metastatic prostate disease. He wants to see where potentially effective drugs fail and to figure out what they should be doing differently. If he develops the kind of data he hopes to explore with the mouse, he would then argue that the same kind of analysis is necessary in humans, to make sure the model and the reality in humans are aligned.
While he’s focused on prostate cancer, Trotman said he would like to find a methodology that allows him to combat and understand cancer on a broader scale.
Born in the United States, Trotman moved to Switzerland when he was 2 years old. He attended high school and received his doctorate in Switzerland. He returned to New York to do his postdoctoral work at Sloan Kettering. He became a faculty member at Cold Spring Harbor Laboratory in 2007. Trotman’s Swiss background enabled him to become fluent in English, German, French and Swedish.
A resident of Oyster Bay, Trotman lives with his wife Eva Frosch, who runs the gallery Frosch & Portmann in New York City, and their sons Liam, 8, and Finn, 5.
Trotman loves summers on Long Island, where he can surf on the south shore and head to the beaches on the North Shore.
Trotman said he hopes his mouse model of prostate cancer can help uncover how cancer progresses, becomes metastatic, and resists drug treatment.
“There are many theories about how diseases like cancer evolve,” he said. His model can “help bring [the research] down to a level where everybody can see it.”