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How Do Cancer Cells Migrate to New Tissues and Take Hold?

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Friday, April 4, 2025

How Do Cancer Cells Migrate to New Tissues and Take Hold? Scientists are looking for answers about how these confounding trips, known as metastases, occur throughout the human body Illustration of a human cancer cell SCIEPRO / SCIENCE PHOTO LIBRARY via Getty Images Back in 2014, a woman with advanced cancer pushed Adrienne Boire’s scientific life in a whole new direction. The cancer, which had begun in the breast, had found its way into the patient’s spinal fluid, rendering the middle-aged mother of two unable to walk. “When did this happen?” she asked from her hospital bed. “Why are the cells growing there?” Why, indeed. Why would cancer cells migrate to the spinal fluid, far from where they’d been birthed, and how did they manage to thrive in a liquid so strikingly poor in nutrients? Boire, a physician-scientist at Memorial Sloan Kettering Cancer Center in New York, decided that those questions deserved answers. The answers are urgent, because the same thing that happened to Boire’s patient is happening to increasing numbers of cancer patients. As the ability to treat initial, or primary, tumors has improved, people survive early rounds with cancer only to come back years or decades later when the cancer has somehow resettled in a new tissue, such as brain, lung or bone. This is metastatic cancer, and it’s the big killer—while precise numbers are scarce, anywhere from half to the large majority of cancer deaths have been attributed to metastasis. Offering people more options and hope will mean understanding how those cancers successfully migrate and recolonize. The prevalence of metastasis belies the arduous journey that cancer cells must make to achieve it. A cell that arises in, say, the breast, is well adapted to live there: to eat the fatty acids available to it, to resist local threats and to grow there in a solid tumor. If it manages to escape into the bloodstream, it finds itself zipping along at up to 15 inches per second with shear stresses sufficient to rip it apart. Should it survive that odyssey and land in a new tissue—say, the brain or spinal fluid—the environment is totally different yet again. The foods the cell is accustomed to may be absent; immune cells or other novel environmental molecules may attack. For a cell to manage this trip, and then adapt to a new environment, is truly a Herculean task. “It is not easy and trivial,” says Ana Gomes, a cancer biologist at the Moffitt Cancer Center in Tampa, Florida. “It’s just against everything in the nature of these cells.” Moving to a new site and forming a new tumor is an arduous journey that few cells can complete. A cell must exit the initial tumor, survive the bloodstream and enter a new tissue. Even then, the cell may remain dormant for a time, until the environment can support its division and growth to create a new tumor. Adapted from Ana Gomes / Knowable Magazine No wonder that, even though tumors regularly shed cells, most escapees perish or languish without successfully establishing themselves as metastases. “Personally, I think metastasis is an accident,” says Matthew Vander Heiden, a physician-scientist and director of the Koch Institute for Integrative Cancer Research at MIT. “It’s really, really inefficient.” The few cells that manage this epic feat are resilient and flexible in how they feed themselves and process the molecules around them. They may tweak their biochemistry to evade local dangers, or to get the fuel they need in sparse environments. Some even send signals ahead to modify the organ where they’ll land, creating a cushy nest with a food supply ready for when they arrive. “Metabolic changes help these cells to face all this challenge,” says Patricia Altea-Manzano, a biomedical researcher at the Andalusian Molecular Biology and Regenerative Medicine Center in Seville, Spain. Such findings suggest ways that metastasizing cells, because they’re so different from the original tumor, might be vulnerable to new kinds of treatment. Someday doctors might not have to wait for metastasis to take hold before they block or slow cancer’s spread: “That is a very big opportunity,” Gomes says. Novel adaptations Metabolically, there’s no place like home: Cancers tend to do best in the tissues where they initially grow, Vander Heiden’s group has found. And when they do move, these primary tumors have preferred target sites—prostate cancers tend to move into bone, for example. Some cells, however, will land in a place to which they are very unlikely to ever adapt: Certain sites, such as the spleen and skeletal muscles, seem to resist metastasis, and there are many possible reasons. Muscle cells, for example, use tons of energy, causing their mitochondria to release lots of a side product of energy processing: reactive oxygen species such as hydrogen peroxide. These vigorously oxidizing molecules are toxic, but local muscle cells can handle them. Yet even though plenty of tumor cells reach the skeletal muscle via the blood that copiously feeds it, they rarely take hold there, stymied, researchers suspect, by those reactive oxygen molecules. But adaptation to other novel environments is possible, as Vander Heiden discovered when his group implanted human breast cancer cells into either mammary fat or the brains of mice. Though the brain lacks the kinds of fat building blocks—fatty acids—that breast cancer cells are accustomed to eating, when the cells were dropped into the brain, they adjusted to manufacture their own fatty acids. The scientists then treated the mice with a drug that blocks fatty acid synthesis, and the cancer cells in brain tissue grew at half-speed. (The breast cells in the mammary fat continued to grow unbothered.) Vander Heiden has consulted for companies that are in the early stages of exploring this approach as a treatment. Sometimes, tumors can even prime a foreign site for their arrival, in a process some researchers call “education of the metastatic niche.” Cancers shed not only cells, but also hormones, DNA and little fatty bubbles called vesicles into the blood and lymph. These bubbles can contain chemical messages, and when these or other signals reach far-off organs, they can reshape the tissues to the tumor cells’ specifications. That “education” helps set up metastasizing cells to thrive in a new location says Gomes. Even microbes can get in on the act: In the case of colorectal cancer, bacteria from the intestines teach the liver to receive metastatic cancer cells. The gut bacteria colonize the intestinal tumor, then break through the multilayer barrier that normally keeps gut contents away from the rest of the body. Then the bacteria can go into the liver, where they induce inflammation in the organ. This creates a pro-tumor environment, so cancer cells that arrive later are able to settle in. The fatty acid connection Altea-Manzano studied this priming process during her time as a postdoctoral scholar with cancer biologist Sarah-Maria Fendt at the VIB-KU Leuven Center for Cancer Biology in Belgium. In this case, it was the lungs that were being primed by tumors residing elsewhere. And much as Vander Heiden observed with breast cancer metastasis to the brain, access to fatty acids was a key factor—specifically, the fatty acid palmitate, whose functions include serving as an energy source and as a component of cellular membranes. The lungs are already awash in a fat-rich material called surfactant, which coats the lungs’ interior and keeps the tissue from collapsing. When the researchers fed mice a high-fat diet, the levels of palmitate and other fatty acids in the lungs rose. And when the researchers injected mouse mammary (breast) cancer cells into the blood of those mice, the high-fat diet resulted in more than twice as much metastasis to the lung. To check whether tumor cells were secreting something that primed the lungs to host them, Altea-Manzano and colleagues grew pieces of mouse mammary tumor in a dish, then collected the liquid containing all the cellular secretions. When they injected this cell-free soup into mice, it boosted the palmitate levels in the lungs; if they also injected cancer cells, this treatment increased the level of lung metastases by those cells, too. Some ingredient made by the cancer cells cultured in that lab dish was sending the lungs a message: Make more palmitate. (The scientists still aren’t sure what the signaling substance is.) The result is that if a breast cancer cell lands in the lungs, it finds a fatty, ready-made feast to nosh on. To make the most of the new menu, however, a newly arrived breast cancer cell will have to alter its cell chemistry. It does that by changing its mitochondria so they can take up more palmitate. In experiments with mice, blocking that change interfered with metastasis, no matter how much palmitate was present. It might do the same in human patients, speculates Altea-Manzano, who with Fendt and others was a co-author of a discussion of metabolic changes that might promote or thwart metastasis for the 2024 Annual Review of Cancer Biology. A person’s lifestyle as well as their environment can influence their metabolism and microbiome. That, in turn, can be a factor in the success or failure of cancer to metastasize. But the relationships are complex: Things that seem good for metabolism on the surface—such as antioxidants—aren’t always things that directly counter cancer spread. Adapted from A. Vandekeere et al. / AR Cancer Biology 2024 / Knowable Magazine Knowing the enemy In addition to fat-rich places like the lungs, cancers can adapt to surprisingly challenging locales, such as the barren wasteland that is the spinal fluid surrounding the brain and spinal cord. Most places in the body where tumors originate are replete with nutrients: fats, amino acids, oxygen, metals—all the foodstuffs a rapidly growing cell needs. In contrast, “the brain is kind of a metabolic princess,” says Boire. “It prefers glucose only, please.” Not only is there precious little to eat, but cancer cells will find themselves surrounded by support cells of the nervous system and resident immune cells, both of which spew out anti-tumor agents. Boire’s work focuses on the spinal fluid. It’s a clear liquid devoid of many nutrients, and yet metastasis to the spinal fluid happens in some 5 percent to 10 percent of solid-tumor patients, and it usually kills within months. For Boire, this makes such a cancer “a worthy adversary. … It’s totally evil.” To learn how such an evil cell survives, Boire and colleagues examined metastatic cells from five patients in whom breast or lung cancers had taken over the spinal fluid. These cells had all ramped up a biochemical system that sops up iron, a necessary metal to produce energy and more cell parts. As one part of the system, the cells secreted a protein called lipocalin-2 that collects the sparse iron in the environment; for the other part, they made a protein called a lipocalin-2-iron transporter that pulls the iron-lipocalin-2 complex into the cells. Mice studied as models for metastasis to the spinal fluid normally all die within fewer than 40 days. But when scientists treated the mice with a drug, deferoxamine, that prevents the cancer from accessing iron, they live for longer. Adapted from Y. Chi et al. / Science 2020 / Knowable Magazine Studying the process further in mice, Boire’s team discovered that the cancer cells boost their iron collection in response to inflammatory molecules produced by local immune cells. The cancer cells then slurp up so much iron that the immune cells can’t meet their own needs for the metal. “They’re like the original jerks at the buffet,” says Boire. “You know these guys—they’re taking everything you want for themselves.” To starve out these cellular creeps, the researchers treated mice with a molecule called deferoxamine that snatches the iron before lipocalin-2 has a chance to grab it. Sure enough, the iron levels in the cancer cells dropped. Moreover, the mice survived nearly twice as long as animals who didn’t get the treatment. Boire has begun testing deferoxamine in a few dozen patients who have metastatic cancer in the spinal fluid and expects to publish results soon. She notes that the treatment doesn’t act directly on the cancer but changes its environment so it can’t fulfill its needs. “It kind of opens up this idea—there are other ways of targeting cancer cell growth,” she says. Stress points In addition to food, traveling cancer cells need protection from changes to their metabolism in new environments. Metastasis itself seems to cause cancer cells to generate reactive oxygen species, which can kill them from within, says Sean Morrison, a cancer biologist at the University of Texas Southwestern Medical Center in Dallas. His team studies this metastasis roadblock by injecting human melanoma cells into mice. The scientists can put the cells right under the skin where they should be comfortable, or stick them into other places, such as the bloodstream or spleen, to see if they can achieve metastasis. In the skin, melanoma cells don’t experience much oxidative stress. But melanoma cells in the blood or other organs experience stress from higher levels of reactive oxygen molecule levels. It could be that higher levels of iron and oxygen in places like the blood drive biochemical changes that produce these dangerous molecules, Morrison suggests. Oxidative stress kills wandering melanoma cells by a process called ferroptosis, in which polyunsaturated fatty acids in the cancer cell membrane react with iron. “It’s like a grease fire starting in the cancer cells as they’re trying to migrate,” says Morrison. But some melanoma cells gain a defense if they cruise the body’s lymphatic system before settling down. In the lymph, their membranes pick up monounsaturated fatty acids that can’t react with iron in the same way, helping them resist ferroptosis, the researchers reported. That’s not all. Melanoma cells that were the most efficient at metastasis rewired their metabolism, the scientists found. As a result, they gorged on a molecule called lactate in their surroundings, and they seemed to use this lactate to manufacture protective, oxidant-fighting molecules. When the scientists blocked the ability of the melanoma cells to suck up this lactate, metastatic disease in the mice was reduced. In contrast, when they treated mice with more antioxidants, metastasizing cells were more likely to survive in the bloodstream and other organs—in some treated mice, the numbers of metastatic cells cruising the bloodstream more than doubled. That result, published in 2015, was a huge surprise, says Morrison: “People think of antioxidants as being good for you.” Well, in his lab mice, antioxidants were good for cancer cells too—really good. The Washington Post called the study “terrifying,” “provocative” and “alarming.” In an experiment, scientists studied a line of mice that had melanoma injected under their skin. Treatment with an antioxidant greatly increased the fraction of cells in blood that were metastasizing melanoma cells (left), as well as the burden—quantity—of metastatic cancer cells in their internal organs (right). Adapted from E. Piskounova et al. / Nature 2015 / Knowable Magazine But the results do jive with past trials of antioxidants in cancer patients. In studies spanning decades, antioxidants such as beta-carotene and vitamin E were linked to increased lung cancer rates and deaths in smokers and higher prostate cancer rates in healthy men. Although those studies did not focus on metastatic cancer, Morrison sees a connection. “The reality is that at certain key phases of the evolution of cancer, the cancer cells are just on the edge of dying of oxidative stress, so they benefit more from the antioxidants than the normal cells do,” he speculates. If antioxidants are good for cancers, then boosting reactive oxygen molecules might fight some kinds of metastasis. Indeed, some current cancer treatments do amplify reactive oxygen molecules to kill cancers. These results imply that diet choices or supplements might influence cancer and metastasis risk. For example, Morrison speculates that a diet high in polyunsaturated fatty acids might lead to more of those pro-ferroptosis fatty acids in the membranes of cancer cells. If the cells are already quite vulnerable, a bit of polyunsaturated fat might be another way to nudge them over the cliff to cell death. For once, that’s an easy diet to swallow: One menu item might be salmon seared in soybean oil, Morrison suggests. Dietary change is not going to vanquish cancer on its own, Fendt says. But, she adds, it might slow progression or help other treatments to work—although as the antioxidant trials illustrate, the effects of diet can be tricky to predict. “It’s important to have really solid and rigorous science on those questions,” cautions Fendt. Some trials are underway—but, for now, there’s no “anti-metastasis” diet to prescribe.Knowable Magazine is an independent journalistic endeavor from Annual Reviews. Get the latest Science stories in your inbox.

Scientists are looking for answers about how these confounding trips, known as metastases, occur throughout the human body

How Do Cancer Cells Migrate to New Tissues and Take Hold?

Scientists are looking for answers about how these confounding trips, known as metastases, occur throughout the human body

Cancer Cell Illustration
Illustration of a human cancer cell SCIEPRO / SCIENCE PHOTO LIBRARY via Getty Images

Back in 2014, a woman with advanced cancer pushed Adrienne Boire’s scientific life in a whole new direction. The cancer, which had begun in the breast, had found its way into the patient’s spinal fluid, rendering the middle-aged mother of two unable to walk. “When did this happen?” she asked from her hospital bed. “Why are the cells growing there?”

Why, indeed. Why would cancer cells migrate to the spinal fluid, far from where they’d been birthed, and how did they manage to thrive in a liquid so strikingly poor in nutrients?

Boire, a physician-scientist at Memorial Sloan Kettering Cancer Center in New York, decided that those questions deserved answers.

The answers are urgent, because the same thing that happened to Boire’s patient is happening to increasing numbers of cancer patients. As the ability to treat initial, or primary, tumors has improved, people survive early rounds with cancer only to come back years or decades later when the cancer has somehow resettled in a new tissue, such as brain, lung or bone. This is metastatic cancer, and it’s the big killer—while precise numbers are scarce, anywhere from half to the large majority of cancer deaths have been attributed to metastasis. Offering people more options and hope will mean understanding how those cancers successfully migrate and recolonize.

The prevalence of metastasis belies the arduous journey that cancer cells must make to achieve it. A cell that arises in, say, the breast, is well adapted to live there: to eat the fatty acids available to it, to resist local threats and to grow there in a solid tumor. If it manages to escape into the bloodstream, it finds itself zipping along at up to 15 inches per second with shear stresses sufficient to rip it apart. Should it survive that odyssey and land in a new tissue—say, the brain or spinal fluid—the environment is totally different yet again. The foods the cell is accustomed to may be absent; immune cells or other novel environmental molecules may attack. For a cell to manage this trip, and then adapt to a new environment, is truly a Herculean task.

“It is not easy and trivial,” says Ana Gomes, a cancer biologist at the Moffitt Cancer Center in Tampa, Florida. “It’s just against everything in the nature of these cells.”

Metastasis Graphic
Moving to a new site and forming a new tumor is an arduous journey that few cells can complete. A cell must exit the initial tumor, survive the bloodstream and enter a new tissue. Even then, the cell may remain dormant for a time, until the environment can support its division and growth to create a new tumor. Adapted from Ana Gomes / Knowable Magazine

No wonder that, even though tumors regularly shed cells, most escapees perish or languish without successfully establishing themselves as metastases. “Personally, I think metastasis is an accident,” says Matthew Vander Heiden, a physician-scientist and director of the Koch Institute for Integrative Cancer Research at MIT. “It’s really, really inefficient.”

The few cells that manage this epic feat are resilient and flexible in how they feed themselves and process the molecules around them. They may tweak their biochemistry to evade local dangers, or to get the fuel they need in sparse environments. Some even send signals ahead to modify the organ where they’ll land, creating a cushy nest with a food supply ready for when they arrive. “Metabolic changes help these cells to face all this challenge,” says Patricia Altea-Manzano, a biomedical researcher at the Andalusian Molecular Biology and Regenerative Medicine Center in Seville, Spain.

Such findings suggest ways that metastasizing cells, because they’re so different from the original tumor, might be vulnerable to new kinds of treatment. Someday doctors might not have to wait for metastasis to take hold before they block or slow cancer’s spread: “That is a very big opportunity,” Gomes says.

Novel adaptations

Metabolically, there’s no place like home: Cancers tend to do best in the tissues where they initially grow, Vander Heiden’s group has found. And when they do move, these primary tumors have preferred target sites—prostate cancers tend to move into bone, for example.

Some cells, however, will land in a place to which they are very unlikely to ever adapt: Certain sites, such as the spleen and skeletal muscles, seem to resist metastasis, and there are many possible reasons. Muscle cells, for example, use tons of energy, causing their mitochondria to release lots of a side product of energy processing: reactive oxygen species such as hydrogen peroxide. These vigorously oxidizing molecules are toxic, but local muscle cells can handle them. Yet even though plenty of tumor cells reach the skeletal muscle via the blood that copiously feeds it, they rarely take hold there, stymied, researchers suspect, by those reactive oxygen molecules.

But adaptation to other novel environments is possible, as Vander Heiden discovered when his group implanted human breast cancer cells into either mammary fat or the brains of mice. Though the brain lacks the kinds of fat building blocks—fatty acids—that breast cancer cells are accustomed to eating, when the cells were dropped into the brain, they adjusted to manufacture their own fatty acids.

The scientists then treated the mice with a drug that blocks fatty acid synthesis, and the cancer cells in brain tissue grew at half-speed. (The breast cells in the mammary fat continued to grow unbothered.) Vander Heiden has consulted for companies that are in the early stages of exploring this approach as a treatment.

Sometimes, tumors can even prime a foreign site for their arrival, in a process some researchers call “education of the metastatic niche.” Cancers shed not only cells, but also hormones, DNA and little fatty bubbles called vesicles into the blood and lymph. These bubbles can contain chemical messages, and when these or other signals reach far-off organs, they can reshape the tissues to the tumor cells’ specifications. That “education” helps set up metastasizing cells to thrive in a new location says Gomes.

Even microbes can get in on the act: In the case of colorectal cancer, bacteria from the intestines teach the liver to receive metastatic cancer cells. The gut bacteria colonize the intestinal tumor, then break through the multilayer barrier that normally keeps gut contents away from the rest of the body. Then the bacteria can go into the liver, where they induce inflammation in the organ. This creates a pro-tumor environment, so cancer cells that arrive later are able to settle in.

The fatty acid connection

Altea-Manzano studied this priming process during her time as a postdoctoral scholar with cancer biologist Sarah-Maria Fendt at the VIB-KU Leuven Center for Cancer Biology in Belgium. In this case, it was the lungs that were being primed by tumors residing elsewhere. And much as Vander Heiden observed with breast cancer metastasis to the brain, access to fatty acids was a key factor—specifically, the fatty acid palmitate, whose functions include serving as an energy source and as a component of cellular membranes.

The lungs are already awash in a fat-rich material called surfactant, which coats the lungs’ interior and keeps the tissue from collapsing. When the researchers fed mice a high-fat diet, the levels of palmitate and other fatty acids in the lungs rose. And when the researchers injected mouse mammary (breast) cancer cells into the blood of those mice, the high-fat diet resulted in more than twice as much metastasis to the lung.

To check whether tumor cells were secreting something that primed the lungs to host them, Altea-Manzano and colleagues grew pieces of mouse mammary tumor in a dish, then collected the liquid containing all the cellular secretions. When they injected this cell-free soup into mice, it boosted the palmitate levels in the lungs; if they also injected cancer cells, this treatment increased the level of lung metastases by those cells, too. Some ingredient made by the cancer cells cultured in that lab dish was sending the lungs a message: Make more palmitate. (The scientists still aren’t sure what the signaling substance is.)

The result is that if a breast cancer cell lands in the lungs, it finds a fatty, ready-made feast to nosh on. To make the most of the new menu, however, a newly arrived breast cancer cell will have to alter its cell chemistry. It does that by changing its mitochondria so they can take up more palmitate. In experiments with mice, blocking that change interfered with metastasis, no matter how much palmitate was present. It might do the same in human patients, speculates Altea-Manzano, who with Fendt and others was a co-author of a discussion of metabolic changes that might promote or thwart metastasis for the 2024 Annual Review of Cancer Biology.

Metastasis Risk Graphic
A person’s lifestyle as well as their environment can influence their metabolism and microbiome. That, in turn, can be a factor in the success or failure of cancer to metastasize. But the relationships are complex: Things that seem good for metabolism on the surface—such as antioxidants—aren’t always things that directly counter cancer spread. Adapted from A. Vandekeere et al. / AR Cancer Biology 2024 / Knowable Magazine

Knowing the enemy

In addition to fat-rich places like the lungs, cancers can adapt to surprisingly challenging locales, such as the barren wasteland that is the spinal fluid surrounding the brain and spinal cord.

Most places in the body where tumors originate are replete with nutrients: fats, amino acids, oxygen, metals—all the foodstuffs a rapidly growing cell needs. In contrast, “the brain is kind of a metabolic princess,” says Boire. “It prefers glucose only, please.”

Not only is there precious little to eat, but cancer cells will find themselves surrounded by support cells of the nervous system and resident immune cells, both of which spew out anti-tumor agents.

Boire’s work focuses on the spinal fluid. It’s a clear liquid devoid of many nutrients, and yet metastasis to the spinal fluid happens in some 5 percent to 10 percent of solid-tumor patients, and it usually kills within months. For Boire, this makes such a cancer “a worthy adversary. … It’s totally evil.”

To learn how such an evil cell survives, Boire and colleagues examined metastatic cells from five patients in whom breast or lung cancers had taken over the spinal fluid. These cells had all ramped up a biochemical system that sops up iron, a necessary metal to produce energy and more cell parts. As one part of the system, the cells secreted a protein called lipocalin-2 that collects the sparse iron in the environment; for the other part, they made a protein called a lipocalin-2-iron transporter that pulls the iron-lipocalin-2 complex into the cells.

Mice and Iron Survival Graphic
Mice studied as models for metastasis to the spinal fluid normally all die within fewer than 40 days. But when scientists treated the mice with a drug, deferoxamine, that prevents the cancer from accessing iron, they live for longer. Adapted from Y. Chi et al. / Science 2020 / Knowable Magazine

Studying the process further in mice, Boire’s team discovered that the cancer cells boost their iron collection in response to inflammatory molecules produced by local immune cells. The cancer cells then slurp up so much iron that the immune cells can’t meet their own needs for the metal. “They’re like the original jerks at the buffet,” says Boire. “You know these guys—they’re taking everything you want for themselves.”

To starve out these cellular creeps, the researchers treated mice with a molecule called deferoxamine that snatches the iron before lipocalin-2 has a chance to grab it. Sure enough, the iron levels in the cancer cells dropped. Moreover, the mice survived nearly twice as long as animals who didn’t get the treatment.

Boire has begun testing deferoxamine in a few dozen patients who have metastatic cancer in the spinal fluid and expects to publish results soon.

She notes that the treatment doesn’t act directly on the cancer but changes its environment so it can’t fulfill its needs. “It kind of opens up this idea—there are other ways of targeting cancer cell growth,” she says.

Stress points

In addition to food, traveling cancer cells need protection from changes to their metabolism in new environments. Metastasis itself seems to cause cancer cells to generate reactive oxygen species, which can kill them from within, says Sean Morrison, a cancer biologist at the University of Texas Southwestern Medical Center in Dallas.

His team studies this metastasis roadblock by injecting human melanoma cells into mice. The scientists can put the cells right under the skin where they should be comfortable, or stick them into other places, such as the bloodstream or spleen, to see if they can achieve metastasis.

In the skin, melanoma cells don’t experience much oxidative stress. But melanoma cells in the blood or other organs experience stress from higher levels of reactive oxygen molecule levels. It could be that higher levels of iron and oxygen in places like the blood drive biochemical changes that produce these dangerous molecules, Morrison suggests.

Oxidative stress kills wandering melanoma cells by a process called ferroptosis, in which polyunsaturated fatty acids in the cancer cell membrane react with iron. “It’s like a grease fire starting in the cancer cells as they’re trying to migrate,” says Morrison.

But some melanoma cells gain a defense if they cruise the body’s lymphatic system before settling down. In the lymph, their membranes pick up monounsaturated fatty acids that can’t react with iron in the same way, helping them resist ferroptosis, the researchers reported.

That’s not all. Melanoma cells that were the most efficient at metastasis rewired their metabolism, the scientists found. As a result, they gorged on a molecule called lactate in their surroundings, and they seemed to use this lactate to manufacture protective, oxidant-fighting molecules. When the scientists blocked the ability of the melanoma cells to suck up this lactate, metastatic disease in the mice was reduced.

In contrast, when they treated mice with more antioxidants, metastasizing cells were more likely to survive in the bloodstream and other organs—in some treated mice, the numbers of metastatic cells cruising the bloodstream more than doubled.

That result, published in 2015, was a huge surprise, says Morrison: “People think of antioxidants as being good for you.” Well, in his lab mice, antioxidants were good for cancer cells too—really good. The Washington Post called the study “terrifying,” “provocative” and “alarming.”

Antioxidants and Metastasis Graphic
In an experiment, scientists studied a line of mice that had melanoma injected under their skin. Treatment with an antioxidant greatly increased the fraction of cells in blood that were metastasizing melanoma cells (left), as well as the burden—quantity—of metastatic cancer cells in their internal organs (right). Adapted from E. Piskounova et al. / Nature 2015 / Knowable Magazine

But the results do jive with past trials of antioxidants in cancer patients. In studies spanning decades, antioxidants such as beta-carotene and vitamin E were linked to increased lung cancer rates and deaths in smokers and higher prostate cancer rates in healthy men. Although those studies did not focus on metastatic cancer, Morrison sees a connection. “The reality is that at certain key phases of the evolution of cancer, the cancer cells are just on the edge of dying of oxidative stress, so they benefit more from the antioxidants than the normal cells do,” he speculates.

If antioxidants are good for cancers, then boosting reactive oxygen molecules might fight some kinds of metastasis. Indeed, some current cancer treatments do amplify reactive oxygen molecules to kill cancers.

These results imply that diet choices or supplements might influence cancer and metastasis risk. For example, Morrison speculates that a diet high in polyunsaturated fatty acids might lead to more of those pro-ferroptosis fatty acids in the membranes of cancer cells. If the cells are already quite vulnerable, a bit of polyunsaturated fat might be another way to nudge them over the cliff to cell death. For once, that’s an easy diet to swallow: One menu item might be salmon seared in soybean oil, Morrison suggests.

Dietary change is not going to vanquish cancer on its own, Fendt says. But, she adds, it might slow progression or help other treatments to work—although as the antioxidant trials illustrate, the effects of diet can be tricky to predict.

“It’s important to have really solid and rigorous science on those questions,” cautions Fendt. Some trials are underway—but, for now, there’s no “anti-metastasis” diet to prescribe.

Knowable

Knowable Magazine is an independent journalistic endeavor from Annual Reviews.

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Giant Sloths and Many Other Massive Creatures Were Once Common on Our Planet. With Environmental Changes, Such Giants Could Thrive Again

If large creatures like elephants, giraffes and bison are allowed to thrive, they could alter habitats that allow for the rise of other giants

Giant Sloths and Many Other Massive Creatures Were Once Common on Our Planet. With Environmental Changes, Such Giants Could Thrive Again If large creatures like elephants, giraffes and bison are allowed to thrive, they could alter habitats that allow for the rise of other giants Riley Black - Science Correspondent July 11, 2025 8:00 a.m. Ancient sloths lived in trees, on mountains, in deserts, in boreal forests and on open savannas. Some grew as large as elephants. Illustration by Diego Barletta The largest sloth of all time was the size of an elephant. Known to paleontologists as Eremotherium, the shaggy giant shuffled across the woodlands of the ancient Americas between 60,000 and five million years ago. Paleontologists have spent decades hotly debating why such magnificent beasts went extinct, the emerging picture involving a one-two punch of increasing human influence on the landscape and a warmer interglacial climate that began to change the world’s ecosystems. But even less understood is how our planet came to host entire communities of such immense animals during the Pleistocene. Now, a new study on the success of the sloths helps to reveal how the world of Ice Age giants came to be, and hints that an Earth brimming with enormous animals could come again. Florida Museum of Natural History paleontologist Rachel Narducci and colleagues tracked how sloths came to be such widespread and essential parts of the Pleistocene Americas and published their findings in Science this May. The researchers found that climate shifts that underwrote the spread of grasslands allowed big sloths to arise, the shaggy mammals then altering those habitats to maintain open spaces best suited to big bodies capable of moving long distances. The interactions between the animals and environment show how giants attained their massive size, and how strange it is that now our planet has fewer big animals than would otherwise be here. Earth still boasts some impressively big species. In fact, the largest animal of all time is alive right now and only evolved relatively recently. The earliest blue whale fossils date to about 1.5 million years ago, and, at 98 feet long and more than 200 tons, the whale is larger than any mammoth or dinosaur. Our planet has always boasted a greater array of small species than large ones, even during prehistoric ages thought of as synonymous with megafauna. Nevertheless, Earth’s ecosystems are still in a megafaunal lull that began at the close of the Ice Age. “I often say we are living on a downsized planet Earth,” says University of Maine paleoecologist Jacquelyn Gill.Consider what North America was like during the Pleistocene, between 11,000 years and two million ago. The landmass used to host multiple forms of mammoths, mastodons, giant ground sloths, enormous armadillos, multiple species of sabercat, huge bison, dire wolves and many more large creatures that formed ancient ecosystems unlike anything on our planet today. In addition, many familiar species such as jaguars, black bears, coyotes, white-tailed deer and golden eagles also thrived. Elsewhere in the world lived terror birds taller than an adult human, wombats the size of cars, woolly rhinos, a variety of elephants with unusual tusks and other creatures. Ecosystems capable of supporting such giants have been the norm rather than the exception for tens of millions of years. Giant sloths were among the greatest success stories among the giant-size menagerie. The herbivores evolved on South America when it was still an island continent, only moving into Central and North America as prehistoric Panama connected the landmasses about 2.7 million years ago. Some were small, like living two- and three-toed sloths, while others embodied a range of sizes all the way up to elephant-sized giants like Eremotherium and the “giant beast” Megatherium. An Eremotherium skeleton at the Houston Museum of Natural Science demonstrates just how large the creature grew. James Nielsen / Houston Chronicle via Getty Images The earliest sloths originated on South America about 35 million years ago. They were already big. Narducci and colleagues estimate that the common ancestor of all sloths was between about 150 and 770 pounds—or similar to the range of sizes seen among black bears today—and they walked on the ground. “I was surprised and thrilled” to find that sloths started off large, Narducci says, as ancestral forms of major mammal groups are often small, nocturnal creatures. The earliest sloths were already in a good position to shift with Earth’s climate and ecological changes. The uplift of the Andes Mountains in South America led to changes on the continent as more open, drier grasslands spread where there had previously been wetter woodlands and forests. While some sloths became smaller as they spent more time around and within trees, the grasslands would host the broadest diversity of sloth species. The grasslands sloths were the ones that ballooned to exceptional sizes. Earth has been shifting between warmer and wetter times, like now, and cooler and drier climates over millions of years. The chillier and more arid times are what gave sloths their size boost. During these colder spans, bigger sloths were better able to hold on to their body heat, but they also didn’t need as much water, and they were capable of traveling long distances more efficiently thanks to their size. “The cooler and drier the climate, especially after 11.6 million years ago, led to expansive grasslands, which tends to favor the evolution of increasing body mass,” Narducci says. The combination of climate shifts, mountain uplift and vegetation changes created environments where sloths could evolve into a variety of forms—including multiple times when sloths became giants again. Gill says that large body size was a “winning strategy” for herbivores. “At a certain point, megaherbivores get so large that most predators can’t touch them; they’re able to access nutrition in foods that other animals can’t really even digest thanks to gut microbes that help them digest cellulose, and being large means you’re also mobile,” Gill adds, underscoring advantages that have repeatedly pushed animals to get big time and again. The same advantages underwrote the rise of the biggest dinosaurs as well as more recent giants like the sloths and mastodons. As large sloths could travel further, suitable grassland habitats stretched from Central America to prehistoric Florida. “This is what also allowed for their passage into North America,” Narducci says. Sloths were able to follow their favored habitats between continents. If the world were to shift back toward cooler and drier conditions that assisted the spread of the grasslands that gave sloths their size boost, perhaps similar giants could evolve. The sticking point is what humans are doing to Earth’s climate, ecosystems and existing species. The diversity and number of large species alive today is vastly, and often negatively, affected by humans. A 2019 study of human influences on 362 megafauna species, on land and in the water, found that 70 percent are diminishing in number, and 59 percent are getting dangerously close to extinction. But if that relationship were to change, either through our actions or intentions, studies like the new paper on giant sloths hint that ecosystems brimming with a wealth of megafaunal species could evolve again. Big animals change the habitats where they live, which in turn tends to support more large species adapted to those environments. The giant sloths that evolved among ancient grasslands helped to keep those spaces open in tandem with other big herbivores, such as mastodons, as well as the large carnivores that preyed upon them. Paleontologists and ecologists know this from studies of how large animals such as giraffes and rhinos affect vegetation around them. Big herbivores, in particular, tend to keep habitats relatively open. Elephants and other big beasts push over trees, trample vegetation underfoot, eat vast amounts of greenery and transport seeds in their dung, disassembling vegetation while unintentionally planting the beginnings of new habitats. Such broad, open spaces were essential to the origins of the giant sloths, and so creating wide-open spaces helps spur the evolution of giants to roam such environments. For now, we are left with the fossil record of giant animals that were here so recently that some of their bones aren’t even petrified, skin and fur still clinging to some skeletons. “The grasslands they left behind are just not the same, in ways we’re really only starting to understand and appreciate,” Gill says. A 2019 study on prehistoric herbivores in Africa, for example, found that the large plant-eaters altered the water cycling, incidence of fire and vegetation of their environment in a way that has no modern equivalent and can’t just be assumed to be an ancient version of today’s savannas. The few megaherbivores still with us alter the plant life, water flow, seed dispersal and other aspects of modern environments in their own unique ways, she notes, which should be a warning to us to protect them—and the ways in which they affect our planet. If humans wish to see the origin of new magnificent giants like the ones we visit museums to see, we must change our relationship to the Earth first. Get the latest Science stories in your inbox.

How changes in California culture have influenced the evolution of wild animals in Los Angeles

A new study argues that religion, politics and war affect how animals and plants in cities evolve, and the confluence of these forces seem to be actively affecting urban wildlife in L.A.

For decades, biologists have studied how cities affect wildlife by altering food supplies, fragmenting habitats and polluting the environment. But a new global study argues that these physical factors are only part of the story. Societal factors, the researchers claim, especially those tied to religion, politics and war, also leave lasting marks on the evolutionary paths of the animals and plants that share our cities.Published in Nature Cities, the comprehensive review synthesizes evidence from cities worldwide, revealing how human conflict and cultural practices affect wildlife genetics, behavior and survival in urban environments.The paper challenges the tendency to treat the social world as separate from ecological processes. Instead, the study argues, we should consider the ways the aftershocks of religious traditions, political systems and armed conflicts can influence the genetic structure of urban wildlife populations. (Gabriella Angotti-Jones / Los Angeles Times) “Social sciences have been very far removed from life sciences for a very long time, and they haven’t been integrated,” said Elizabeth Carlen, a biologist at Washington University in St. Louis and co-lead author of the study. “We started just kind of playing around with what social and cultural processes haven’t been talked about,” eventually focusing on religion, politics and war because of their persistent yet underexamined impacts on evolutionary biology, particularly in cities, where cultural values and built environments are densely concentrated.Carlen’s own work in St. Louis examines how racial segregation and urban design, often influenced by policing strategies, affect ecological conditions and wild animals’ access to green spaces.“Crime prevention through environmental design,” she said, is one example of how these factors influence urban wildlife. “Law enforcement can request that there not be bushes … or short trees, because then they don’t have a sight line across the park.” Although that design choice may serve surveillance goals, it also limits the ability of small animals to navigate those spaces.These patterns, she emphasized, aren’t unique to St. Louis. “I’m positive that it’s happening in Los Angeles. Parks in Beverly Hills are going to look very different than parks in Compton. And part of that is based on what policing looks like in those different places.” This may very well be the case, as there is a significantly lower level of urban tree species richness in areas like Compton than in areas like Beverly Hills, according to UCLA’s Biodiversity Atlas. A coyote wanders onto the fairway, with the sprinklers turned on, as a golfer makes his way back to his cart after hitting a shot on the 16th hole of the Harding golf course at Griffith Park. (Mel Melcon / Los Angeles Times) The study also examines war and its disruptions, which can have unpredictable effects on animal populations. Human evacuation from war zones can open urban habitats to wildlife, while the destruction of green spaces or contamination of soil and water can fragment ecosystems and reduce genetic diversity.In Kharkiv, Ukraine, for example, human displacement during the Russian invasion led to the return of wild boars and deer to urban parks, according to the study. In contrast, sparrows, which depend on human food waste, nearly vanished from high-rise areas.All of this, the researchers argue, underscores the need to rethink how cities are designed and managed by recognizing how religion, politics and war shape not just human communities but also the evolutionary trajectories of urban wildlife. By integrating ecological and social considerations into urban development, planners and scientists can help create cities that are more livable for people while also supporting the long-term genetic diversity and adaptability of the other species that inhabit them.This intersection of culture and biology may be playing out in cities across the globe, including Los Angeles.A study released earlier this year tracking coyotes across L.A. County found that the animals were more likely to avoid wealthier neighborhoods, not because of a lack of access or food scarcity, but possibly due to more aggressive human behavior toward them and higher rates of “removal” — including trapping and releasing elsewhere, and in some rare cases, killing them. In lower-income areas, where trapping is less common, coyotes tended to roam more freely, even though these neighborhoods often had more pollution and fewer resources that would typically support wild canines. Researchers say these patterns reflect how broader urban inequities are written directly into the movements of and risks faced by wildlife in the city.Black bears, parrots and even peacocks tell a similar story in Los Angeles. Wilson Sherman, a PhD student at UCLA who is studying human-black bear interactions, highlights how local politics and fragmented municipal governance shape not only how animals are managed but also where they appear. (Carolyn Cole / Los Angeles Times) “Sierra Madre has an ordinance requiring everyone to have bear-resistant trash cans,” Sherman noted. “Neighboring Arcadia doesn’t.” This kind of patchwork governance, Sherman said, can influence where wild animals ultimately spend their time, creating a mosaic of risk and opportunity for species whose ranges extend across multiple jurisdictions.Cultural values also play a role. Thriving populations of non-native birds, such as Amazon parrots and peacocks, illustrate how aesthetic preferences and everyday choices can significantly influence the city’s ecological makeup in lasting ways.Sherman also pointed to subtler, often overlooked influences, such as policing and surveillance infrastructure. Ideally, the California Department of Fish and Wildlife would be the first agency to respond in a “wildlife situation,” as Sherman put it. But, he said, what often ends up happening is that people default to calling the police, especially when the circumstances involve animals that some urban-dwelling humans may find threatening, like bears.Police departments typically do not possess the same expertise and ability as CDFW to manage and then relocate bears. If a bear poses a threat to human life, police policy is to kill the bear. However, protocols for responding to wildlife conflicts that are not life-threatening can vary from one community to another. And how police use non-lethal methods of deterrence — such as rubber bullets and loud noises — can shape bear behavior.Meanwhile, the growing prevalence of security cameras and motion-triggered alerts has provided residents with new forms of visibility into urban biodiversity. “That might mean that people are suddenly aware that a coyote is using their yard,” Sherman said. In turn, that could trigger a homeowner to purposefully rework the landscape of their property so as to discourage coyotes from using it. Surveillance systems, he said, are quietly reshaping both public perception and policy around who belongs in the city, and who doesn’t. A mountain lion sits in a tree after being tranquilized along San Vicente Boulevard in Brentwood on Oct. 27, 2022. (Wally Skalij / Los Angeles Times) Korinna Domingo, founder and director of the Cougar Conservancy, emphasized how cougar behavior in Los Angeles is similarly shaped by decades of urban development, fragmented landscapes and the social and political choices that structure them. “Policies like freeway construction, zoning and even how communities have been historically policed or funded can affect where and how cougars move throughout L.A.,” she said. For example, these forces have prompted cougars to adapt by becoming more nocturnal, using culverts or taking riskier crossings across fragmented landscapes.Urban planning and evolutionary consequences are deeply intertwined, Domingo says. For example, mountain lion populations in the Santa Monica and Santa Ana mountains have shown signs of reduced genetic diversity due to inbreeding, an issue created not by natural processes, but by political and planning decisions — such as freeway construction and zoning decisions— that restricted their movement decades ago.Today, the Wallis Annenberg Wildlife Crossing, is an attempt to rectify that. The massive infrastructure project is happening only, Domingo said, “because of community, scientific and political will all being aligned.”However, infrastructure alone isn’t enough. “You can have habitat connectivity all you want,” she said, but you also have to think about social tolerance. Urban planning that allows for animal movement also increases the likelihood of contact with people, pets and livestock — which means humans need to learn how to interact with wild animals in a healthier way.In L.A., coexistence strategies can look very different depending on the resources, ordinances and attitudes of each community. Although wealthier residents may have the means to build predator-proof enclosures, others lack the financial or institutional support to do the same. And some with the means simply choose not to, instead demanding lethal removal., “Wildlife management is not just about biology,” Domingo said. “It’s about values, power, and really, who’s at the table.”Wildlife management in the United States has long been informed by dominant cultural and religious worldviews, particularly those grounded in notions of human exceptionalism and control over nature. Carlen, Sherman and Domingo all brought up how these values shaped early policies that framed predators as threats to be removed rather than species to be understood or respected. In California, this worldview contributed not only to the widespread killing of wolves, bears and cougars but also to the displacement of American Indian communities whose land-based practices and beliefs conflicted with these approaches. A male peacock makes its way past Ian Choi, 21 months old, standing in front of his home on Altura Road in Arcadia. (Mel Melcon / Los Angeles Times) Wildlife management in California, specifically, has long been shaped by these same forces of violence, originating in bounty campaigns not just against predators like cougars and wolves but also against American Indian peoples. These intertwined legacies of removal, extermination and land seizure continue to influence how certain animals and communities are perceived and treated today.For Alan Salazar, a tribal elder with the Fernandeño Tataviam Band of Mission Indians, those legacies run deep. “What happened to native peoples happened to our large predators in California,” he said. “Happened to our plant relatives.” Reflecting on the genocide of Indigenous Californians and the coordinated extermination of grizzly bears, wolves and mountain lions, Salazar sees a clear parallel.“There were three parts to our world — the humans, the animals and the plants,” he explained. “We were all connected. We respected all of them.” Salazar explains that his people’s relationship with the land, animals and plants is itself a form of religion, one grounded in ceremony, reciprocity and deep respect. Salazar said his ancestors lived in harmony with mountain lions for over 10,000 years, not by eliminating them but by learning from them. Other predators — cougars, bears, coyotes and wolves — were also considered teachers, honored through ceremony and studied for their power and intelligence. “Maybe we had a better plan on how to live with mountain lions, wolves and bears,” he said. “Maybe you should look at tribal knowledge.”He views the Wallis Annenberg Wildlife Crossing — for which he is a Native American consultant — as a cultural opportunity. “It’s not just for mountain lions,” he said. “It’s for all animals. And that’s why I wanted to be involved.” He believes the project has already helped raise awareness and shift perceptions about coexistence and planning, and hopes that it will help native plants, animals and peoples.As L.A. continues to grapple with the future of wildlife in its neighborhoods, canyons and corridors, Salazar and others argue that it is an opportunity to rethink the cultural frameworks, governance systems and historical injustices that have long shaped human-animal relations in the city. Whether through policy reform, neighborhood education or sacred ceremony, residents need reminders that evolutionary futures are being shaped not only in forests and preserves but right here, across freeways, backyards and local council meetings. The Wallis Annenberg Wildlife Crossing under construction over the 101 Freeway near Liberty Canyon Road in Agoura Hills on July 12, 2024. (Myung J. Chun / Los Angeles Times) The research makes clear that wildlife is not simply adapting to urban environments in isolation; it is adapting to a range of factors, including policing, architecture and neighborhood design. Carlen believes this opens a crucial frontier for interdisciplinary research, especially in cities like Los Angeles, where uneven geographies, biodiversity and political decisions intersect daily. “I think there’s a lot of injustice in cities that are happening to both humans and wildlife,” she said. “And I think the potential is out there for justice to be brought to both of those things.”

Something Strange Is Happening to Tomatoes Growing on the Galápagos Islands

Scientists say wild tomato plants on the archipelago's western islands are experiencing "reverse evolution" and reverting back to ancestral traits

Something Strange Is Happening to Tomatoes Growing on the Galápagos Islands Scientists say wild tomato plants on the archipelago’s western islands are experiencing “reverse evolution” and reverting back to ancestral traits Sarah Kuta - Daily Correspondent July 9, 2025 4:29 p.m. Scientists are investigating the production of ancestral alkaloids by tomatoes in the Galápagos Islands. Adam Jozwiak / University of California, Riverside Some tomatoes growing on the Galápagos Islands appear to be going back in time by producing the same toxins their ancestors did millions of years ago. Scientists describe this development—a controversial process known as “reverse evolution”—in a June 18 paper published in the journal Nature Communications. Tomatoes are nightshades, a group of plants that also includes eggplants, potatoes and peppers. Nightshades, also known as Solanaceae, produce bitter compounds called alkaloids, which help fend off hungry bugs, animals and fungi. When plants produce alkaloids in high concentrations, they can sicken the humans who eat them. To better understand alkaloid synthesis, researchers traveled to the Galápagos Islands, the volcanic chain roughly 600 miles off the coast of mainland Ecuador made famous by British naturalist Charles Darwin. They gathered and studied more than 30 wild tomato plants growing in different places on various islands. The Galápagos tomatoes are the descendents of plants from South America that were probably carried to the archipelago by birds. The team’s analyses revealed that the tomatoes growing on the eastern islands were behaving as expected, by producing alkaloids that are similar to those found in modern, cultivated varieties. But those growing on the western islands, they found, were creating alkaloids that were more closely related to those produced by eggplants millions of years ago. Tomatoes growing on the western islands (shown here) are producing ancestral alkaloids.  Adam Jozwiak / University of California, Riverside Researchers suspect the environment may be responsible for the plants’ unexpected return to ancestral alkaloids. The western islands are much younger than the eastern islands, so the soil is less developed and the landscape is more barren. To survive in these harsh conditions, perhaps it was advantageous for the tomato plants to revert back to older alkaloids, the researchers posit. “The plants may be responding to an environment that more closely resembles what their ancestors faced,” says lead author Adam Jozwiak, a biochemist at the University of California, Riverside, to BBC Wildlife’s Beki Hooper. However, for now, this is just a theory. Scientists say they need to conduct more research to understand why tomato plants on the western islands have adapted this way. Scientists were able to uncover the underlying molecular mechanisms at play: Four amino acids in a single enzyme appear to be responsible for the reversion back to the ancestral alkaloids, they found. They also used evolutionary modeling to confirm the direction of the adaptation—that is, that the tomatoes on the western islands had indeed returned to an earlier, ancestral state. Among evolutionary biologists, “reverse evolution” is somewhat contentious. The commonly held belief is that evolution marches forward, not backward. It’s also difficult to prove an organism has reverted back to an older trait through the same genetic pathways. But, with the new study, researchers say they’ve done exactly that. “Some people don’t believe in this,” says Jozwiak in a statement. “But the genetic and chemical evidence points to a return to an ancestral state. The mechanism is there. It happened.” So, if “reverse evolution” happened in wild tomatoes, could something similar happen in humans? In theory, yes, but it would take a long time, Jozwiak says. “If environmental conditions shifted dramatically over long timescales, it’s possible that traits from our distant past could re-emerge, but whether that ever happens is highly uncertain,” Jozwiak tells Newsweek’s Daniella Gray. “It’s speculative and would take millions of years, if at all.” Get the latest stories in your inbox every weekday.

Lifesize herd of puppet animals begins climate action journey from Africa to Arctic Circle

The Herds project from the team behind Little Amal will travel 20,000km taking its message on environmental crisis across the worldHundreds of life-size animal puppets have begun a 20,000km (12,400 mile) journey from central Africa to the Arctic Circle as part of an ambitious project created by the team behind Little Amal, the giant puppet of a Syrian girl that travelled across the world.The public art initiative called The Herds, which has already visited Kinshasa and Lagos, will travel to 20 cities over four months to raise awareness of the climate crisis. Continue reading...

Hundreds of life-size animal puppets have begun a 20,000km (12,400 mile) journey from central Africa to the Arctic Circle as part of an ambitious project created by the team behind Little Amal, the giant puppet of a Syrian girl that travelled across the world.The public art initiative called The Herds, which has already visited Kinshasa and Lagos, will travel to 20 cities over four months to raise awareness of the climate crisis.It is the second major project from The Walk Productions, which introduced Little Amal, a 12-foot puppet, to the world in Gaziantep, near the Turkey-Syria border, in 2021. The award-winning project, co-founded by the Palestinian playwright and director Amir Nizar Zuabi, reached 2 million people in 17 countries as she travelled from Turkey to the UK.The Herds’ journey began in Kinshasa’s Botanical Gardens on 10 April, kicking off four days of events. It moved on to Lagos, Nigeria, the following week, where up to 5,000 people attended events performed by more than 60 puppeteers.On Friday the streets of Dakar in Senegal will be filled with more than 40 puppet zebras, wildebeest, monkeys, giraffes and baboons as they run through Médina, one of the busiest neighbourhoods, where they will encounter a creation by Fabrice Monteiro, a Belgium-born artist who lives in Senegal, and is known for his large-scale sculptures. On Saturday the puppets will be part of an event in the fishing village of Ngor.The Herds’ 20,000km journey began in Kinshasa, the Democratic Republic of the Congo. Photograph: Berclaire/walk productionsThe first set of animal puppets was created by Ukwanda Puppetry and Designs Art Collective in Cape Town using recycled materials, but in each location local volunteers are taught how to make their own animals using prototypes provided by Ukwanda. The project has already attracted huge interest from people keen to get involved. In Dakar more than 300 artists applied for 80 roles as artists and puppet guides. About 2,000 people will be trained to make the puppets over the duration of the project.“The idea is that we’re migrating with an ever-evolving, growing group of animals,” Zuabi told the Guardian last year.Zuabi has spoken of The Herds as a continuation of Little Amal’s journey, which was inspired by refugees, who often cite climate disaster as a trigger for forced migration. The Herds will put the environmental emergency centre stage, and will encourage communities to launch their own events to discuss the significance of the project and get involved in climate activism.The puppets are created with recycled materials and local volunteers are taught how to make them in each location. Photograph: Ant Strack“The idea is to put in front of people that there is an emergency – not with scientific facts, but with emotions,” said The Herds’ Senegal producer, Sarah Desbois.She expects thousands of people to view the four events being staged over the weekend. “We don’t have a tradition of puppetry in Senegal. As soon as the project started, when people were shown pictures of the puppets, they were going crazy.”Little Amal, the puppet of a Syrian girl that has become a symbol of human rights, in Santiago, Chile on 3 January. Photograph: Anadolu/Getty ImagesGrowing as it moves, The Herds will make its way from Dakar to Morocco, then into Europe, including London and Paris, arriving in the Arctic Circle in early August.

Dead, sick pelicans turning up along Oregon coast

So far, no signs of bird flu but wildlife officials continue to test the birds.

Sick and dead pelicans are turning up on Oregon’s coast and state wildlife officials say they don’t yet know why. The Oregon Department of Fish and Wildlife says it has collected several dead brown pelican carcasses for testing. Lab results from two pelicans found in Newport have come back negative for highly pathogenic avian influenza, also known as bird flu, the agency said. Avian influenza was detected in Oregon last fall and earlier this year in both domestic animals and wildlife – but not brown pelicans. Additional test results are pending to determine if another disease or domoic acid toxicity caused by harmful algal blooms may be involved, officials said. In recent months, domoic acid toxicity has sickened or killed dozens of brown pelicans and numerous other wildlife in California. The sport harvest for razor clams is currently closed in Oregon – from Cascade Head to the California border – due to high levels of domoic acid detected last fall.Brown pelicans – easily recognized by their large size, massive bill and brownish plumage – breed in Southern California and migrate north along the Oregon coast in spring. Younger birds sometimes rest on the journey and may just be tired, not sick, officials said. If you find a sick, resting or dead pelican, leave it alone and keep dogs leashed and away from wildlife. State wildlife biologists along the coast are aware of the situation and the public doesn’t need to report sick, resting or dead pelicans. — Gosia Wozniacka covers environmental justice, climate change, the clean energy transition and other environmental issues. Reach her at gwozniacka@oregonian.com or 971-421-3154.Our journalism needs your support. Subscribe today to OregonLive.com.

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