Scientists find the genetic switch that makes pancreatic cancer resist chemotherapy

 Researchers at Duke-NUS Medical School have discovered a molecular "switch" that determines whether pancreatic cancer cells respond to chemotherapy or resist it. The finding points to a way to potentially shift some of the most treatment resistant tumors into a state where existing drugs can work more effectively.

The study, published in the Journal of Clinical Investigation, explains how this switch operates at a molecular level. The results suggest that pairing targeted therapies with standard chemotherapy may improve outcomes for patients whose tumors no longer respond to treatment.

Why Pancreatic Cancer Is So Difficult to Treat

Pancreatic cancer is one of the deadliest cancers worldwide. In Singapore, it ranks as the ninth most common cancer but the fourth leading cause of cancer related death. Because symptoms often appear late and current treatments have limited impact, most patients depend on chemotherapy, which typically provides only modest benefit.

Over the past decade, scientists have identified two main molecular subtypes of pancreatic cancer, classical and basal. Tumors in the classical subtype tend to be more organized at the cellular level, and patients with this form are more likely to respond to treatment. In contrast, basal subtype tumors are more disorganized and aggressive, and they are often resistant to chemotherapy.

Importantly, pancreatic cancer cells are not fixed in one subtype. They can shift between these states, moving from a more treatable form to a more resistant one. This flexibility is known as cancer cell plasticity.

The Role of GATA6 in Tumor Behavior

The research team focused on a gene called GATA6, which helps maintain pancreatic cancer cells in the more structured and less aggressive classical state. When GATA6 levels are high, tumors tend to grow in a more organized way and are more likely to respond to chemotherapy. When GATA6 levels fall, cells lose that structure, become more aggressive, and are harder to treat.

Professor David Virshup of Duke-NUS's Programme in Cancer & Stem Cell Biology, the study's lead author, said:

"We have known that pancreatic cancer cells can switch between these two states. What we didn't understand was the mechanism driving that switch. By identifying the pathway that suppresses GATA6, we now have a clearer picture of how tumors become resistant -- and potentially how to reverse that process."

KRAS and ERK Pathway Drive the Switch

The researchers traced the switch to a chain of signals inside pancreatic cancer cells. A gene called KRAS, which is mutated in nearly all pancreatic cancers, sends constant growth signals that drive tumor development. KRAS passes these signals through a partner protein known as ERK, which relays the instructions further inside the cell.

When the ERK pathway becomes highly active, it protects another protein that interferes with the production of GATA6. As GATA6 levels drop, cancer cells lose their organized structure, shift toward the more aggressive basal state, and become much less responsive to chemotherapy.

Using genetic screening, molecular analysis in cancer cells, and drug treatments, the team demonstrated that blocking the KRAS and ERK pathway lifts this suppression. When that happens, GATA6 levels rise again. The cancer cells then shift back toward the more organized state and regain sensitivity to chemotherapy.

Combination Therapy Shows Stronger Effects

The study also found that higher levels of GATA6 on their own made pancreatic cancer cells more responsive to treatment. When drugs that inhibit the KRAS and ERK pathway were combined with standard chemotherapy, the anti cancer effects were stronger than with either approach alone. However, this enhanced benefit occurred only when GATA6 was present, highlighting its central role in determining which patients might benefit most from combination therapy.

These findings help clarify why patients with higher GATA6 levels often respond better to certain chemotherapy regimens. They also provide a scientific foundation for ongoing clinical trials that are testing new treatments aimed at KRAS and related pathways.

Professor Lok Sheemei, Duke-NUS' Interim Vice-Dean for Research, said:

"Pancreatic cancer remains one of the toughest cancers to treat. These findings provide a mechanistic explanation for why tumors respond poorly to chemotherapy and offers a rational strategy for combining targeted therapies with existing drugs."

Broader Implications for Other KRAS Driven Cancers

The implications may extend beyond pancreatic cancer. Many other cancers fueled by KRAS mutations show similar shifts in cell behavior and treatment response. Understanding how cancer cells transition between different states could help researchers address therapy resistance in additional cancer types.

Professor Patrick Tan, Dean and Provost's Chair in Cancer and Stem Cell Biology at Duke-NUS, commented:

"This work demonstrates how basic science can uncover actionable insights into treatment resistance. Understanding how cancer cells switch states gives us a more strategic way to design combination treatments."

Duke-NUS Medical School is internationally recognized for its leadership in medical education and biomedical research, combining fundamental discoveries with translational expertise to improve health outcomes in Singapore and beyond.

Source: ScienceDaily

Scientists discover sleep switch that builds muscle, burns fat, and boosts brainpower

 Deep sleep does more than help you feel rested. It actively rebuilds your body, strengthening muscles, supporting bone growth, and helping burn fat. For teenagers, it is also essential for reaching full height potential.

At the center of all this is growth hormone, which surges during sleep. But scientists have long puzzled over why poor sleep, especially the early deep stage known as non-REM sleep, leads to lower levels of this critical hormone.

Scientists Discover the Brain Circuit Behind It

Researchers at the University of California, Berkeley, have now uncovered the answer. In a study published in Cell, they mapped the brain circuits that control growth hormone release during sleep and identified a new feedback system that keeps those levels in balance.

This discovery offers a clearer understanding of how sleep and hormones work together. It may also open the door to new treatments for sleep disorders linked to metabolic diseases like diabetes, as well as neurological conditions such as Parkinson's and Alzheimer's.

"People know that growth hormone release is tightly related to sleep, but only through drawing blood and checking growth hormone levels during sleep," said study first author Xinlu Ding, a postdoctoral fellow in UC Berkeley's Department of Neuroscience and the Helen Wills Neuroscience Institute. "We're actually directly recording neural activity in mice to see what's going on. We are providing a basic circuit to work on in the future to develop different treatments."

Lack of sleep does more than leave you tired. Because growth hormone helps control how the body processes sugar and fat, poor sleep can increase the risk of obesity, diabetes, and heart disease.

The Brain Regions Driving Growth Hormone

The system behind this process is buried deep in the hypothalamus, an ancient part of the brain shared by all mammals. Here, specialized neurons release signals that either trigger or suppress growth hormone.

Two key players are growth hormone releasing hormone (GHRH), which stimulates release, and somatostatin, which inhibits it. Together, they coordinate hormone activity across the sleep-wake cycle.

Once growth hormone enters the system, it activates the locus coeruleus, a brainstem region that controls alertness, attention, and cognitive function. Disruptions in this area are linked to a wide range of neurological and psychiatric disorders.

"Understanding the neural circuit for growth hormone release could eventually point toward new hormonal therapies to improve sleep quality or restore normal growth hormone balance," said Daniel Silverman, a UC Berkeley postdoctoral fellow and study co-author. "There are some experimental gene therapies where you target a specific cell type. This circuit could be a novel handle to try to dial back the excitability of the locus coeruleus, which hasn't been talked about before."

How Sleep Stages Control Hormone Release

To study this system, researchers recorded brain activity in mice by inserting electrodes and stimulating neurons with light. Because mice sleep in short bursts throughout the day and night, they provided a detailed view of how growth hormone changes across sleep stages.

The team found that GHRH and somatostatin behave differently depending on whether the brain is in REM or non-REM sleep.

During REM sleep, both hormones increase, leading to a surge in growth hormone. During non-REM sleep, somatostatin drops while GHRH rises more modestly, still boosting hormone levels but in a different pattern.

A Surprising Feedback Loop in the Brain

The researchers also uncovered a feedback loop that links growth hormone to wakefulness. As sleep continues, growth hormone gradually builds up and stimulates the locus coeruleus, nudging the brain toward waking.

But there is a twist. When this brain region becomes too active, it can actually trigger sleepiness instead, creating a delicate balance between sleep and alertness.

"This suggests that sleep and growth hormone form a tightly balanced system: Too little sleep reduces growth hormone release, and too much growth hormone can in turn push the brain toward wakefulness," Silverman said. "Sleep drives growth hormone release, and growth hormone feeds back to regulate wakefulness, and this balance is essential for growth, repair and metabolic health."

Why It Matters for Brain and Body

This balance does more than affect physical growth. Because growth hormone works through brain systems that control alertness, it may also influence how clearly you think and how focused you feel.

"Growth hormone not only helps you build your muscle and bones and reduce your fat tissue, but may also have cognitive benefits, promoting your overall arousal level when you wake up," Ding said.

Funding and Research Team

The research was supported by the Howard Hughes Medical Institute (HHMI) and the Pivotal Life Sciences Chancellor's Chair fund. Yang Dan holds the Pivotal Life Sciences Chancellor's Chair in Neuroscience. The study also included collaborators from UC Berkeley and Stanford University.

Source: ScienceDaily

One fat helped pancreatic cancer grow while another cut disease in half

 For years, the common assumption has been simple: eating less fat may help lower cancer risk. New research suggests the picture is much more complicated.

Scientists report that when it comes to pancreatic cancer, the specific type of fat in the diet may be more important than the total amount consumed.

The findings, published in Cancer Discovery, a journal of the American Association for Cancer Research, indicate that different fats can have dramatically different effects on cancer development.

"It's really the type of fat that you're consuming, not just total fat content," says Christian Felipe Ruiz, PhD, an associate research scientist in Yale School of Medicine's Department of Genetics and lead author of the study. "Depending on the type of fat that you consume, it can go completely different ways. We found that some fats promote cancer, as we would expect, while other fats are really good at suppressing cancer."

Oleic Acid Linked to Faster Tumor Growth

One of the study's most unexpected findings involved oleic acid, the primary fatty acid found in olive oil.

Researchers found evidence that oleic acid may encourage tumor growth in pancreatic cancer, a result that surprised the team because of the fatty acid's long-standing reputation as a heart-healthy dietary fat.

"It's traditionally been considered a healthy type of fat for cardiovascular health," Ruiz says.

The cancer examined in the study was pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer and one of the deadliest cancers overall. Only about 13% of people diagnosed with PDAC survive for five years.

"More than 65,000 people are expected to be diagnosed with PDAC in the U.S. this year, with over 50,000 deaths," Ruiz notes. "At the moment, effective treatment options are limited, especially for advanced disease. Therefore, prevention strategies are sorely needed to move the needle on PDAC mortality."

Although previous research has linked high-fat diets to a greater risk of PDAC, scientists have struggled to identify exactly how dietary fat influences the disease. The new study, led by senior author Mandar Deepak Muzumdar, MD, associate professor of genetics and of internal medicine at YSM, sought to answer that question.

Muzumdar is also a member of Yale Cancer Center and the Yale Cancer Biology Institute at West Campus.

Comparing Different Types of Dietary Fat

To isolate the effects of specific fats, the researchers created 12 different high-fat diets. Each diet contained the same number of calories, with the only difference being the source of fat. The diets were designed to reflect common patterns of fat consumption in the modern American diet.

According to Ruiz, many earlier studies relied on a simpler approach.

For decades, researchers commonly "gave mice very high levels of fat in their diet, often using a single fat source." In many cases, those diets derived 60% of calories from lard, which does not accurately reflect typical human eating habits and makes it difficult to determine the effects of individual fatty acids.

"Exactly what components of dietary fat cause cancer has remained a mystery," Ruiz adds.

The results were striking. Mice carrying a genetic mutation that produces a disease closely resembling human PDAC developed tumors more rapidly when fed diets rich in oleic acid. Oleic acid is a monounsaturated fatty acid (MUFA) found in foods such as olive oil, high-oleic safflower oil, high-oleic sunflower oil, peanuts, and lard.

In contrast, diets rich in polyunsaturated fatty acids (PUFAs) slowed cancer development. The strongest protective effects were seen with omega-3 fatty acids, including those found in fish oil.

"When we fed mice diets enriched with fish oil, we saw a 50% reduction in disease compared with mice fed a standard fat diet."

How Dietary Fats Affect Cancer Cell Survival

The findings led researchers to investigate ferroptosis, a form of programmed cell death caused by lipid oxidation.

When fatty acids become part of pancreatic cell membranes, their chemical characteristics influence how easily those cells can be damaged by oxidation. PUFAs are more prone to oxidation, making cancer cells more vulnerable to ferroptosis and death. MUFAs are more resistant to oxidation, helping protect cancer cells from this process.

"Monounsaturated fats really protect the cancer cells from lipid oxidation," Ruiz explains. "Because oxidation is reduced, they're less likely to undergo ferroptosis."

The researchers observed a direct relationship between fat composition and disease severity.

"When we increased the ratio of MUFAs to PUFAs in the diet, disease burden increased. Conversely, when we decreased the ratio, disease burden was reduced."

Source: ScienceDaily

Scientists finally crack an “undruggable” pancreatic cancer target and nearly double survival

 For a long time, the likelihood of surviving pancreatic cancer has been extremely low. For patients who were diagnosed with metastatic pancreatic cancer between 2015 and 2021, about 97% died within five years of their diagnosis.

Pancreatic cancer is so deadly in part because there are no effective screening tests, and it rarely causes noticeable symptoms in its earliest stages. By the time a patient experiences signs, such as jaundice – a yellowing of the skin – or abdominal pain, the cancer has often already spread to other organs.

As a gastrointestinal oncologist and researcher specializing in early-phase clinical trials, I have seen the critical need for more effective therapies for patients with pancreatic cancer. For decades, successfully targeting the central mechanism that causes the vast majority of pancreatic cancers was considered impossible.

However, that narrative is rapidly changing with a new drug that can shut down the key protein that drives pancreatic cancer, nearly doubling survival rates for patients with advanced stages of the disease.

‘Undruggable’ tumors

The standard treatment for advanced pancreatic cancer has historically relied on chemotherapy, potent drugs designed to kill rapidly dividing cells. While chemotherapy can slow the progression of the disease, its effectiveness is often limited by the ability of pancreatic cancer cells to develop resistance against these drugs.

Pancreatic cancer’s success lies in its genetics. More than 90% of pancreatic tumors are driven by mutations in a gene called KRAS. This gene codes for proteins that function as switches that turn cell growth on and off. When the KRAS gene is mutated, the switch becomes permanently stuck in the “on” position, commanding cancer cells to multiply endlessly.

For decades, scientists considered KRAS to be “undruggable.” The surface of the protein is exceptionally smooth, lacking the molecular pockets that standard drugs require to bind to and turn the switch off.

Because existing drugs haven’t been able to target this protein, treatment for pancreatic cancer has primarily relied on toxic drugs that act more like blunt instruments than precise tools. Chemotherapy attempts to control the disease through widespread cell destruction, causing significant collateral damage to healthy tissues that lead to side effects.

What is daraxonrasib?

A new drug called daraxonrasib offers a critical advance in treating metastatic pancreatic cancer.

Daraxonrasib is taken daily by mouth. Instead of binding to KRAS directly, it attaches to a molecule called cyclophilin A in cells that helps fold proteins into their final 3D structures. This protein complex is then able to bind to the active KRAS protein and shut down its ability to signal cancer cells to multiply.

The company developing the drug, Revolution Medicines, presented results on May 31, 2026, from its Phase 3 clinical trial of 500 patients with metastatic pancreatic cancer who had received prior treatment. Compared to standard chemotherapy, daraxonrasib nearly doubled overall survival from 6.7 months to 13.2 months after diagnosis. Overall, daraxonrasib reduced the risk of death for metastatic pancreatic cancer patients by 60%.

The most common side effect is a prominent skin rash, which affected more than 86% of patients in the study. Patients also frequently dealt with stomatitis – painful swelling and sores inside the mouth – as well as diarrhea, nausea and vomiting. However, patients taking daraxonrasib were far less likely to stop treatment due to severe side effects compared to chemotherapy, and they had improved quality of life with reduced pain.

Next steps for daraxonrasib

By successfully targeting the specific genetic mutation that drives the vast majority of pancreatic cancers, researchers have demonstrated that this “undruggable” disease is treatable with targeted therapy.

Source: ScienceDaily

Scientists discover the deep sleep circuit that builds muscle, burns fat, and boosts the brain

 A good night's sleep does far more than leave you feeling refreshed. It also triggers the release of growth hormone, a key hormone that helps build muscle and bone, burn fat, and support healthy growth. That's why athletes value quality sleep for recovery, and why teenagers need enough sleep to reach their full height potential.

Scientists have long known that growth hormone levels rise during sleep, especially during the deep, non-REM stage. What has remained unclear is exactly how the brain controls this process.

Now, researchers at the University of California, Berkeley have uncovered the brain circuitry responsible for regulating growth hormone during sleep. Their study, published in the journal Cell, also reveals a previously unknown feedback system that helps keep growth hormone levels in balance.

The discovery offers new insight into the close relationship between sleep and hormone regulation. It could eventually guide new treatments for sleep disorders linked to metabolic diseases such as diabetes, as well as neurodegenerative conditions including Parkinson's and Alzheimer's disease.

"People know that growth hormone release is tightly related to sleep, but only through drawing blood and checking growth hormone levels during sleep," said study first author Xinlu Ding, a postdoctoral fellow in UC Berkeley's Department of Neuroscience and the Helen Wills Neuroscience Institute. "We're actually directly recording neural activity in mice to see what's going on. We are providing a basic circuit to work on in the future to develop different treatments."

Because growth hormone also helps regulate glucose and fat metabolism, consistently poor sleep may increase the risk of obesity, diabetes, and cardiovascular disease.

How the Brain Controls Growth Hormone During Sleep

The nerve cells that coordinate growth hormone release are located deep within the hypothalamus, an ancient brain region found across mammals. These include growth hormone-releasing hormone (GHRH) neurons, along with two different types of somatostatin neurons.

Once growth hormone is released, it activates neurons in the locus coeruleus, a brainstem region involved in alertness, attention, thinking, and responding to new experiences. Problems affecting the locus coeruleus have been linked to numerous neurological and psychiatric disorders.

"Understanding the neural circuit for growth hormone release could eventually point toward new hormonal therapies to improve sleep quality or restore normal growth hormone balance," said Daniel Silverman, a UC Berkeley postdoctoral fellow and study co-author. "There are some experimental gene therapies where you target a specific cell type. This circuit could be a novel handle to try to dial back the excitability of the locus coeruleus, which hasn't been talked about before."

Mapping the Sleep Growth Hormone Circuit

Working in the laboratory of Yang Dan, professor of neuroscience and molecular and cell biology at UC Berkeley, the research team studied the brain circuits in mice by placing electrodes in their brains and stimulating hypothalamic neurons with light while recording neural activity.

Mice naturally sleep in short bursts lasting only a few minutes throughout the day and night. That pattern allowed researchers to repeatedly observe changes in growth hormone activity across many sleep and wake cycles.

Using advanced circuit tracing techniques, the team discovered that the two peptide hormones responsible for regulating growth hormone release behave differently depending on the stage of sleep. GHRH promotes growth hormone release, while somatostatin suppresses it.

During REM sleep, both GHRH and somatostatin increase, leading to greater growth hormone release. During non-REM sleep, however, somatostatin levels fall while GHRH rises only moderately, creating a different pattern of hormone regulation.

A Feedback Loop That Balances Sleep and Wakefulness

The researchers also identified a previously unknown feedback mechanism involving the locus coeruleus.

As growth hormone gradually builds up during sleep, it stimulates the locus coeruleus and encourages wakefulness. But if activity in the locus coeruleus becomes too high, it unexpectedly begins promoting sleepiness instead, a finding Silverman reported earlier this year.

"This suggests that sleep and growth hormone form a tightly balanced system: Too little sleep reduces growth hormone release, and too much growth hormone can in turn push the brain toward wakefulness," Silverman said. "Sleep drives growth hormone release, and growth hormone feeds back to regulate wakefulness, and this balance is essential for growth, repair and metabolic health."

Because growth hormone influences the locus coeruleus, which plays a central role in maintaining alertness during the day, this newly identified system may also affect attention and other aspects of cognitive function.

Source: ScienceDaily

Giant Greenland iceberg slams into Joe Island and survives

 Summer is the busiest time of year for iceberg activity in Greenland's glacier-fed fjords, and 2026 delivered a particularly dramatic example. In August, a huge iceberg broke away from Petermann Glacier on Greenland's northwest coast. About the size of St. Thomas in the U.S. Virgin Islands, it marked the largest calving event from any Arctic glacier since 2020.

Iceberg calving is a normal part of the life cycle of outlet glaciers, but scientists monitor these events closely for clues about longer-term signs of instability. Petermann is one of Greenland's largest marine-terminating glaciers and helps control the flow of ice from the Greenland Ice Sheet into the ocean. Because of that role, changes in its stability could have implications for sea level rise.

A Giant Ice Island Breaks From Petermann Glacier

The summer 2026 calving was first identified on August 4 by Adam Garbo, a doctoral student in glaciology at the University of Ottawa, using imagery from the European Space Agency's Sentinel-1 mission. Garbo and an international group of researchers have been relying on remote sensing to monitor Petermann Glacier and follow changes in its floating ice tongue.

According to the team, the large flat-topped iceberg, known as an "ice island," measured just over 76 square kilometers (29 square miles) when it separated from the glacier. That made it the largest iceberg to break from Petermann since the 2012 event, which produced an ice island covering 130 square kilometers. Earlier major calving events occurred in 2008 (31 square kilometers) and 2010 (just over 250 square kilometers).

Scientists had actually been preparing for an even larger break. Garbo and his colleagues were watching one of several major rifts that appeared likely to eventually cut across the entire ice tongue. Instead, the glacier fractured along a different crack.

"What surprised us was that the calving instead followed a different fracture, producing a smaller ice island than we had originally anticipated," Garbo said.

As of late August, two large rifts were still present. Researchers expect them to eventually release new ice islands measuring roughly 94 square kilometers and 84 square kilometers, although no one knows exactly when those breaks will occur.

The Iceberg Heads Toward Nares Strait

Glaciologist Mauri Pelto of Nichols College has also been tracking the iceberg using imagery from NASA-USGS Landsat satellites. After separating from the glacier, the berg moved down Petermann Fjord toward Nares Strait at an average speed of about 3 kilometers per day during its first week.

It eventually approached the point where the fjord meets Nares Strait and collided with a small rocky outcrop called Joe Island (Joe Ø). The encounter was captured by the OLI (Operational Land Imager) aboard Landsat 9 on August 23 and August 24. A closer look at the August 24 scene is shown at the top of this article.

Joe Island sits near the entrance to Petermann Fjord, putting it directly in the path of many ice islands leaving the glacier. Such collisions can trigger the beginning of an iceberg's breakup. One notable example occurred when a 2010 ice island struck Joe Island and split into two pieces.

Pelto noted that icebergs from Petermann are generally thinner and more fragile than those produced by Greenland glaciers such as Jakobshavn and Helheim. They are also much thinner than the enormous icebergs that break away from Antarctica.

A Collision That Failed to Break It Apart

Despite that fragility, the new Petermann ice island remained intact after striking Joe Island.

"We were certainly watching closely as it interacted with Joe Island and were impressed that it survived the interaction without further fragmentation," Garbo said.

At the time it broke away, the ice island was estimated to be less than 150 meters thick. Winds and surface currents later carried it out of Petermann Fjord, while satellite observations showed it pivoting away from Joe Island and moving southwest through Nares Strait.

Its journey will gradually become more destructive. Tides, winds, ocean currents, and melting will continue weakening the iceberg until it eventually fractures into smaller pieces.

Where Greenland's Ice Islands Can Go Next

Some thicker icebergs that break from tidewater glaciers without floating ice shelf extensions can scrape along the seabed or become grounded inside a fjord. Ice islands from Petermann may instead travel farther before running aground. Many have eventually become "grounded" near the coasts of Coburg and Baffin islands.

Garbo and his colleagues noted that Petermann ice islands and the fragments they produce can travel long distances through Arctic waters. Along the way, they can create hazards for ships, marine operations, and infrastructure.

At the same time, they play another role in the ocean. As the ice slowly melts, it releases freshwater into surrounding waters, carrying the influence of Greenland's glaciers far beyond the fjord where the iceberg first broke free.

Source: ScienceDaily

Antarctica gained a record 695 billion tons of ice. Scientists found the surprising reason

 A persistent patch of unusually warm tropical ocean helped intensify snowfall over East Antarctica, contributing to a temporary net ice sheet mass gain of about 695 billion tons, according to a new study published in Nature on August 19.

Researchers found that sustained warming in the tropical warm pool during 2021-23 set off a chain of atmospheric changes that ultimately affected weather thousands of miles away in Antarctica. The warming generated a Rossby wave train that traveled toward the continent, helped establish a north-south circulation pattern over East Antarctica, altered the movement of moisture, and increased regional snowfall. Together, these changes temporarily slowed the Antarctic Ice Sheet's overall loss of mass.

A Remarkable Antarctic Ice Gain

The Antarctic Ice Sheet is a major source of uncertainty when scientists estimate how much global sea levels could rise in the future. During the past two decades, Antarctica has lost ice at an average rate of approximately 140.5 billion tons per year.

Yet between 2021-23, that pattern briefly shifted. The ice sheet gained about 695 billion tons of mass, making it the largest Antarctic mass gain observed by the GRACE satellite missions.

To understand what caused the unusual increase, researchers led by the Institute of Oceanology of the Chinese Academy of Sciences (IOCAS) brought together several types of evidence. They analyzed gravity satellite measurements, snow accumulation records preserved in ice cores, and simulations of atmospheric circulation. Their goal was to determine where the extra moisture came from and how weather patterns delivered it to East Antarctica.

A Climate Signal From the Tropics

The team identified sustained warming in the tropical warm pool during 2021-23. This region lies where the tropical western Pacific meets the eastern Indian Ocean and contains some of the planet's warmest ocean waters.

That warming triggered what scientists call a Rossby wave train, a large-scale pattern of atmospheric waves capable of transmitting changes in weather and circulation across enormous distances. The disturbance traveled toward the high southern latitudes and helped reorganize atmospheric conditions around Antarctica.

Eddy mean flow feedbacks strengthened and prolonged the resulting circulation pattern. This produced a north-south dipole, with unusual low pressure south of Australia and unusual high pressure along the East Antarctic coast.

The resulting pressure pattern changed the routes taken by moisture moving through the atmosphere. In particular, it strengthened the transport of water vapor from the midlatitude Indian Ocean toward East Antarctica through atmospheric rivers.

Atmospheric Rivers Fueled Heavy Snowfall

Atmospheric rivers are relatively narrow corridors in the atmosphere that can carry enormous amounts of water vapor over long distances. When they reach cold regions such as Antarctica, that moisture can fall as heavy snow.

Water vapor tracking simulations showed that the dipole circulation directed moist air from the midlatitude Indian Ocean toward East Antarctica and allowed more atmospheric rivers to reach the continent. This produced sustained heavy snowfall across the Queen Mary Land-Wilkes Land region, adding substantial mass to the ice sheet.

Atmospheric circulation model experiments provided further evidence that warming of the tropical warm pool directly drove both the circulation changes and the increase in snowfall.

The researchers also examined how much of the snowfall increase could be attributed to anthropogenic forcing. They found that this contribution was equivalent to only 9% of the observed snowfall anomaly. That result suggests that the general increase in atmospheric moisture associated with global warming was not the main explanation for this particular event.

A Remote Antarctic "Regulator"

Additional observations and simulations indicate that comparable periods of sustained warming in the tropical warm pool occur approximately once every decade.

The researchers therefore describe the tropical warm pool as a remote "regulator" that can influence snowfall and ice mass in East Antarctica over periods lasting several years. Changes in tropical ocean temperatures can alter atmospheric circulation in ways that ultimately affect how much snow falls on the distant Antarctic continent.

The findings reveal a long-distance climate connection in which conditions in the tropics can have major consequences for Antarctica.

Antarctica Is Still Losing Ice Over the Long Term

Despite the striking 695 billion-ton increase, the researchers emphasize that the event was temporary and does not reverse the long-term decline of the Antarctic Ice Sheet.

Source: ScienceDaily