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CHICAGO—At the world’s largest oncology conference, Ozempic, a diabetes drug, found its way to the center of the conversation. As thousands of attendees bounced between presentations at the American Society of Clinical Oncology (ASCO) meeting, some of the biggest buzz focused on the connection between taking Ozempic and similar glucagonlike peptide 1 (GLP-1) receptor agonists and having a decreased risk of several types of cancer.

GLP-1 drugs, originally designed to treat type 2 diabetes, have become blockbuster treatments for weight loss and metabolic conditions such as heart, liver, and kidney disease. Now researchers are investigating whether certain cancers, such as breast cancer, could be added to that list. At the conference, scientists announced their findings that people taking GLP-1 drugs were less likely to be diagnosed with certain cancers, have them spread, or die from them when compared with nonusers and those on other diabetes medications. Even though the findings are largely based on observational studies, they reinforce animal research that shows GLP-1 drugs do more than just shed pounds and improve metabolic health. The drugs may also dial down the inflammation that can drive cancer development—and might even act directly on tumors.

Obesity has long been identified as a risk factor for at least 13 types of cancer. Excess weight promotes chronic inflammation, raises insulin levels in the blood, and increases estrogen circulating in the body—all potential drivers of cancer development. Whether GLP-1 treatments reduce cancer risk by reversing these pathways through weight loss, or through some other mechanism entirely, remains an open question. Several lines of research presented at ASCO offer evidence of the drugs’ protective effect against cancer, including several not typically associated with weight, such as leukemia and lung cancer, says Elizabeth McDonald, radiologist at the Hospital of the University of Pennsylvania.

McDonald’s team at the University of Pennsylvania found GLP-1 drugs were linked to a 30 percent lower likelihood of a breast cancer diagnosis in more than 111,000 women who underwent breast imaging. Another large analysis from the Virginia Commonwealth University (VCU) Massey Comprehensive Cancer Center, published in JAMA Network Open before the conference, followed breast cancer patients for up to 10 years and found that those who took GLP-1s had a lower risk of death from any cause—and a reduced risk of cancer recurrence—compared with patients who did not take them. And in another investigation, co-led by researchers at Massey, found that GLP-1 drugs were associated with improved survival among people with colorectal cancer as well. A Cleveland Clinic study tracking people across seven cancer types found that those taking the drugs were significantly less likely to progress to stage four disease in lung, breast, colorectal, and liver cancers—with a 43 percent risk reduction seen in breast cancer and a 50 percent reduction in lung cancer.

These studies collectively provide an “interesting signal,” says Jasmine Sukumar, a breast medical oncologist at the University of Texas MD Anderson Cancer Center, who also presented research on GLP-1s’ protective effect against breast cancer. The data are still observational, which means the research teams cannot prove cause and effect, she adds. Still, Sukumar and other scientists are trying to understand what might be driving these findings.

The most straightforward explanation is the weight loss that the drugs can cause. Reducing weight also reduces the pathways by which obesity fuels cancer, explains Bernard Fuemmeler, associate director of population science at the VCU Massey Comprehensive Cancer Center and a co-author of the breast cancer study and the colorectal cancer study presented at ASCO. The drugs may also reduce deaths through their effect on cardiovascular disease, he says. Additionally, fat tissue is a source of estrogen, so shrinking fat tissue reduces the hormones that promote certain types of breast cancer tumors.

But some of the new research suggests a mechanism that goes beyond weight loss. GLP-1 drugs could be working on inflammation, which is a key driver linked to tumor development. Chronic inflammation can create conditions that help cancers take root and spread. Because GLP-1 receptors are found throughout the body, not just in the gut and pancreas, activating them appears to dampen inflammation through multiple pathways—such as by acting on immune cells and endothelial cells, and other vascular cells or by influencing body-wide inflammatory cascades that affect multiple organs.

GLP-1 drugs might also act on tumors directly. In animal studies, tirzepatide—the dual-receptor drug sold as Zepbound—appears to have target tumors in breast cancer and endometrial cancer, possibly by reversing the inflammatory effects of obesity and inhibiting tumor growth.

Certain cancers might be more responsive to GLP-1 treatment. For instance, the Cleveland Clinic researchers found that, across seven tumor types, people who had tumors packed with GLP-1 receptors were 33 percent less likely to die during the follow-up period; people with breast cancer tumors had the greatest improvements in survival. High amounts of such receptors in breast cancer tumors might explain the higher survival rate, but it’s not fully understood, says Mark Orland of the Cleveland Clinic Taussig Cancer Institute, who led the analysis.

“Each of these cancers has to be looked at fairly individually and very specifically, stage by stage and mutation by mutation,” Orland says.

He and his Cleveland Clinic colleague Jaroslaw Maciejewski, a co-author of the research, speculate that the drugs might also be working through something more systemic. Early-stage cancers can only progress in the right environment, one often shaped by aging-related chronic inflammation. “Such an effect would not necessarily be tumor-specific,” Maciejewski says. One possibility is that GLP-1 drugs might be narrowing the gap between chronological age and biological age, the apparent age of various tissues. This could mean GLP-1 drugs may affect biological aging more broadly, the researchers suggest.

Orland says that the field is still far from calling GLP-1 drugs the next big deal for cancer treatment. “It would be a little bit aggressive to say it’s going to cure my cancer or stop my cancer,” he says.

While there isn’t strong evidence to suggest that the drugs worsen cancer in humans, the Food and Drug Administration has warned against their use among people with a family history of certain thyroid cancers, with the agency citing rodent studies. Cancer patients and survivors would also need to carefully monitor their loss of muscle mass, a common side effect of the drugs, during any potential GLP-1-based cancer therapy, Fuemmeler says. For now, clinicians are holding off on prescribing GLP-1 drugs to prevent or treat cancer until there is more research, particularly human clinical trials, which some researchers are already beginning to design. “We don’t know for sure if these [initial] results will hold up in a randomized clinical trial,” Fuemmeler says. “All of these mechanisms are really ripe for future investigation.”

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Alvaro Medina Jurado

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Key Takeaways

• Research shows that college graduates could be haunted by a weak job market in the form of reduced earnings and employment opportunities.
• Unemployment for 22‑ to 27‑year‑old college grads is around 5.6 percent, noticeably higher than in recent years and unusually elevated relative to the broader workforce.
• More than 40% of employed recent graduates are working in jobs that do not require a college degree, the highest share since 2020.

Today’s class of college graduates is entering one of the weakest labor markets in years, and research suggests that those early setbacks could echo through their earnings and careers for at least a decade. 

According to a recent report from The New York Times, recent college graduates are stepping into the most challenging job market since the depths of the pandemic. An analysis from the Federal Reserve Bank of New York shows that unemployment among 22- to 27-year-old college graduates has increased over the past three years, reaching 5.6% in the first quarter of the year. 

That’s above the 4.2% overall jobless rate. College graduates usually enjoy lower unemployment than the broader workforce, so the current gap is a sign that entry-level hiring has weakened disproportionately. 

At the same time, underemployment has surged. More than 40% of employed recent graduates are in roles that do not typically require a college degree, the highest level since 2020, per the Federal Reserve Bank of New York. 

“The overall labor market is not in a recession right now,” Larry Katz, a labor economist at Harvard, told the Times. “But it’s clearly feeling like a recession for young college graduates entering the labor market.”

Economists told the Times that the tough job market means graduates are likely to earn less and face more challenges in advancing their careers. Research has repeatedly found that the year a worker leaves college, and the state of the economy at that moment, can shape how much they earn in the long term.

One study examined the effects of a weak job market on wages 

One influential study by Lisa Kahn, an economist at the University of Rochester, examined what happened to students who graduated around the deep recession of the early 1980s, following them for many years before, during and after that downturn. 

She compared them to cohorts who were otherwise similar, but who entered the labor market under very different macroeconomic conditions, when the economy was a little better. 

Khan’s core finding was that graduating from college when unemployment is high and jobs are scarce has a clear, measurable and long-lasting negative impact on wages. 

New graduates who started their careers in that weak labor market accepted lower‑paying jobs than they likely would have in better times, and those smaller paychecks did not simply snap back when the economy recovered. Instead, their earnings grew from a lower base, so even as conditions improved, the initial penalty continued to linger.

Fifteen years after graduation, workers who entered the job market during the downturn were still earning less, on average, than similar peers who began their careers in healthier job markets. 

Now Kahn warns that the current group of college graduates could be haunted by a weak job market in the form of reduced earnings and employment opportunities. 

“There are going to be lasting effects,” Kahn told the Times. “The cohorts that were lucky enough to just finish a little bit earlier or a little bit later I think are going to be doing better.”

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Young graduates are entering the toughest hiring climate since the pandemic

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When Jeffrey Epstein wanted his favorite Zweigle’s Pop Open hot dogs ferried from his townhouse on the Upper East Side of Manhattan to his sprawling Zorro Ranch in New Mexico, he did what any exceedingly rich person might.

He had his staff reach out to a close friend with a private jet. Stephen Hanson, then head of a Manhattan restaurant empire that at its peak served more than 20,000 people a day at 25 theatrical, high-volume restaurants like Blue Water Grill, Dos Caminos, and Ruby Foo’s, was happy to make the delivery himself.

“In the white freezer in downstairs kitchen of 71st street, there are packages of frozen hot dogs,” Mr. Epstein’s private chef emailed an assistant. “JE would like to have hot dogs for lunch tmrw and these are the new dogs he likes.”

There was one other favor Mr. Epstein wanted on that August weekend in 2012. He asked Mr. Hanson to make room for a woman who would be bringing a wallet he’d left behind, according to documents the Department of Justice collected as it investigated Mr. Epstein. She was later paid settlements from funds established for Mr. Epstein’s victims.

The Justice Department files attest to Mr. Epstein’s transactional relationships with many powerful men. Billionaires like the Victoria’s Secret magnate Les Wexner and the private equity investor Leon Black helped build his fortune. Boldfaced names like Woody Allen and Andrew Mountbatten-Windsor, the former British prince, provided cachet and social access.

What Mr. Hanson offered, a review of the thousands of emails and texts the two men exchanged over a decade, shows was access to the world of food and hospitality — as well as a wingman who enjoyed the company of attractive women, and had the means to help manage and entertain them.

Mr. Hanson got the young women tables in his dining rooms. He arranged cooking classes for them. When Mr. Epstein asked him to help women land visas or find jobs in his restaurants, the answer was almost always yes.

During their long friendship, Mr. Hanson became one of the most powerful people in the restaurant business. In 2003, Bon Appétit magazine named him restaurateur of the year, and he expanded his reach to Las Vegas. By 2007, his company, BR Guest Hospitality, was valued at $300 million.

Mr. Hanson still found time, the files show, to aid his friend in all kinds of ways. He recruited people to manage Mr. Epstein’s private Caribbean island compound and set up tastings to help him hire the perfect private chef. No errand was too small. When the beef jerky that fueled one of Mr. Epstein’s odd dietary binges didn’t taste quite right, Mr. Hanson worked on the recipe. He even had his executive assistant send a sample to a laboratory to test its nutritional value.

Nothing in the files or other public records indicates that Mr. Hanson had sex with minors, as Mr. Epstein did. In a video interview in 2021, a victim of Mr. Epstein’s told the F.B.I. that a decade earlier, when she was in her early 20s, Mr. Epstein had sent the restaurateur to her New York City apartment, where Mr. Hanson paid her for oral sex at least a dozen times.

The woman, who first met Mr. Epstein when she was 17, said she had become dependent on Mr. Epstein and did whatever he requested. Her name was redacted in the files, and her lawyer, Gloria Allred, declined to comment. A Justice Department spokeswoman would not say whether the agency had investigated further, but Mr. Hanson has never been charged with a crime.

In response to questions for this article, Mr. Hanson did not address the woman’s allegations, but issued a brief statement through his lawyer, Gerald B. Lefcourt, a former attorney for Mr. Epstein. “Mr. Epstein knew and relied upon Mr. Hanson for advice on certain matters given Mr. Hanson’s hospitality industry experience,” it read in part. “Mr. Epstein was adept at deception and manipulation. He pulled the wool over the eyes of leading academics, scientists, and titans of business. The suggestion, assumption, or insinuation that there was anything untoward about, in relation to, or concerning, any connection between Mr. Hanson and Mr. Epstein is untrue.”

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The bond between Stephen Hanson, left, and Jeffrey Epstein stretched over decades, a review of Department of Justice files shows. It included vacations like this 2013 trip to Las Vegas. Credit…U.S. Department of Justice

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“When a clown moves into a palace, he doesn’t become a king, the palace instead becomes a circus. — Turkish proverb,”

 

Hmmmmm…History is repeating itself yet again!

 

Isaiah 59:14

New Living Translation

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You might find these videos enlightening!

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A. R. Bernard: one of many

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The first case of the New World screwworm in a U.S. cow in about 60 years has been detected, the U.S. Department of Agriculture confirmed yesterday. It is the first instance of the agricultural pest in cattle since it was eliminated in the U.S. in 1966.

Screwworms are parasitic flies that lays their eggs in open wounds or cuts or in the eyes, ears, mouth, nose, or genitals of warm-blooded animals—including humans. The maggots hatch and burrow through the skin, causing painful, foul-smelling wounds.

Livestock in the southern U.S. and Mexico suffered devastating screwworm outbreaks in the first half of the 20th century. But the parasite was eliminated in those nations thanks to a wildly successful effort called the sterile insect technique, which involved the release of sterile flies in Panama that caused the fly population to collapse.

Yet the New World screwworm remained endemic to the Caribbean and South America, where, in 2005, it was estimated to cause annual economic losses of around $6.1 billion in today’s dollars. And in recent years, the fly has been spreading northward through Central America. Experts had been warning that it was only a matter of time before it arrived in the U.S.

The new infection was detected in a three-week-old calf in Zavala County, Texas; it was found in the calf’s umbilical area, according to the USDA.

“Protecting our livestock industry is a national security issue of the utmost importance, and USDA is wasting no time in taking action,” said Dudley Hoskins, the agency’s undersecretary for marketing and regulatory programs, in a statement. “The United States has defeated this pest before, and we will do it again.”

USDA and Texas officials are taking “immediate action” to contain the threat, according to the statement. Efforts include forming an incident command team with the Texas Animal Health Commission, establishing a 20-kilometer perimeter around the site of the infection with quarantines and movement controls, releasing sterile New World screwworm flies from the ground and the air, trapping flies along the border, screening wildlife in the area, and doing outreach in local communities.

People who live around Zavala County should check their pets or livestock for signs of an infection—for example, draining or growing wounds and screwworm maggots and eggs in or around body openings, the USDA says. If they suspect an infection, people should contact their state animal health official or local USDA veterinarian.

New World screwworms rarely infect humans, but they can infect people who live in or travel to areas where the flies are endemic. People who spend a lot of time outside and have open wounds are most at risk. Anyone who suspects they may have an infection should seek immediate medical care. People should not try to remove maggots themselves—a health care provider may need to remove them surgically, according to the U.S. Centers for Disease Control and Prevention.

To prevent infection, the CDC advises keeping wounds clean and covered, sleeping indoors with closed windows or screens, and using insect repellant or wearing long-sleeved clothing.

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Key Points

• Colorectal cancer diagnoses are rising among younger people, and new research suggests that early-life exposure to colibactin, a toxin produced by certain E. coli strains, may contribute to this trend.
• Researchers found that colibactin-related mutations were 3.3 times more common in early-onset colorectal cancer cases than in late-onset cases.
• Researchers are continuing to study how childhood microbiome factors, including exposure to colibactin-producing bacteria, may influence colorectal cancer risk later in life.

Colorectal cancer, which the Cancer Research Institute explained was “once considered a disease of older age,” is skyrocketing among younger people. According to the institute, 1 in 5 diagnoses now occurs in someone under 55, and the disease is quickly becoming “a leading cause of cancer-related death in young people.” While a number of factors are at play, one study suggests that E. coli could play a major role. 

In 2025, researchers led by a team at the University of California, San Diego published their study in the journal Nature, which outlined how colibactin, a toxin produced by certain strains of E. coli that appears to damage DNA early in childhood, could be fueling this colon cancer crisis.

To identify this connection, the team examined the colorectal cancer genomes of 981 patients with either early- or late-onset colon cancer. They found that colibactin-related mutations were 3.3 times more common in patients with early-onset colon cancer than in those with late-onset.

“These mutation patterns are a kind of historical record in the genome, and they point to early-life exposure to colibactin as a driving force behind early-onset disease,” said Ludmil Alexandrov, the study’s senior author and a professor in the Shu Chien-Gene Lay Department of Bioengineering and the Department of Cellular and Molecular Medicine at UC San Diego, in a press release. “If someone acquires one of these driver mutations by the time they’re 10 years old,” he added, “they could be decades ahead of schedule for developing colorectal cancer, getting it at age 40 instead of 60.”

Alexandrov also explained to NPR that the team found colibactin mutations were far less common in places like rural Africa and Asia, but turned up more often in the U.S. and Western Europe. That, he added, could be due to a number of factors, including the use of antibiotics and childhood nutrition choices, as well as whether someone was breastfed and how they were delivered, either by cesarean section or vaginal delivery. 

“All of these factors are known to substantially affect the microbiome, and there is some evidence they may impact this [colibactin-producing] bacteria, but we really need to investigate each one carefully,” the researcher said. 

It’s important to note that if you do contract this particular strain and have this particular toxin in your body, it doesn’t mean you’ll automatically get colon cancer.

“We don’t have definitive data on whether having the toxin means you will definitely get young-onset colorectal cancer: this study only looked at cancers themselves, not at the bowels of healthy people without cancer,” Trevor Graham, a professor of genomics and evolution and director of the Center for Evolution and Cancer at The Institute of Cancer Research, who was not involved in the study, said in a statement. “So, it’s quite possible that [this certain] E. coli are very common and only a few people with the ‘bad bugs’ will actually go on to get bowel cancer.”

Graham added, “I think it is very likely cancer only occurs in some cases, because even though someone might have the ‘bad bugs’ that cause mutations, those bugs have to cause the right mutations to make a cancer grow.” 

While this strain of E. coli may be a player in the game, it’s only a piece of the ever-growing colorectal puzzle. The Cancer Research Institute noted that several risk factors are at play, not the least of which is genetics. There are, however, things the institute said you can control, including your lifestyle.

“A diet high in processed and red meats and low in fiber, fruits, and vegetables is associated with increased colorectal cancer risk,” the Institute said. It cited The World Cancer Research Fund’s recommendations to limit red meat to 12–18 ounces per week and minimize processed meats to reduce your risk. Additionally, you may want to cut back on alcohol, as the institute also said that “heavy alcohol consumption” can increase risk.

For now, Alexandrov said in the statement that the team is continuing to investigate the issue and exploring whether probiotics could eliminate these and other harmful bacterial strains. The team is also developing early-detection tests that analyze stool samples for colibactin-related mutations and continues to monitor how colorectal cancers are evolving around the world to better understand what we can control in cancer risk. “This reshapes how we think about cancer,” he said. “It might not be just about what happens in adulthood — cancer could potentially be influenced by events in early life, perhaps even the first few years. Sustained investment in this type of research will be critical to the global effort to prevent and treat cancer before it’s too late.”

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Israeli security forces in Kochav Yair, Israel, on Sunday, after a shooting. Credit…Jack Guez/Agence France-Presse — Getty Images

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“Universal” biological signatures of aging shared across different mammalian species—including humans—could offer new clues to identifying longevity and antiaging treatments or interventions, a new study finds.

Age isn’t just the number of candles on a cake. That’s a representation of your chronological age, while your “biological age” is a measure of how your body’s various tissues and cells are holding up over time—and the two don’t necessarily match. Instead, your biological age may be higher or lower than your chronological age for several reasons, such as your lifestyle choices, a chronic disease if you have one, your genes, and more. Researchers use molecular “clocks” to estimate biological age, such as by looking at changes to our DNA. But some of these biomarkers don’t help explain why aging is occurring.

In the new study, published on Wednesday in the journal Nature, researchers analyzed more than 11,000 “transcriptomes”—collections of RNA transcripts that show which genes are being turned on or off in any given cell or tissue at any given time—across various tissues in mice, rats, monkeys, and humans.

What they found was that biological hallmarks of aging in different tissues appear to be highly conserved, meaning they are shared across species, says Alexander Tyshkovskiy, the paper’s lead author and a researcher at Brigham and Women’s Hospital and Harvard Medical School. “The same genes are associated with aging in, for example, liver and heart in rats and humans,” he says.

The hallmarks of aging carried across individual cell types, too, such as liver or blood cells. “Even though the cells have very different functions, very different origin, they still share the same aging-related biomarkers,” Tyshkovskiy adds.

The researchers call this type of aging one’s “transcriptomic age.” Both humans and animals with chronic diseases had a higher transcriptomic age, the researchers found, suggesting it reflects higher levels of cellular damage. And using a large dataset from the U.K. Biobank, the team found that proteins associated with some universal biomarkers also appear to correlate with disease and mortality.*

Overall, the results suggest that aging seems to be a “very systemic process” that affects different tissues, cell types, and species in similar ways, Tyshkovskiy says.

The study is a “major advance,” says David Sinclair, a professor at the department of genetics at Harvard Medical School, who has long studied longevity. Sinclair was not involved with the study.

“[The authors] developed transcriptomic clocks that don’t just estimate age; they measure the progressive loss of cellular function and predict biological decline and mortality risk across mammals,” Sinclair says. The findings could help researchers understand “the underlying process of aging itself, not just the passage of time.”

Tyshkovskiy and his colleagues hope the results will one day lead to potential treatments to slow aging in humans. To that end, the team has developed an online tool called “Transcriptomic Age Calculator Online,” or TACO, to enable other researchers to predict the age of tissue samples using RNA data they may have already collected. For instance, if a researcher has collected tissue from one animal model that was treated with a drug and from another that was not treated, the scientist can measure changes in the biological age between the samples “regardless of the tissue [and] regardless of the species,” says Vadim Gladyshev, the study’s senior author and a professor of medicine at Brigham and Women’s Hospital and Harvard Medical School.

The project could help narrow down possible longevity treatments. “Currently in humans, we don’t have a single intervention that extends lifespan,” Gladyshev says. “We think, using these tools, we could identify candidates that can be tested in the future, and maybe some of them will extend lifespan. That is the hope.”

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