Cancer drug calmed age-related inflammation in lab models, study says

Scientists have long known that the body tends to run a low, steady fire of inflammation as it gets older. A study led by researchers at The University of Texas MD Anderson Cancer Center now points to one reason that fire may keep burning. They also report that a drug already used for a blood cancer dampened it in preclinical (lab) models.¹ The work was published in the journal Nature Aging and led by Rugang Zhang, professor and chair of Experimental Therapeutics at MD Anderson.¹ Biohack did not have access to the full paper; this article is based on the cancer center’s announcement and an independent scientific review of the field.

What the researchers found

The study focuses on aging cells that have stopped dividing and entered what the researchers call a “retired” state, known as senescence. In that state, cells start releasing inflammatory signals that feed chronic inflammation.¹ Until now, according to the announcement, little was known about why those signals are released.¹

The team points to a structure called an R-loop. It forms briefly while a cell reads its genes: a paired strand of RNA and DNA becomes tangled with a third, loose strand of DNA.¹ Normally R-loops stay inside the nucleus, the cell’s core.² The study found that retired cells increasingly push R-loops out into the cytoplasm, the fluid between the nucleus and the cell’s outer wall.¹

Out there, the R-loops attach to fragments of DNA debris. The immune system mistakes this for a threat and triggers inflammation, which the announcement compares to “an alarm that won’t turn off.”¹

The researchers also named two proteins involved. One, called DDX1, grabs the R-loop inside the nucleus and carries it out. The other, XPO1, acts as an “exit gate” from the nucleus, working together with DDX1.¹

Testing a cancer drug

The team noted that pushing R-loops out and the build-up of DNA debris happen separately, and the immune reaction only starts when the two meet. That suggested it might be possible to block one without touching the other.²

To test this, they used a drug called KPT-330, also known as selinexor. It is approved by the US Food and Drug Administration to treat multiple myeloma, a blood cancer, and it works by blocking the cell’s nuclear exit.¹ With the exit closed, the R-loops stay trapped inside the nucleus and cannot set off the inflammatory response.¹

In the preclinical models, blocking XPO1 suppressed age-related inflammation, reduced liver fibrosis (scarring of the liver), lowered inflammation markers throughout the body, reversed age-related changes in body make-up, and significantly extended lifespan, the researchers report.¹ The announcement lists the body changes as less fat gain and less muscle loss.²

“Chronic, widespread inflammation is a driving factor in many age-related diseases, including cancer, and our research has discovered one reason why this happens,” Zhang said.¹

He added that the team “saw encouraging results using a drug that has already been tested in humans, paving the way for potential clinical use to alleviate age-related conditions.”¹

What it does not show yet

The results come from preclinical models. The announcement does not describe those models in detail. A lifespan result suggests living animals were involved, but the release does not say which ones, how many, or at what age the drug was given.¹ Without the full paper, Biohack cannot report effect sizes or how long the experiments ran.

No one was treated with the drug for aging or age-related inflammation. The announcement says the drug “already has been tested and proven safe for humans” and that the findings “show translational promise,” meaning they may carry over to people.¹ That is the institution’s own framing. Whether the drug would have the same effects in older people, and what side effects it might cause in that use, has not been tested.

The researchers also flag a trade-off. In a separate experiment, they found that the same inflammatory alarm helps the immune system find and remove precancerous cells, cells that could become cancer. They say this points to a need to refine the alarm rather than silence it completely.¹ They also say it is still unknown why cells push out more R-loops as they age.²

Who is behind it

The study was led by MD Anderson, a cancer center in Houston.² According to the announcement, the work was funded by the National Institutes of Health, the National Cancer Institute, the Department of Defense, and the Cancer Prevention and Research Institute of Texas.¹ The announcement says a full list of authors, disclosures and funding is in the Nature Aging paper; Biohack did not review those disclosures.¹ The Newswise version of the story is a reprint of the cancer center’s release, not separate reporting.²

How it fits the field

“Inflammaging” is the name scientists use for chronic, low-grade inflammation throughout the body that rises with age even without an obvious infection. It was first defined in 2000 by Franceschi and colleagues, according to a December 2025 review in Frontiers in Immunology by researchers at the University of Georgia.³

The review describes inflammaging as a force behind age-related diseases, including heart, brain, metabolic and autoimmune disorders.³ It is usually tracked through raised levels of inflammatory messengers in the blood, such as IL-6, TNF-alpha and IL-1-beta.³ The authors suggest that also measuring calming, anti-inflammatory messengers, such as IL-10, and comparing the two may give a better picture of inflammatory balance in older adults.³

The review notes renewed interest in the subject, driven by work showing that senescent, or “retired,” cells drive chronic inflammatory signaling.³ It also describes how cells can sense stray DNA in the cytoplasm and switch on inflammation.³ The MD Anderson study adds a specific proposed step to that picture: R-loops leaving the nucleus and meeting DNA debris.¹

The review also stresses that inflammaging is not fully understood and is different from immunosenescence, the general weakening of the immune system with age.³ One study pointing to one trigger does not mean it is the only cause.

What to watch next

• A more targeted approach. Because DDX1 is the protein that carries R-loops out, the researchers say future studies could try blocking it instead of shutting down all traffic out of the nucleus, which might cause fewer side effects.¹
• Why cells change with age. The team says more work is needed on why aging cells export more R-loops.¹
• Independent checks. Other labs would need to confirm the findings, and any test in people would be a separate, later step.

Biohack will follow this thread as new research on what starts and sustains age-related inflammation appears.