A new study led by a team of researchers at Moffitt Cancer Center reveals that lymphoma can accelerate the biological aging of the immune system and other tissues, providing new insight into how cancer reshapes the body beyond tumor growth.

The study, published in Cancer Cell, shows that B cell lymphoma rapidly transforms young T cells, which are key immune fighters, into a state resembling those of T cells in much older individuals. These changes included increased inflammation, impaired protein balance and altered iron regulation. The effects were not limited to immune cells. Markers of aging also appeared in the blood vessels, kidneys and intestines.

"Cancer doesn't just grow in isolation; it has widespread effects on patients. We found that lymphoma alone, without treatment, is enough to provoke systemic signs of aging," said John Cleveland, Ph.D., senior author and chief scientific officer at Moffitt. "This helps explain why many cancer patients experience symptoms typically associated with aging."

The findings challenge the long-held belief that accelerated aging in cancer patients is primarily caused by treatments like chemotherapy or radiation. While those therapies are known to age cells, this study shows that the cancer itself can push immune and tissue systems into an aged state.

"Our results also suggest there may be opportunities to reverse some cancer-driven aging effects," said Rebecca Hesterberg, Ph.D., the study's lead author and a researcher in Moffitt's Department of Tumor Microenvironment and Metastasis. "By understanding the biology, we can begin to think about interventions that not only treat the cancer but also protect or even restore healthy immune function."

Researchers discovered that lymphoma-exposed T cells accumulated excess iron, making them resistant to a type of cell death called ferroptosis. They also exhibited defects in protein quality control, a hallmark of aging. Some of these changes were reversible when tumors were eliminated in animal models, pointing to new therapeutic opportunities.

With the global population aging and cancer risk rising with age, the study underscores the importance of understanding how cancer interacts with aging biology.

The research was supported by the National Institutes of Health (CA241713, CA244328, P01-CA250984, CA267032, AG063543, P30-CA076292 and CA233399), the Leukemia and Lymphoma Society and the Florida Department of Health (23L10).

Read more …Scientists discover cancer’s hidden power to accelerate aging

Researchers led by Hiroshi Ohno at the RIKEN Center for Integrative Medical Sciences (IMS) in Japan have discovered why smoking tobacco helps people suffering from ulcerative colitis, a chronic disease typified by inflammation of the large intestine. Published in the scientific journal Gut, the study shows that smoking produces metabolites that encourage bacteria from the mouth to grow in the large intestines where they trigger an immune response. These findings imply that protection against ulcerative colitis can be achieved through prebiotics like hydroquinone or probiotic therapy with bacteria like Streptococcus mitis, thus eliminating the need to smoke and all the associated risks for other diseases.

Inflammatory bowel disease comes in two main varieties, Crohn's disease and ulcerative colitis. Although both cause chronic abdominal pain, diarrhea, fatigue and weight loss, their causes and the exact type and location of the inflammation differ. Along with these differences is a mystery that has puzzled doctors and scientists for over 40 years; smoking increases the risk of Crohn's disease but somehow protects against ulcerative colitis. As both diseases are related to gut inflammation -- which is an immune response -- and gut immunity depends in part on the types of bacteria in the gut, Ohno and his team at RIKEN IMS set out to investigate whether the differential effects of smoking on these diseases can be explained by gut bacteria.

The researchers used a combination of human clinical data and experiments with mice to reach their conclusions. Among those with ulcerative colitis, they found that smokers had certain bacteria usually found in the mouth, such as Streptococcus, growing in the gut, specifically in the colonic mucosa that cover the inner lining of the intestines. This phenomenon did not occur in ex-smokers. Thus, while these bacteria normally pass all the way through the digestive system as we swallow saliva throughout the day, smoking somehow allows them to settle down in the gut mucosa.

The next question was why? The researchers also examined gut metabolites -- small substances produced in the gut when food is broken down and processed by the body and gut bacteria. They found that levels of several gut metabolites were higher in smokers with ulcerative colitis than in ex-smokers with colitis. In mice, the researchers found that one of these metabolites, called hydroquinone, promoted the growth of Streptococcus in the gut mucosa. So, smoking-related metabolites like hydroquinone allow mouth bacteria like Streptococcus to flourish in the mucus layer that covers the inner lining of the intestines. But how do these bacteria help reduce inflammation? And why don't they help in Crohn's disease?

The researchers then went back to the oral bacteria that they had discovered was growing in the gut mucosa of smokers with ulcerative colitis, and isolated 10 strains from the saliva of smokers. When they treated mouse models of Crohn's disease and ulcerative colitis with each of these 10 strains for five days, they found that giving the mice Streptococcusmitis had almost the same effect as smoking. Inflammation was reduced in mice with ulcerative colitis and exacerbated in mice with Crohn's disease.

Analysis showed that S. mitis triggered the emergence of helper Th1 cells, which are an important part of the gut's immune response to invaders. In Crohn's disease this likely worsens the condition because the original inflammation is actually caused by these same helper Th1 cells. But in colitis, the Th1 cells fight against an initial Th2-immune response, and this ends up reducing inflammation.

As smoking poses high risks for cancer, heart disease, and many other illnesses, it is not a sustainable treatment for ulcerative colitis. "Our results indicate the relocation of bacteria from the mouth to the gut, particularly those of the Streptococcus genus, and the subsequent immune response in the gut, is the mechanism through which smoking helps protect against the disease," says Ohno. "Logically, direct treatment with this kind of bacteria, or indirect treatment with hydroquinone, is thus likely to mimic the beneficial effects of smoking but avoid all the negative effects."

Read more …Smoking’s hidden gut bacteria trick may lead to new colitis treatments

Graphic saying '95% Drop in U.S. childhood hepatitis B infections since 1991, when routine infant vaccination began'
The Conversation, CC BY-ND[1]

Before the United States began vaccinating all infants at birth with the hepatitis B vaccine in 1991, around 18,000 children every year contracted the virus before their 10th birthday[2] – about half of them at birth. About 90% of that subset developed a chronic infection.

In the U.S., 1 in 4 children chronically infected with hepatitis B will die prematurely from cirrhosis or liver...

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