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Feb 14 (Reuters) -

Welcome to Health Rounds! Pancreas cancer rates are climbing in the U.S., but they’re rising faster in younger women than in their male counterparts, a large study shows. Researchers say the increases are relatively small, but while they work to figure out the reasons, they hope awareness might refocus people on the need for lifestyle changes that help decrease the risk.

In other news, a drug that delivers a cancer-killing virus directly into tumors may be an effective new alternative for patients with a hard-to-treat form of breast cancer. And instead of looking for new ways to kill antibiotic-resistant bacteria, researchers suggest finding ways to disable the organisms and make them less harmful.

Pancreas cancer rates rising faster in young women

Pancreas cancer rates in the United States are increasing faster in younger women than in their male counterparts, a large study has found.

And while survival rates are improving overall, "that improvement is largely among men. The mortality rate among women is not improving," Dr. Srinivas Gaddam of Cedars Sinai Medical Center in Los Angeles said in a statement.

Gaddam's team used databases covering more than half the country to study pancreatic cancer rates between 2001 and 2018. During that period, the cancers were diagnosed in 454,611 patients, roughly half of whom were female. Over that period, the rate of new diagnoses rose by roughly 1%, with a similar pattern seen in adults of both sexes over the age of 55.

Among those younger than 55, however, the rate of new pancreatic cancer diagnoses rose by 2.36% in women versus 0.62% in men.

The difference was most pronounced in the youngest patients. Among women under age 34, the rate went up by 6.45%, compared to 2.97% in similarly aged men. The greatest increase in this age group was in Black women, the research team reported in Gastroenterology.

The researchers also found that rates of pancreatic head adenocarcinoma, an especially aggressive and deadly type of tumor at the head of the pancreas, appear to be increasing.

The increases are small and the findings should not cause alarm, Gaddam said. The research team plans to look for explanations for these trends, which might include differences between pancreatic tumors in women and in men.

The study was funded in part by The Widjaja Family Fund for Pancreatic Cancer Research.

Cancer-killing virus tested in hard-to-treat breast cancer

Adding a drug that contains a cancer cell-killing virus to treatment with chemotherapy yielded impressive results in a small trial of patients with triple-negative breast cancer, with nearly half seeing their tumors disappear.

Triple-negative breast cancer has few treatment options because many drugs do not bind to the cancer cells and so cannot attack them. A new approach employs talimogene laherperepvec (T-VEC), sold as Imlygic by Amgen Inc, which contains a so-called oncolytic, or cancer-killing, herpes virus already in use for treating advanced melanoma.

With funding from Amgen, researchers at the Moffitt Cancer Center in Tampa, Florida injected T-VEC directly into triple-negative breast cancer tumors in 37 patients receiving chemotherapy in advance of mastectomy or lumpectomy. The average tumor size was about four centimeters (1.65 inches), all the patients had stage 2 or stage 3 disease, and in nearly half, the cancer had spread to the lymph nodes.

As reported in Nature Medicine, the treatment led to a complete response in 46% of the patients, meaning the tumor was no longer detectable. Another 21% of the patients had significant shrinkage of their tumors.

Two years after the treatment and the surgery, 89% of the patients remained cancer free, and there were no recurrences in the patients who had strong responses to the treatment.

The researchers noted that Merck and Co's immunotherapy Keytruda is already approved for use along with chemotherapy in patients with triple-negative breast cancer and has led to significantly improved survival, but with a risk for autoimmune side effects.

Side effects with T-VEC were similar to what would be expected of chemotherapy. There were higher rates of low grade fevers, chills, headaches and injection site pain, researchers reported.

"Locally administered agents like oncolytic viruses may boost tumor anti-immunity without increasing systemic toxicities," they said.

If you can't kill MRSA, try disabling it

Instead of trying to kill antibiotic-resistant bacteria, limiting the damage they can do might be an option, laboratory experiments suggest.

"If we can disarm it, then we may not have to worry about it evading antimicrobial agents," study leader Seth Dickey of the University of Maryland said in a statement.

There is a huge unmet need for new medicines or approaches to tackle bacteria resistant to many current drugs.

Dickey's team has discovered that two proteins enable MRSA bacteria (methicillin-resistant Staphylococcus aureus) to secrete the toxins that make people sick. They also learned how those proteins work and what happens if they are disabled, according to a report released on Tuesday and scheduled for publication this week in PNAS.

"We were looking for an alternative way of approaching MRSA," Dickey said. "We were interested in understanding how the bacterium causes disease to see if we could interfere directly with the virulence factors that the bug produces."

When they removed one of those proteins in test-tube experiments, toxins could not leave the single-cell organisms, the researchers found. Instead, the toxins merely built up inside the bacteria, where they cannot hurt anyone. When the other protein was removed, the bacteria were damaged by their own toxins.

The researchers theorize that if therapies could be developed that target these two proteins, MRSA bacteria could be disabled, making them less deadly and possibly even harmless.

The research, funded by the U.S. National Institutes of Health, has implications beyond MRSA because many other bacteria also have dual transport protein systems similar to the one found in MRSA. (Reporting by Nancy Lapid; Editing by Bill Berkrot)