Flu, COVID can reawaken dormant breast cancer cells: Study
The study, published in Nature, found that common viruses can reawaken small numbers of dormant breast cancer cells in the lungs.
Researchers began investigating the link after the team noticed that U.K. patients who were in remission from breast cancer and tested positive for COVID later showed a two-fold increase in cancer-related deaths.
They also analyzed a U.S. database that included nearly 37,000 patients and found that COVID infection was associated with a more than 40 percent increased risk of metastatic breast cancer in the lungs.
Studies on mice found that influenza and COVID infections triggered dormant breast cancer cells after just days of infection. Within two weeks, researchers observed 'massive expansion' of the cancer cells into metastatic lesions by more than 100 times.
Scientists have suspected that common viruses like Epstein-Barr can trigger some cancers. Human papillomavirus (HPV) is already documented to trigger cervical cancer.
When it comes to breast cancer, however, research on human cells was limited, and it's not entirely known how the virus triggers the disease to spread.
The findings suggest the body's immune response plays a role.
After breast cancer goes into remission, a tiny number of cells remain dormant in lung, bone and liver tissue. Sometimes, inflammation can wake up the cells.
In the mouse experiments, both influenza A and coronavirus only reawakened dormant cells if they triggered an inflammatory cytokine response.
More research is needed to see if vaccination makes a difference when it comes to the possibility of reawakening dormant cells.
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Research on reversing Alzheimer's reveals lithium as potential key
Seven years of investigation by scientists at Harvard Medical School has revealed that the loss of the metal lithium plays a powerful role in Alzheimer's disease, a finding that could lead to earlier detection, new treatments and a broader understanding of how the brain ages. Researchers led by Bruce A. Yankner, a professor of genetics and neurology at Harvard Medical School, reported that they were able to reverse the disease in mice and restore brain function with small amounts of the compound lithium orotate, enough to mimic the metal's natural level in the brain. Their study appeared Wednesday in the journal Nature. Subscribe to The Post Most newsletter for the most important and interesting stories from The Washington Post. 'The obvious impact is that because lithium orotate is dirt cheap, hopefully we will get rigorous, randomized trials testing this very, very quickly,' said Matt Kaeberlein, former director of the Healthy Aging and Longevity Research Institute at the University of Washington, who did not participate in the study. 'And I would say that it will be an embarrassment to the Alzheimer's clinical community if that doesn't happen right away.' Yankner, who is also the co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard, said: 'I do not recommend that people take lithium at this point, because it has not been validated as a treatment in humans. We always have to be cautious because things can change as you go from mice to humans.' He added that the findings still need to be validated by other labs. Although there have been recent breakthroughs in the treatment of Alzheimer's, no medication has succeeded in stopping or reversing the disease that afflicts more than 7 million Americans, a number projected to reach almost 13 million by 2050, according to the Alzheimer's Association. Lithium is widely prescribed for patients with bipolar disorder, and previous research indicated that it held potential as an Alzheimer's treatment and an antiaging medication. A 2017 study in Denmark suggested the presence of lithium in drinking water might be associated with a lower incidence of dementia. However, the new work is the first to describe the specific roles that lithium plays in the brain, its influence on all of the brain's major cell types and the effect that its deficiency later in life has on aging. Results of the study by Yankner's lab and researchers at Boston Children's Hospital and the Rush Alzheimer's Disease Center in Chicago also suggest that measuring lithium levels might help doctors screen people for signs of Alzheimer's years before the first symptoms begin to appear. Yankner said doctors might be able to measure lithium levels in the cerebrospinal fluid or blood, or through brain imaging. - - - How our brains use lithium In a healthy brain, lithium maintains the connections and communication lines that allow neurons to talk with one another. The metal also helps form the myelin that coats and insulates the communication lines and helps microglial cells clear cellular debris that can impede brain function. 'In normal aging mice,' Yankner said, 'lithium promotes good memory function. In normal aging humans,' higher lithium levels also correspond to better memory function. The depletion of lithium in the brain plays a role in most of the deterioration in several mouse models of Alzheimer's disease. Loss of lithium accelerates the development of harmful clumps of the protein amyloid beta and tangles of the protein tau that resemble the structures found in people with Alzheimer's. Amyloid plaques and tau tangles disrupt communication between nerve cells. The plaques in turn undermine lithium by trapping it, weakening its ability to help the brain function. Lithium depletion is involved in other destructive processes of Alzheimer's: decay of brain synapses, damage to the myelin that protects nerve fibers and reduced capacity of microglial cells to break down amyloid plaques. Lithium's pervasive role comes despite the fact that our brains contain only a small amount of it. After examining more than 500 human brains from Rush and other brain banks, Yankner's team discovered the naturally occurring lithium in the brain is 1,000 times less than the lithium provided in medications to treat bipolar disorder. Li-Huei Tsai, director of the Picower Institute for Learning and Memory at Massachusetts Institute of Technology and who was not involved in the study, called it 'very exciting,' especially when many in the field, including her own lab, have focused on genetic risk factors for Alzheimer's. 'But clearly genetic risk factors are not the only things,' said Tsai, who is also Picower professor of neuroscience. 'There are a lot of people walking around carrying these risk genes, but they are not affected by Alzheimer's disease. I feel this study provides a very important piece of the puzzle.' - - - Pathways for treatment Alzheimer's treatments mostly help to manage symptoms and slow the decline it causes in thinking and functioning. 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Targeting a Vaccine
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