Can vitamin A turn back the clock on breast cancer?

A derivative of vitamin A, known as retinoic acid, found abundantly in sweet potato and carrots, helps turn pre-cancer cells back to normal healthy breast cells, according to research published this month in the International Journal of Oncology. The research could help explain why some clinical studies have been unable to see a benefit of vitamin A on cancer: the vitamin doesn’t appear to change the course of full-blown cancer, only pre-cancerous cells, and only works at a very narrow dose.Because cells undergo many changes before they become fully aggressive and metastatic, Sandra V. Fernandez, Ph.D., Assistant Research Professor of Medical Oncology at Thomas Jefferson University, and colleagues, used a model of breast cancer progression composed of four types of cells each one representing a different stage of breast cancer: normal, pre-cancerous, cancerous and a fully aggressive model.When the researchers exposed the four breast cell types to different concentrations of retinoic acid – one of the chemicals that the body converts vitamin A into – they noticed a strong change in the pre-cancerous cells. Not only did the pre-cancerous cells begin to look more like normal cells in terms of their shape, they also changed their genetic signature back to normal. Dr. Fernandez’s pre-cancerous cells had 443 genes that were either up or downregulated on their way to becoming cancerous. All of these genes returned to normal levels after treatment with retinoic acid. “It looks like retinoic acid exerts effects on cancer cells in part via the modulation of the epigenome,” says Fernandez.“We were able to see this effect of retinoic acid because we were looking at four distinct stages of breast cancer,” says Dr. Fernandez. “It will be interesting to see if these results can be applied to patients.”Interestingly, the cells that were considered fully cancerous did not respond at all to retinoic acid, suggesting that there may be a small window of opportunity for retinoic acid to be helpful in preventing cancer progression. …

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Eat more, weigh less: Worm study provides clues to better fat-loss therapies for humans

Oct. 10, 2013 — Scientists at The Scripps Research Institute (TSRI) have discovered key details of a brain-to-body signaling circuit that enables roundworms to lose weight independently of food intake. The weight-loss circuit is activated by combined signals from the worm versions of the neurotransmitters serotonin and adrenaline, and there are reasons to suspect that it exists in a similar form in humans and other mammals.”Boosting serotonin signaling has been seen as a viable strategy for weight loss in people, but our results hint that boosting serotonin plus adrenaline should produce more potent effects — and there is already some evidence that that’s the case,” said TSRI Assistant Professor Supriya Srinivasan, who was principal investigator for the study, published online before print on October 10, 2013 by the journal Cell Metabolism.Serotonin signaling, which can be increased artificially by some diet and antidepressant drugs, has long been known to reduce weight. Until recently, scientists assumed that it does so largely by suppressing appetite and food intake. However, Srinivasan reported in 2008 — while she was a postdoctoral fellow at the University of California, San Francisco — that serotonin changes food intake and fat levels via separate signaling pathways. “We could make the animals we studied lose fat even as they ate more,” she said. Her experiments were conducted on C. elegans roundworms, whose short lifespans and well-characterized nervous systems make them a preferred species for quick-turnaround lab studies. Indeed, other researchers soon found that serotonin’s food-intake-suppressing and weight-loss effects are separable in mammals, too.Now with her own laboratory at TSRI, Srinivasan has been examining the C. elegans weight loss circuitry in more detail. …

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New study redefines how plaques grow in heart disease

Aug. 11, 2013 — The growth of deadly plaque inside the walls of arteries may not happen as scientists believed, research from the University of Toronto and Massachusetts General Hospital has found.The research also suggests a new potential target in the treatment of atherosclerosis, a leading cause of cardiovascular disease and death globally.The research team found that macrophages, white blood cells that drive atherosclerosis, replicate inside plaques. Moreover, this growth is not reliant on cells outside the plaques called monocytes, as scientists had assumed.”Until now, the thinking was that inflammatory macrophages arise mainly from the recruitment of their precursors — monocytes — from the bloodstream,” said Clint Robbins, lead author on the study and an Assistant Professor in U of T’s Departments of Laboratory Medicine and Pathobiology, and Immunology. “Our study shows that the accumulation of macrophages also depends on their proliferation locally within the developing plaque.”The journal Nature Medicine published the study results today.The impact of the research on clinical treatments could be large. Many pharmaceutical companies are pouring resources into potential therapies that can block the recruitment of white blood cells into plaques. But if macrophages self-sustain through local cell division, blocking recruitment may not be the best strategy.”I think this work will force some major re-evaluations,” said Filip Swirski, the study’s principal investigator who is a scientist in the Center for Systems Biology at Massachusetts General Hospital and an Assistant Professor at Harvard Medical School. “People have been thinking of targeting monocyte influx to treat atherosclerosis, but they need to consider macrophage proliferation as an additional or alternative approach, especially in established disease.”That approach might be better than targeting circulating monocytes, since interrupting disease-causing processes within plaques could spare other beneficial immune responses that monocytes control, said Swirski.As well, it could help improve the current standard of care in treating atherosclerosis: statin therapy. Statins, in addition to lowering blood lipids that contribute to plaque, have anti-inflammatory properties. The researchers are now looking at whether statins might limit the spread of macrophages within plaques.”Additional targeting of macrophage proliferation may further decrease inflammation in atherosclerosis and prove clinically advantageous,” said Robbins, who is also a scientist in the Toronto General Research Institute at University Health Network.The researchers conducted their study in mice, and they caution that much more research is needed to see how the work will translate to humans. But encouragingly, they found evidence of macrophage growth in plaques from human carotid arteries.Next, the team will compare macrophage proliferation to monocyte recruitment during different stages of atherosclerosis, and look at whether all macrophages, or only subsets, replicate.

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