Clinical OMICS

NOV-DEC 2017

Healthcare magazine for research scientists, labs, pathologists, hospitals, cancer centers, physicians and biopharma companies providing news articles, expert interviews and videos about molecular diagnostics in precision medicine

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Page 28 of 47 November/December 2017 Clinical OMICs 27 explained how the gut microbiome impacts on C. difficile infection: "The intact gut microbiome is hostile to C. diffi- cile. When the gut microbiome is damaged, typically by antibiotics, this provides a niche which can be exploited by C. difficile." Wilcox and his colleagues advocate prevention as a way of tackling recurrent C. difficile infections. "By preventing the damage to the gut microbiome, we can potentially avoid C. difficile infection and the recurrences that typically occur in about a quarter of affected patients," he said. The research team has developed a laboratory gut model that allows accurate prediction of which antibiotics put patients at higher risk of developing C. difficile infection and which are most likely to be effective for treatment purposes. The team also had success using targeted antibiotics to treat C. difficile infection. These include ridinilazole—a drug that appears to be better at preserving the gut microbiome and reducing the risk of recurrent infections than more tra- ditional, less specific, antibiotics such as vancomycin. Cracking Open the Cancer Microbiome Jennifer Wargo, M.D., is associate professor of surgical oncology at University of Texas, MD Anderson Cancer Cen- ter in Houston. She first became interested in the influence that bacteria have on cancer while working at Harvard University. "We identified bacteria within tumors that could mediate therapeutic resistance. Specifically, in 75% of patients with pancreatic cancer you could identify bacteria within their tumors and these bacteria could actually break down che- motherapy," she explained. After moving to MD Anderson in 2013, Wargo and her group began to focus more on how differences in the gut microbiome could impact on cancer treatment. Working with her colleague Vancheswaran Gopalakrishnan, Ph.D., also based at MD Anderson, Wargo and her team collected oral and gut microbiome samples from more than 200 patients with metastatic melanoma both before and after treatment with anti-PD1 based immunotherapy. "Patients who had a higher diversity of bacteria within their gut had a better response to therapy than those who did not," explained Wargo. Adding that "component taxa also mattered." Gopalakrishnan continued: "Taking our findings in our human cohort forward, we understood that the data was compelling, but it was mostly correlative and so we wanted to delve into the mechanism a little more. With that in mind we planned and performed experiments in germ-free mice." The researchers transplanted stool samples from human responders and non-responders to therapy into the mice. The mice were injected with cancer cells and subsequently treated. "Strikingly, we saw that the mice that were trans- Sriram Subramaniam / National Cancer Institute, National Institutes of Health (continued on next page) 3D structure of a melanoma cell derived by ion abrasion scanning electron microscopy. Metastatic Melanoma Cells: The ability of cancer cells to move and spread depends on actin-rich core structures such as the podosomes (yellow) shown here in melanoma cells. Cell nuclei (blue), actin (red), and an actin regulator (green) are also shown. Julio C. Valencia, NCI Center for Cancer Research

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