Anti-Parasitic Drug Prevents Pancreatic Cancer’s Initiation, Progression and Metastasis in Mice

AHA Publisher — Wed, 04 Aug 2021 07:00:22 +0000

Johns Hopkins Medicine via News-Medical – As the third-most lethal cancer in the United States, with only a 1% five-year survival rate for people with its most aggressive form, pancreatic cancer has long been a target of researchers who search for ways to slow or stop its growth and spread. Now, a team of Johns Hopkins Medicine researchers have found that an anti-parasitic drug prevents pancreatic cancer’s initiation, progression and metastasis in genetically engineered mice. In a study published in the journal Oncotarget on July 6, Gregory Riggins, M.D., Ph.D., professor of neurosurgery and oncology at the Johns Hopkins University School of Medicine, and his team used two different mouse models to determine that the anti-parasitic drug mebendazole could slow or stop the growth and spread of both early and late-stage pancreatic cancer. “We think that mebendazole could have a role in all stages. It was particularly effective for pancreatic cancer that was detected early.” (Gregory Riggins, M.D., Ph.D., Professor of Neurosurgery and Oncology, Johns Hopkins University School of Medicine) Riggins and his team administered mebendazole to mice that were genetically engineered to develop pancreatic cancer. The team measured the inflammation and the change in tissue, as well as the stage, grade and metastatic status in each tumor. Originally used to fight roundworm, hookworm and other parasitic infections by cutting off the parasites’ supply of nutrition, mebendazole inhibits the formation of tubulin. Tubulin, Riggins explains, is both a micro-skeleton of the inner cell and a highway for transport. The drug gets into the parasite’s gut and collapses the tubulin, starving the parasite to death. The study shows that mebendazole may act similarly in pancreatic cancer by collapsing cancer cells’ structure, along with other mechanisms such as reducing inflammation. Riggins says he hopes to continue his team’s research through human clinical trials. “We are advocating for use of mebendazole as a therapy for those diagnosed before metastasis to see if we can slow or prevent pancreatic cancer,” Riggins says. “For those with more advanced cancers, it could be an alternative to certain surgeries. Mebendazole may have utility as a therapy after initial treatment to prevent tumor recurrence in the 15% to 20% of pancreatic adenocarcinoma patients who undergo surgery. It may also increase the durability of response to standard chemotherapy in the remaining 80% to 85% of patients with advanced disease.” The Virginia and D.K. Ludwig Fund for Cancer Research provided funding for the research. Other scientists who conducted the research include Tara Williamson, Michelle Carvalho de Abreu, Dimitri G. Trembath, Cory Brayton, Byunghak Kang, Thais Biude Mendes, Paulo Pimentel de Assumpção and Janete M. Cerutti. Riggins and Williamson are inventors on intellectual property related to mebendazole owned and managed by Johns Hopkins University conflict of interest policies. Riggins has a financial interest in Benizole Therapeutics, PBC. The technology is available for licensing through Johns Hopkins Technology Ventures. To read the original article click here.

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Protein in Prostate Cancer May Inhibit Tumor Growth

AHA Publisher — Wed, 16 Jun 2021 07:00:57 +0000

University of Georgia via EurekAlert – Prostate cancer is the second most common cancer among men, according to the American Cancer Society. It’s also one of the trickiest cancers to diagnose and treat. But new research from the University of Georgia has identified a protein that appears to prevent the cancer from spreading to and colonizing the bone, providing a new target for future therapeutics. “Unfortunately, prostate cancer that has spread to the bone is very aggressive, often lethal and very difficult to treat,” said Brian Cummings, corresponding author of the study and head of the College of Pharmacy’s pharmaceutical and biomedical sciences department. “Even in cases of successful treatment, the patient’s quality of life is severely lessened due to bone loss.” Prostate cancer that hasn’t spread beyond nearby organs has nearly a 100% survival rate, meaning almost all of these patients will live at least another five or more years after their initial diagnosis and treatment. But for men whose cancer has spread to other organs or the bone, that five-year survival rate plummets to 30%, according to the American Cancer Society. In the U.S., about one in every eight men will be diagnosed with prostate cancer and more than 34,000 men die each year from the disease. The new study, published by Scientific Reports, focused on cancer-associated fibroblasts, which are the most abundant type of cell in tumors and are responsible for cancer growth and spread. The researchers found that knocking out a specific protein, called glypican-1, could prevent tumor cells from spreading into nearby bone. The study supports a previous report from Cummings’ laboratory suggesting that this protein may prevent tumor growth. The researchers found that the protein doesn’t alter the cancer cells themselves. Instead it affects a group of neighboring cells called fibroblasts. Fibroblasts are cells that help make up connective tissues in people and animals. But fibroblasts can also be present in cancerous tumors, where they facilitate cancer growth and spread. To determine the glypican-1 protein’s role in helping cancer spread, the researchers combined human prostate cancer cells and human bone-derived cells to examine how the cancer cells transformed the fibroblast. Then they genetically modified the cancer cells and the fibroblast to knock out the protein. Without the protein, the prostate cancer cells had problems transforming the fibroblast. The study was the first to demonstrate such a role for glypican-1 and suggests that this protein may have the same effect on tumor growth in people. “Part of the significance of this study is that it demonstrates how cancer cells are able to change their environment in ways to facilitate their own growth,” Cummings said. “Prostate cancer cells alter their environment so that they can colonize bone. This study identifies a role for a protein that appears to inhibit the harmful changes that prostate cancer makes to the bone.” “This protein appears to stop the ability of cancer cells to change their environment, which decreases the cancer’s aggressiveness. The fact that this protein is found in the bone, where many aggressive prostate cancer cells reside, further increases the potential impact of this work.” To read the original article click here.

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Anti-Parasitic Drug Prevents Pancreatic Cancer’s Initiation, Progression and Metastasis in Mice

Protein in Prostate Cancer May Inhibit Tumor Growth