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Research into cancer can provide new insight into how this disease works and how it can be stopped. The Experimental Biology 2018 meeting (EB 2018) will showcase innovative research that could lead to new ways to treat and prevent cancer.
Pancreatic ductal adenocarcinoma (PDAC), which makes up 90 percent of all pancreatic cancers, has a 5-year survival rate of less than five percent. The cancer is not only difficult to detect but treatment is often complicated by mutations in the p53 tumor suppressor gene that make the cancer cells resistant to chemotherapy. Researchers from the Human BioMolecular Research Institute, University of California San Diego and ChemRegen, Inc. developed a new compound that could be useful for treating pancreatic cancer. They previously showed that the compound killed PDAC cells with and without mutant p53 and strongly inhibited tumor growth in an invasive PDAC tumor mouse model. In new work, the researchers showed that the compound works by uniquely targeting two human cell death pathways: programmed cell death, or apoptosis, and the intracellular degradation system known as autophagy. They also showed that the compound's potency comes from its ability to induce crosstalk between PDAC cell death pathways, as portal eurekalert.org says.
Jiongjia Cheng will present this research at the American Society for Pharmacology and Experimental Therapeutics (ASPET) annual meeting from 12:30-2:30 p.m. Tuesday, April 24, in Exhibit Halls A-D (poster C197).
Patients receiving anti-cancer drugs often experience debilitating pain because of a condition known as chemotherapy-induced peripheral neuropathy. Scientists don't fully understand why the drugs cause this condition, which currently has no treatment. In a new study, researchers from the University of Texas Health Science Center at San Antonio discovered that exposure to vinca alkaloids and taxanes chemotherapy drugs was associated with an immediate pain response activated through the peripheral nerves that detect pain stimuli. Their experiments revealed that the chemotherapy drugs cause overexcitation of sensory neurons by specifically activating the an ion channel (TrpA1) involved in pain perception. The study represents the first demonstration of direct activation of sensory neurons by anti-cancer drugs and supports a role for TrpA1 in the development of chemotherapy-induced peripheral neuropathy. The findings could lead to new treatments for pain associated with chemotherapy drugs.
Indomethacin is a highly potent nonsteroidal anti-inflammatory drug (NSAID) that has shown anticancer properties in people and animal models. To find out if this drug inhibits colon cancer, researchers from University of Texas Health Sciences Center in Houston conducted a study involving unmodified indomethacin and indomethacin modified with phosphatidylcholine to protect against NSAID injury in the gastrointestinal tract. In cultured cancer cells from mice, doses of both indomethacin formulations significantly inhibited colon cancer cell growth in culture, with the phosphatidylcholine formulation showing slightly more potency at the lowest dose tested. Similarly, in mice injected with colon cancer cells, treatment with both forms of indomethacin brought significant reductions in the number of tumors compared to mice receiving no treatment. The researchers conclude that indomethacin and phosphatidylcholine-indomethacin are strong and effective inhibitors of colon cancer cell growth and hold potential for preventing, and possibly treating, colorectal cancer in people.
Cold-inducible RNA binding protein (CIRP) plays an important role in regulating gene expression and how cells respond to stress. To better understand CIRP's role in breast cancer, researchers from the University of New Mexico Health Sciences Center are studying a mouse model of breast cancer that expresses CIRP at levels that are higher than normal. The researchers report that the increased levels of CIRP inhibited growth, progression and metastasis of tumors. These anti-cancer effects were associated with changes in immune system signals known as cytokines. Specifically, the mice exhibited decreased levels of cytokines that promote an environment favorable for tumor growth and increased levels of cytokines that create an antitumorigenic environment. The researchers continue to study the mechanisms involved in CIRP's ability to influence signaling between cancer and immune cells so that this information could be used to improve standard therapies and immunotherapeutic approaches for treating breast cancer.
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