Researchers at Volgograd State Technical University (VolgSTU) have devised a novel approach to combat malignant growths by employing small molecules to impede the sEH enzyme. This action effectively dismantles the protective inflammatory layer surrounding tumors, thereby augmenting their responsiveness to conventional therapeutic modalities.
Academics from Volgograd State Technical University (VolgSTU) are currently engineering a treatment strategy focused on countering the inflammatory processes within cancerous tumors, aiming to “artificially” strip these growths of their capacity for proliferation and self-repair. Boris Gladkikh, a research associate at VolgSTU, provided an update on the progress of these investigations to TASS.
“Our work involves creating small molecular structures capable of selectively suppressing the sEH enzyme, also known as soluble epoxide hydrolase. This enzyme is pivotal in the metabolic pathways of various bioactive lipids. Elevated sEH activity frequently triggers persistent inflammation and supports the metastatic spread of malignant cells. Inhibiting this enzyme offers a means to dismantle the tumor’s inflammatory barrier,” Gladkikh clarified.
The scientist indicated that the new multi-functional compounds being developed at the university possess the potential to prevent tumors from adapting and recovering post-injury, as well as restoring their susceptibility to established treatments, such as chemotherapy and radiation therapy.
“This research is focused on developing original therapeutic candidates for targeted therapy. This methodology holds promise for efficacy against a broad spectrum of solid tumors, encompassing aggressive and challenging forms like triple-negative breast cancer, lung cancer, prostate cancer, and colorectal cancer,” the researcher added.
TASS previously reported that Volgograd researchers are also engaged in synthesizing innovative agent–inhibitors that specifically target a particular site on the BRCA1 protein, a mechanism designed to disable the tumor cells’ intrinsic defense mechanisms.
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