Breakthrough Experimental Therapy Treats Colon Cancer and Chronic Inflammatory Bowel Disease

SCIENTISTS have discovered a groundbreaking experimental therapy that is capable of suppressing the development of ulcerative colitis (UC), a disease that causes inflammation in the digestive tract and colon cancer (COC). The treatment uses a chemical inhibitor that may block an RNA molecule (microRNA-214) involved in the transmission of genetic information.

High levels of microRNA-214 are usually found in UC patients, who have an increased risk of developing COC. It is still unclear why colitis patients also develop COC. Thirty percent of all patients who report gastrointestinal pain are usually diagnosed with ‘indeterminate inflammatory bowel disease’ by their gastroenterologist. Even if the patient has all available biomarkers and underwent a colonoscopy, many clinicians are still unable to determine whether the patient has UC or Crohn’s disease (CrD).

In a 2-year study, researchers from David Geffen School of Medicine at UCLA, Los Angeles, California, USA examined 401 colon tissue samples from patients in the USA and Europe with UC, CrD, irritable bowel syndrome, sporadic colorectal cancer, and colitis-associated COC, and compared them with samples from individuals without these conditions. Their aim was to aid physicians in diagnosing this disease correctly and provide appropriate treatment, according to study author Dr Dimitrios Iliopoulos, Director, Center for Systems Biomedicine and Associate Professor of Medicine, Division of Digestive Diseases, David Geffen School of Medicine at UCLA.

They developed a systems approach that could accelerate the drug delivery process by utilising sophisticated computer programs and high-tech robotics, combining molecular and clinical information to identify the most important genes to develop new drugs. The integration of these complex data led them to discover a new chemical inhibitor of microRNA-214 for the treatment of UC and COC. “The first steps of the drug discovery process usually take 5-6 years and by using our novel approach we expedited the drug discovery process only in 2 years,” said Dr Iliopoulos.

Previous trials have indicated findings related to inflammatory responses in both sporadic and colitis-associated COCs, but it was unclear until now whether the inflammatory signals regulated the same signalling pathways. “We evaluated this drug in mice with UC and colon tumours and found that in both cases it was highly effective to suppress these diseases,” explained Dr Iliopoulos.

Dr Iliopoulos hopes to eventually begin Phase I clinical trials for patients with UC next year.

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