Ground Breaking Research Sheds Light on New Potential Treatment Target for Colorectal Cancer

ChristianaCare’s Helen F. Graham Cancer Center & Research Institute

WILMINGTON, DE — In an informing breakthrough, scientists at ChristianaCare’s Helen F. Graham Cancer Center & Research Institute have discovered a critical link between two chief cellular pathways implicated in the development of colorectal cancer. The discovery of an enzyme named CYP26A1 has sparked significant hope for the global healthcare industry, as it indicates a potential new treatment target for drug-resistant colorectal cancers.

A leading killer, colorectal cancer holds the notorious rank of the second most deadly cancer worldwide, with an equal rate of occurrence in both genders. Traditional therapies have, until now, struggled to fully combat the mutated cells responsible for the accelerated growth and progression of this aggressive form of cancer.

The latest discovery by Dr. Bruce Boman and his research team has introduced a new ray of hope in this battle. “The identification of CYP26A1 as a link between WNT and RA signaling brings us a step closer to specifically targeting the stem cell population that fuels tumor growth,” says Dr. Boman, senior author and chief of the research team.

Retinoid drugs, derived from vitamin A, have shown significant potential in treating a range of cancers. However, in cases of colorectal cancer, the treatment-resistant stem cells that fuel the tumor’s growth have proven formidable opponents to conventional treatments.

The team’s research has centered on how these resilient stem cells develop in the presence of a mutation in the APC (adenomatous polyposis coli) tumor suppressor gene. They found that when APC is mutated, it triggers WNT signaling, which subsequently heightens CYP26A1 expression, causing a reduction in RA signaling. Increased CYP26A1 levels prevent the differentiation of APC-mutated colorectal cancer stem cells by diminishing retinoid acid, hence reducing RA signaling.

The implication of these findings is clear: to restore retinoid-induced differentiation and cut back tumor-driving stem cell numbers, CYP26A1 levels will need to be reduced. This suggests that inhibiting WNT signaling could allow cells to respond more effectively to retinoid drugs. As a consequence, the inhibiting action on the CYP26A1 enzyme activity is essential for attaining the full effect of the retinoids.

With the new understanding of how the dysregulated CYP26A1 expression contributes to tumor growth, the team has embarked on drug testing to target this mechanism. Initial stages involve combining CYP26A1 and WNT signaling inhibitors with cell differentiation-inducing agents. This discovery, underscored by the promising initial testing results, is expected to bear significant potential for clinical applications.

This research breakthrough paves the way for exciting future strides in the treatment of colorectal cancer. Understanding the critical role of the CYP26A1 enzyme in tumor growth may well be a game changer in the development of more effective therapeutic treatments for this deadly cancer.

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