Researchers at Wilmington, Del.-based ChristianaCare’s Helen F. Graham Cancer Center & Research Institute identified a developmental genetic pattern tied to colorectal cancer growth, aggressiveness and patient survival, according to a news release shared with Becker’s by the system May 26.
The study found that disruptions in WNT and retinoic acid signaling caused colon stem cells to stop maturing and overgrow, leading to changes in HOX genes that drive cancer growth and resistance. The HOX gene network contains 39 transcription factors involved in embryonic development.
The research team, led by Bruce Boman, MD, PhD, identified an eight-gene HOX signature linked to poor survival in colorectal cancer patients. Six genes were overactive in tumors and associated with shorter survival, while two protective genes were underactive, removing natural growth controls.
Researchers also found that different cancer stem cell types depended on different HOX genes, which may help explain why tumors adapt and resist treatment. One stem cell type relied on HOXB genes common in normal colon tissue, while another depended on HOXC genes that increase in cancer.The findings build on earlier research published in January in the International Journal of Translational Medicine examining oncofetal reprogramming, a process in which cancer cells reactivate genes normally active before birth. Researchers said the studies suggest future therapies may need to target cancer plasticity alongside tumor growth.
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