This technology identifies a gene that is positively correlated with colorectal cancer disease progression whose selective inhibition restricts aggressive cancer growth.
Colorectal cancer (CRC) is a prevalent malignancy with a high rate of mortality in patients diagnosed after stage I. Patients with familial adenomatous polyposis (FAP), a rare inherited polyposis syndrome accounting for less than 1% of all cases of colorectal cancer, will develop cancer from colon polyps by age 40, and there is currently no effective treatment option. The tumor microenvironment and gut microbiome are becoming increasingly recognized as predominant drivers in carcinogenesis and disease progression; however, the mechanisms by which specific microbes influence cell proliferation and metastasis remain largely unknown. There is an urgent need to understand the molecular underpinnings that drive cancer growth in the intestine to facilitate development of effective prevention and treatment options.
This technology describes a gene that is highly correlated with colorectal cancer (CRC) progression and metastasis across various colorectal cancers, including FAP. Gene expression is induced by the presence of an intestinal microbe, Fusobacterium nucleatum, that is frequently found in individuals with CRC. Importantly, genetic knock-down of this target restricts cell growth on the leading edge of the tumor, suggesting that modulation of this protein may be therapeutically beneficial for reducing the risk of metastasis. Additionally, this technology provides methods for both prevention and treatment of CRC, as well as strategies for minimizing chemo-resistance of CRC.
This technology has been validated in human colon cancer cell lines.
Patent Pending
IR CU17129, CU19196
Licensing Contact: Ron Katz