Glitch in Gatekeeper Gene may Trigger Colon Cancer

Singapore scientists used human tissue samples and animal models in a new study and have found that the absence or inactivation of the RUNX3 gatekeeper gene may initiate the growth and development of colon cancer.

In earlier studies, the scientists have shown that RUNX3 plays a role in gastric, breast, lung and bladder cancers.

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The inactivation of RUNX3 occurs at a very early stage of colon cancer. Thus, due to the easy detection of the inactivation of RUNX3, and the possibility to reactivate the inactivated RUNX3, the findings may prove to be a crucial step in the development of an early diagnostic test as well as a therapeutic target for colon cancer.

Since a long time scientists believe that most of the time colon cancer involves the disruption of a tumor suppressor gene called APC, which in turn activates bete-catenin and TCF4, a protein complex that plays an important role in cancer development.

The latest findings have for the first time shown that the activity of beta- catenin/TCF4 also is inhibited by RUNX3.

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In an earlier research, the same team of researchers reported that RUNX3 is a major tumor suppressor of gastric cancer.

Led by Yoshiaki Ito, M.D., NUS Yong Loo Lin Professor in Medical Oncology and a principal investigator at IMCB, the research analyzed animal models as well as tissue samples from patients diagnosed with colon cancer, to examine how RUNX3 is involved in colon cancer.

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"My team and I have been working on our research for the past six years, and we are extremely excited about how our research findings can be translated into practical clinical applications to help patients suffering from cancers such as bladder, breast, colon and lung. We certainly look forward to our continuous teamwork with our clinical colleagues in improving the lives of cancer patients," said Ito.

He said that the disruption of the RUNX3 gene can cause colon cancer as well as many other types of cancers, including those of the bladder, breast, colon and lung.

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Source-ANI
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