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Home / Specialties / Oncology / Deficiency of a Gene May Increase Risk of Diabetes and Liver Cancer in Males

Deficiency of a Gene May Increase Risk of Diabetes and Liver Cancer in Males

Sep 5, 2014

Why doesn’t this gene affect females in the same way?…

Michigan State University researchers have discovered that a deficiency in a certain gene may cause males to become more susceptible to type 2 diabetes and liver cancer. This may be part of the explanation as to why diabetes is thought to be a risk factor for development of liver cancer, as well as why liver cancer is 2-4 times more prevalent in males as compared to females. The gene is called NCOA5 and is found in both males and females, although due to the genes interaction with estrogen a female with a deficiency of this gene will not have the same risks. It has also previously been thought that this same gene comes with a protective function against both of these diseases for women.

This susceptibility was discovered in a mouse study which identified that 94% of the male mice with a NCOA5 deficiency had development of cells which could lead to liver cancer, specifically a type called hepatocellular carcinoma. During this study it was also discovered that 100% of the male mice which had a deficiency of this gene had some level of glucose intolerance, which could later develop into type 2 diabetes. The expression of glucose intolerance occurred before the development of cancer cells.

With this new information, potential treatments need to be investigated regarding a way to reverse this deficiency in males in order to give them increased protection against development of these diseases.

Practice Pearls:

  • Deficiency of the NCOA5 gene in males has been found to increase the risk of developing type 2 diabetes and hepatocellular carcinoma.
  • Women do not have the same risks with this gene due to the gene’s interaction with elevated levels of estrogen.
  • In mice studies 100% of male mice with a NCOA5 deficiency had some level of glucose intolerance.

Cancer Cell, December 2013