The National Institutes of Health published a new breakthrough in research on the 15th of this month, discovering that the human DKK2 gene, an important key factor in inhibiting liver cancer, will help future development to predict the risk of developing liver cancer, the risk of recurrence and the development of new drugs.
Liver cancer is one of the most lethal cancers, with more than 10,000 deaths per year. The National Institutes of Health (NIH) has been working for 10 years on sequencing chromosome 4 of Rongyang's team to find the oncogene DKK2, which is associated with liver cancer, and has discovered a new genetic mechanism of cancer, which will be helpful for the future development of liver cancer risk prediction, screening, and new strategies for personalized and precise medical treatment. The results of the study were published on May 20, 2012 in the international journal PLOS Geics.
Frequent pairwise gene deletions on chromosome 4Past studies have found that human liver cancer tissue cells often have pairwise gene deletions in a specific region on the long arm of chromosome 4, suggesting that oncogenes associated with liver cancer formation may be present in this region. Dr. Yung-Feng Lin and Dr. Shih-Feng Tsai, Distinguished Research Fellow at the Institute of Molecular and Genetic Medicine, National Institutes of Health (NIH), and members of an inter-agency team analyzed the genes in the deletion region of chromosome 4 and their variations, and developed a new assay to identify the three oncogenes UNC5C, DKK2, and ZGRF1, all of which have been implicated in the formation of hepatocellular carcinoma.
DKK2 is like the engine of the engine, and is a breakthrough for the cancer genetics
The Taiwanese team studied the DKK2 gene and found that an oncogene regulates the growth of liver cancer by a completely new mechanism, which is an important breakthrough in the genetic mechanism of cancer. The team analyzed and compared the sequences of DKK2 gene in cancer cells and normal human cells, and found that the variations appeared in the nucleic acid sequences of the initiation region of the DKK2 gene, which is responsible for the switching on and off of the DKK2 gene, instead of in the protein structure that the DKK2 gene is made of.A specific sequence combination is found in most cancer tissue samples, and the test found that this sequence combination causes the initiation region of the switch to fail, which in turn prevents the protein function of the DKK2 gene from being expressed properly. According to Tsai Shih-Feng, DKK2 is like the starter of a car engine. If the starter is broken, the car will not run even if the engine itself is not malfunctioning. Therefore, if there is a mutation in a specific region of DKK2 in the human body that cannot control the growth of cancer cells, the risk of developing liver cancer will increase.
New Breakthrough in Cancer Genetic Mechanisms Enabling Personalized Precision Medicine
This study validates a new genetic mechanism of cancer, whereby cancer cells influence the function of oncogenes through a screening process in the region of the pairwise gene initiator, ultimately leading to the formation of liver cancer. This discovery brings a new direction for exploring the mechanism of liver cancer, which can be applied to the risk assessment and early detection of liver cancer in the future, and is expected to develop the genotyping analysis of liver cancer tumors on this basis to classify patients, which will be helpful for the development of personalized and precise medical treatment of liver cancer. The National Institutes of Health (NIH) has a long history of supporting medical research on genomics, and has collaborated with many institutions such as Yang Ming University. In addition to continuing the achievements of the Rong Yang team in the transnational project "Human Genome Project", the Taiwan team has also established a solid foundation for the development of a large database of tumor genomics in the local community.
Topics: genes, anticancer, cancer, precision medicine, liver cancer, heredity