Cancer is a genetic disease, in which cancer cells arise from mutations of genes in an otherwise normal cell. The mutations are usually caused by either environmental insults on DNA or spontaneous errors in cellular processes, such as gene expression, DNA replication, and chromosome segregation. Cancer does not occur from a single mutation in a single gene. Instead, development of the disease involves multiple vital genes whose mutations act in concert to drive tumorigenesis.
These vital genes fall into two classes, proto-oncogenes and tumor suppressor genes, which have been analogous to the gas pedal and the brake of a car, respectively. A defective oncogene would be comparable to a gas pedal that remains down at all times. In contrast, inactivation of a tumor suppressor genes means that the brake system is disabled. In either case, cancer cells can start growing unchecked and both instances together often synergize to thrust the process.
世界杯365bet下载365bet滚球注册365bet体育投注正规Physiological functions of cancer genes under normal condition and their pathological roles during tumorigenesis are a central research theme in our institute. Equipped with a large panel of isogenic cell lines and human cancer cell lines, and a variety of genetically and somatically modified mouse models of tumors, our scientists will elucidate the oncogenic changes and their mechanisms that propel tumor initiation, progression, and metastasis; identify biomarkers for diagnosis of the disease, selection of therapeutics, and prediction of outcome; pre-clinically test new therapeutic strategies such as oncoprotein-targeted therapies, synthetic lethal therapies and rational combination therapies. Our ultimate goal is to translate our breakthrough research into clinical applications for the personalized treatment of cancer.