Oncogenes & Tumor Suppressor Genes

Oncogenes and tumor suppressor genes (TSGs) both play a role in oncogenesis via opposite mechanisms. Proto-oncogenes promote normal cell growth. Occasionally, a mutation increases their activity or a duplication, translocation, or other genetic event increases their expression. Under such conditions, these genes, now called oncogenes, cause abnormal unchecked cell growth. Examples of proto-oncogenes include growth factors, tyrosine kinases, regulatory GTPases, and transcription factors. TSGs inhibit cell growth in normal cells. However, decreases in TSG activity, often caused by mutation or promoter hypermethylation, prevents their ability to stop abnormal cell growth. Examples of TSGs include genes that regulate apoptosis, cell adhesion, or DNA damage signaling. Genes may have oncogenic properties, tumor suppressor properties, or both. These properties depend not only on the tumor type, but also on the known or observed differences in gene expression or epigenetic marks. Genetic differences in oncogenes and/or TSGs in tumor samples may correlate with biological phenotypes or clinical outcomes such as staging, therapy selection, metastasis, or survival rate. Analyzing these genes may provide insights into the molecular mechanisms and biological pathways behind oncogenesis and cancer pathology, including deregulation of apoptosis, cell cycle, cell adhesion, and DNA damage and repair.

QIAGEN provides a broad range of assay technologies for oncogene and tumor suppressor gene research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for oncogene and tumor suppressor gene studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.