It is now well established that cancer is the result of a number of genetic changes within a cell, manifesting alterations of growth regulation, cell survival, angiogenesis, immune surveillance, and metastatic properties. Knowledge of cancer genetics involves the understanding of the factors that contribute to gene regulation, mutagenesis and genetic instability, and how these factors ultimately influence the malignant phenotype. While classic genetics deals with heritable changes of genomic sequences, epigenetics is related to gene expression or cellular phenotype caused by mechanisms other than changes in the DNA sequence, which often involve DNA methylation and chromatin remodeling. Accumulating evidence indicate that both types of changes can lead to cancer phenotype. The mission of the Cancer Genetics Program is to understand how genetic alterations impact cancer initiation, progression and metastasis. Our approaches are to determine the molecular and genetic determinants of cancer predisposition, genetic alterations related to tumor aggressiveness and their response to therapy. The program is strongly based on fundamental understanding of cell and tissue development and homeostasis, animal models of disease, and clinical samples and studies. The translational aspects of the program are to develop better and sensitive genetic testing techniques so that the identification of these genetic factors, following appropriate screening, risk reduction, and prevention recommendations can significantly reduce the cancer risk. The program has three primary focuses. The first focus is to determine how epigenetic regulation influences cancer initiation, progression and metastasis. This includes regulatory RNAs and chromatin remodeling. Given that only about 2% of human genome codes for protein-coding genes, there exists a large amount of non-coding RNAs, among which microRNAs and lncRNAs (large non-coding RNAs) have been shown to play fundamental roles in regulation of gene expression. These non-coding RNAs may impact cancer genetics in several ways, including gene expression, genetic diversity and cancer risk factors. Several members of the program have been investigating how non-coding RNAs regulate expression of genes involved in various cellular pathways and how dysregulation of non-coding RNAs leads to cancer development. The second focus is to understand how inherited genetic variation influences predisposition to cancer. A variety of epidemiological and family-based studies have demonstrated that cancer predisposition is a hereditary trait. For instance, approximately 5-10% of cancer is inherited. Individuals with a genetic predisposition will have a far higher chance of developing cancer within their lifetime and at an earlier age.
However, despite this knowledge, the nature of the genetic variation that leads to increased cancer risk among some individuals largely remains a mystery. The third focus is in area of genetic instability, which encompasses the sources and causes of mutations along with how the cell tries to repair DNA damage to avoid mutations. The causes of genetic instability represent excellent targets for prevention of cancer, while the products of the result mutations are excellent targets for novel therapeutics. Ultimately, we are able to prevent cancer, or to detect it as early as possible by identifying individuals at increased risk or to provide more effective therapies if cancer occurs. In this way, we would be able to better serve our patients by providing individualized cancer risk assessment and health management recommendations to those at increased risk for cancer due to their personal and/or family history of cancer.
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