One Step Forward Toward Identification of the Genetic Signature of Glioblastomas
- Boris Pasche, MD, PhD;
- Richard M. Myers, PhD
- Author Affiliations: Division of Hematology/Oncology, University of Alabama at Birmingham, and UAB Comprehensive Cancer Center, Birmingham (Dr Pasche); and HudsonAlpha Institute for Biotechnology, Huntsville, Alabama (Mr Myers). Dr Pasche is also Contributing Editor, JAMA.
Since this article does not have an abstract, we have provided the first 150 words of the full text.
- KEYWORDS:
- ANNEXIN A7
- BRAIN NEOPLASMS
- CHROMOSOMES, HUMAN
- EPIDERMAL GROWTH FACTOR
- GENES
- GENETIC PREDISPOSITION TO DISEASE
- GENOME, HUMAN
- GLIOBLASTOMA
- HAPLOTYPES
- RECEPTOR, EPIDERMAL GROWTH FACTOR
- SEQUENCE ANALYSIS, DNA
Cancer is a disease of the genome at the level of gene expression, epigenetic modifications such as DNA methylation, and DNA alterations. For more than 3 decades, many lines of research have shown that acquisition of genetic changes is a major and required step in the development of most cancers. First, ionizing radiation and chemicals that damage DNA and cause mutations also cause cancer.1 Second, genomic alterations such as translocations that result in the production of a specific gene fusion product are associated with some types of cancer. Such is the case for the translocations between chromosomes 9 and 22 in chronic myeloid leukemia and the translocation between chromosomes 15 and 17 in acute promyelocytic leukemia.2 Third, the introduction of genomic DNA from human cancer cells into normal cells can render the normal cells cancerous.3
In the past 2 decades, many genomic alterations have been identified in …
