PUBLICATION
An indicator of cancer: downregulation of Monoamine Oxidase-A in multiple organs and species
- Authors
- Rybaczyk, L.A., Bashaw, M.J., Pathak, D.R., and Huang, K.
- ID
- ZDB-PUB-080331-4
- Date
- 2008
- Source
- BMC Genomics 9: 134 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Down-Regulation*
- Gene Expression Regulation, Neoplastic*
- Humans
- Mice
- Monoamine Oxidase/genetics*
- Monoamine Oxidase/metabolism
- Neoplasms/enzymology*
- Neoplasms/genetics*
- Organ Specificity
- Rats
- Serotonin/metabolism
- Species Specificity
- Zebrafish
- PubMed
- 18366702 Full text @ BMC Genomics
Citation
Rybaczyk, L.A., Bashaw, M.J., Pathak, D.R., and Huang, K. (2008) An indicator of cancer: downregulation of Monoamine Oxidase-A in multiple organs and species. BMC Genomics. 9:134.
Abstract
BACKGROUND: Identifying consistent changes in cellular function that occur in multiple types of cancer could revolutionize the way cancer is treated. Previous work has produced promising results such as the identification of p53. Recently drugs that affect serotonin reuptake were shown to reduce the risk of colon cancer in man. Here, we analyze an ensemble of cancer datasets focusing on genes involved in the serotonergic pathway. Genechip datasets consisting of cancerous tissue from human, mouse, rat, or zebrafish were extracted from the GEO database. We first compared gene expression between cancerous tissues and normal tissues for each type of cancer and then identified changes that were common to a variety of cancer types. Results: Our analysis found that significant downregulation of MAO-A, the enzyme that metabolizes serotonin, occurred in multiple tissues from humans, rodents, and fish. MAO-A expression was decreased in 95.4% of human cancer patients and 94.2% of animal cancer cases compared to the non-cancerous controls. Conclusion: These are the first findings that identify a single reliable change in so many different cancers. Future studies should investigate links between MAO-A suppression and the development of cancer to determine the extent that MAO-A suppression contributes to increased cancer risk.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping