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Tumor suppressor gene networks as molecular targets for developing new cancer treatments
Lee W.  Bioinformatics and bioengineering (Proceedings of the 4th IEEE Symposium on Bioinformatics and Bioengineering, May 19-21, 2004) 12004. Type: Proceedings
Date Reviewed: Jun 27 2005

This short paper provides a brief summary of the importance of biological interactions, or epistasis, between the breast cancer susceptibility gene 2 (BRCA2) and the RAD51 gene in determining cancer cell sensitivity to chemotherapy and radiation therapy. According to the Chilibot literature search tool [1], there are at least 30 abstracts in PubMed in which BRCA2 and RAD51 co-occur. This suggests that these two genes do in fact interact with one another.

The role of epistasis, or gene-gene interaction, in disease susceptibility is becoming increasingly important, as biology moves away from describing single molecules, and moves toward the characterization of gene networks and biochemical systems. Epistasis can occur among biomolecules in an individual, or can occur as a statistical pattern among individuals in a population. The conceptual divide between biological and statistical epistasis has been recently explored [2]. Lee’s paper hypothesizes that perturbing the interaction between BRCA2 and RAD51 will sensitize cancer cells to chemotherapy and radiation therapy. It will be interesting to see if the proposed disruption of the biological interaction at the cellular level in individuals will result in a statistical pattern of interaction across multiple individuals.

Reviewer:  Jason Moore Review #: CR131430 (0605-0551)
1) Chen, H.; Sharp, B. Content-rich biological network constructed by mining PubMed abstracts. BMC Bioinformatics 5, (2004), 147–147.
2) Moore, J.; Williams, S. Traversing the conceptual divide between biological and statistical epistasis: systems biology and a more modern synthesis. BioEssays 27, 6(2005), 637–646.
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