Using Boolean Logic Modeling of Gene Regulatory Networks to Exploit the Links Between Cancer and Metabolism for Therapeutic Purposes.

The uncontrolled cell proliferation that is characteristically associated with cancer is usually accompanied by alterations in the genome and cell metabolism. Indeed, the phenomenon of cancer cells metabolizing glucose using a less efficient anaerobic process even in the presence of normal oxygen levels, termed the Warburg effect, is currently considered to be one of the hallmarks of cancer. Diabetes, much like cancer, is defined by significant metabolic changes.

Boolean modeling and fault diagnosis in oxidative stress response.

Background: Oxidative stress is a consequence of normal and abnormal cellular metabolism and is linked to the development of human diseases. The effective functioning of the pathway responding to oxidative stress protects the cellular DNA against oxidative damage; conversely the failure of the oxidative stress response mechanism can induce aberrant cellular behavior leading to diseases such as neurodegenerative disorders and cancer. Thus, understanding the normal signaling present in oxidative stress response pathways and determining possible signaling alterations leading to disease could provide us with useful pointers for therapeutic purposes.

Comparative non-cholinergic neurotoxic effects of paraoxon and diisopropyl fluorophosphate (DFP) on human neuroblastoma and astrocytoma cell lines.

The objective of this study was to evaluate the comparative non-cholinergic neurotoxic effects of paraoxon, which is acutely neurotoxic, and diisopropyl fluorophosphate (DFP), which induces OPIDN, in the human neuroblastoma SY5Y and the human astrocytoma cell line CCF-STTG1. SY5Y cells have been studied extensively as a model for OP-induced neurotoxicity, but CCF cells have not previously been studied. We conducted a preliminary human gene array assay of OP-treated SY5Y cells in order to assess at the gene level whether these cells can distinguish between OP compounds that do and do not cause OPIDN.