enhance data interpretation. the existing knowledge base–driven pathway analysis methods in each generation have been summarized in recent literature. applications of pathway analysis in medicine colorectal cancer (crc) a program package matchminer was used to scan hugo names for cloned genes of interest are scanned, then are input into gominer, which leveraged the go to identify the biological processes, functions and components represented in the gene profile. also, database for annotation, visualization, and integrated discovery (david) and kegg database can be used for the analysis of microarray expression data and the analysis of each go biological process (p), cellular component (c), and molecular function (f) ontology. in addition, david tools can be used to analyze the roles of genes in metabolic pathways and show the biological relationships between genes or gene-products and may represent metabolic pathways. these two databases also provide bioinformatics tools online to combine specific biochemical information on a certain organism and facilitate the interpretation of biological meanings for experimental data. by using a combined approach of microarray-bioinformatic technologies, a potential metabolic mechanism contributing to colorectal cancer (crc) has been demonstrated several environmental factors may be involved in a series of points along the genetic pathway to crc. these include genes associated with bile acid metabolism, glycolysis metabolism and fatty acid metabolism pathways, supporting a hypothesis that some metabolic alternations observed in colon carcinoma may occur in the development of crc. parkinson's disease (pd) cellular models are instrumental in dissecting a complex pathological process into simpler molecular events. parkinson's disease (pd) is multifactorial and clinically heterogeneous; the aetiology of the sporadic (and most common) form is still unclear and only a few molecular mechanisms have been clarified so far in the neurodegenerative cascade. in such a multifaceted picture, it is particularly important to identify experimental models that simplify the study of the different networks of proteins and genes involved. cellular models that reproduce some of the features of the neurons that degenerate in pd have contributed to many advances in our comprehension of the pathogenic flow of the disease. in particular, the pivotal biochemical pathways (i.e. apoptosis and oxidative stress, mitochondrial impairment and dysfunctional mitophagy, unfolded protein stress and improper removal of misfolded proteins) have been widely explored in cell lines, challenged with toxic insults or genetically modified. the central role of a-synuclein has generated many models aiming to elucidate its contribution to the dysregulation of various cellular processes. classical cellular models appear to be the correct choice for preliminary studies on the molecular action of new drugs or potential toxins and for understanding the role of single genetic factors. moreover, the availability of novel cellular systems, such as cybrids or induced pluripotent stem cells, offers the chance to exploit the advantages of an in vitro investigation, although mirroring more closely the cell population being affected. alzheimer's disease (ad) synaptic degeneration and death of nerve cells are defining features of alzheimer's disease (ad), the most prevalent age-related neurodegenerative disorders. in ad, neurons in the hippocampus and basal forebrain (brain regions that subserve learning and memory functions) are selectively vulnerable. studies of postmortem brain tissue from ad people have provided evidence for increased levels of oxidative stress, mitochondrial dysfunction and impaired glucose uptake in vulnerable neuronal populations. studies of animal and cell culture models of ad suggest that increased levels of oxidative stress (membrane lipid peroxidation, in particular) may disrupt neuronal energy metabolism and ion homeostasis, by impairing the function of membrane ion-motive atpases, glucose and glutamate transporters. such oxidative and metabolic compromise may thereby render neurons vulnerable to excitotoxicity and apoptosis. recent studies suggest that ad can manifest systemic alterations in energy metabolism (e.g., increased insulin resistance and dysregulation of glucose metabolism). emerging evidence that dietary restriction can forestall the development of ad is consistent with a major "metabolic" component to these disorders, and provides optimism that these devastating brain disorders of aging may be largely preventable.