الفهرس 
? An overview on DNA microarrays technologyOnly 14 pages are availabe for public view
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Abstract
Fabrication of a DNA microarray begins with the application of ‘‘probes’’ on a surface in an arrayed manner .There are two main microarray technological platforms, spotted arrays and in-situ oligonucleotide arrays .
Once microarrays have been made and obtained, the next stage is to obtain samples for labeling and hybridization. Labeling RNA for expression analysis generally involves three steps,isolation of RNA, labeling the RNA by a reverse transcription procedure with fluorescent markers and purification of the labeled products .
The fundamental basis of DNA microarrays is the process of hybridization. Two DNA strands hybridize if they are complementary to each other . Hybridization of the labeled target to the probes on a microarray is performed by adding the targets dissolved in hybridization buffer to the slide within a confined space, followed by incubation for a given amount of time at a certain temperature .
The final step of the laboratory process is to produce an image of the surface of the hybridized array. The slide is placed in a scanner ( laser scanning confocal microscope ) which is a device that reads the surface of the slide.
Once the microarrays have been hybridized, the resulting images are used to generate a dataset.This dataset needs to be “preprocessed” prior to the analysis and interpretation of the results. Normalization is a preprocessing step that aims to correct for systematic differences between genes or arrays.
DNA microarrays had been used to compare the gene expression profile of malignant melanoma with that of nevi. Also,microarrays were used to identify mechanisms of early malignant transformation of melanoma cells. Using microarrays, the question of gene expression profiles of non-metastatic versus metastatic melanoma cell lines had been addressed . The nodular melanoma ( NM ) and superficial spreading melanoma (SSM) show different gene expression patterns.
Genes involved in many crucial aspects of cellular biology, including metabolism, transcription, cell cycle regulation, cell adhesion, cell migration, cell proliferation and cell motility were amongst the largest groups of upregulated genes, while oxidative phosphorylation, lipid metabolism, translation, and apoptosis were among the main categories down-regulated in BCCs compared to normal skin.
In SCC, the majority of up-regulated genes were involved in adhesion, cell communication, and metabolism, and one each in apoptosis and in proliferation . In contrast, the majority of down-regulated genes were involved in metabolism, in proliferation, differentiation, and detoxification, and 5 in adhesion.
In CTCL, genes with known function that were upregulated in advanced-stage disease included those involved in cell proliferation, cell survival, and resistance to drugs. In contrast, the downregulated genes comprised promoters of cell adhesion and apoptosis, negative regulators of cell signaling and the cell cycle, and genes involved in DNA repair .
Th1-specific genes were identified to be down-regulated in Sezary syndrome as well as in a proportion of mycosis fungoides samples.
Of special interest was the finding that several of the central p53 target genes remained unaffected following UVB exposure in spite of p53 protein accumulation. S100A6, S100A7, S100A8, S100A9 and S100P protein genes were upregulated in human epidermis following UVB radiation.
A group of p53 targets were induced in melanocytes exposed to UVB light . These genes include CDKN1A, the WNT pathway regulator DKK1 , the receptor tyrosine kinase EPHA2, GDF15, FDXR , TP53I3 .
In psoriases, S100 calcium binding proteins showed the largest expression difference between involved and uninvolved skin in
comparison to normal skin.
In psoriasis skin, CCL-4 , CCL-20 , chemokine (C-X-C motif) ligand 2(CXCL-2) , IL-8, and IL-8R showed increase of gene expression compared with AD skin
Of approximately 4,000 genes, 32 were differentially expressed in fibroblast cell strains from the skin of scleroderma patients in comparison with those from normal skin. The aberrantly expressed genes comprised 7 autoantigen and 25 nonautoantigen genes.
Global analysis of 284 known biological pathways revealed that 13 were differentially regulated in SSc PBCs, including two pathways (interleukin 2 receptor, beta(IL2RB) and GATA binding protein 3(GATA3) ) that lead to TH2 polarization