The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis-0

Measured utilizing Breslow's depth of invasion. All procured lymph node metastases were macroscopically involved, often completely replacing the entire lymph node parenchyma. Distant metastatic (subcutaneous and solid organ) melanoma often exhibited varying degrees of pigmentation, however, surrounding stroma was avoided in procurement of melanoma samples. B: A distinct change in the gene expression patterns is apparent within the comparative groups of thin/I.M. to thick PCM samples. Gene over-expression (upper graph) is evident at the I.M. thickness sample set, with an average Breslow's tumor thickness of 2.1 mm and 19 mm for thick melanomas. Contrary, there is a decrease in gene expression (lower graph) of the same set of genes, with a comparative difference in gene down-regulation evident at the same interphase of I.M. to thick PCM. Proceeding from left to right: normal skin, BCC, SCC, MIS, I.M., thick primary, metastatic melanoma (subcutaneous, lymph node and distant) and melanoma cell lines derived from patients with stage IV melanoma.<p><b>Copyright information:</b></p><p>Taken from "The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis"</p><p>http://www.biomedcentral.com/1755-8794/1/13</p><p>BMC Medical Genomics 2008;1():13-13.</p><p>Published online 28 Apr 2008</p><p>PMCID:PMC2408576.</p><p></p

The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis-2

Band (-), faintly visible band (+/-), visible band (+), strongly visible band (++), N = Not Done. β-actin served as the internal comparative control. The grey values of PCR products of each gene are analyzed by the AlphaEase 3 software and standardized according to β-actin in every sample. B: a, b, Daughter melanoma cell lines secrete SPP1 (osteopontin). The melanoma cell lysates and conditioned cell-free media was resolved by SDS-PAGE and transferred to a PVDF membrane. The blot was probed with anti-SPP1 antibody. , Antibodies for DSC-3 (c), CLCA2 (d), PDGFRL (e) and α-tubulin (f) as an internal control. Lanes 1–3 are PCM and lanes 4–6 are MM cell lines.<p><b>Copyright information:</b></p><p>Taken from "The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis"</p><p>http://www.biomedcentral.com/1755-8794/1/13</p><p>BMC Medical Genomics 2008;1():13-13.</p><p>Published online 28 Apr 2008</p><p>PMCID:PMC2408576.</p><p></p

The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis-1

oncogenes (GDF15, SPP-1) in PCM (n = 7) and MM (n = 13) samples. Relative quantitation of target gene expression for each sample was determined using the equation 2, where GAPDH was used as the internal reference and normal skin as the calibrator. Values were Log base 10 transformed (y-axis) so that all values below zero represent a down-regulation in gene expression and values above zero represent an up-regulation in gene expression, compared to normal skin. B: Correlative microarray analysis of gene expression levels in primary and metastatic melanoma samples compared with normal skin. The statistical differences of gene expression between primary (PCM) and metastatic melanoma (MM) samples were analyzed by Wilcoxon's signed rank test; two-tailed significance level was set at α = 0.05. Compared to PCM samples (n = 7), the expression levels of 4 putative tumor suppressor genes (CST6, p < 0.0001; DSC3, p < 0.0001; PITX1, p = 0.0043, POU2F3, p < 0.0001) were significantly decreased in MM samples (n = 40), while the expression of putative oncogenes (GDF15, p = 0.0027; SPP1, p < 0.0001) were significantly increased in MM samples.<p><b>Copyright information:</b></p><p>Taken from "The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis"</p><p>http://www.biomedcentral.com/1755-8794/1/13</p><p>BMC Medical Genomics 2008;1():13-13.</p><p>Published online 28 Apr 2008</p><p>PMCID:PMC2408576.</p><p></p