Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151195 | ENA |
REPOSITORIES: ENA
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Project description:Perturbations in microRNA (miRNA) expression profiles has been reported for cutaneous malignant melanoma (CMM). With regards to a rapidly growing number of newly discovered miRNA sequences, the availability of up-to-date miRNA expression profiles for primary cutaneous malignant melanoma (PCMM), cutaneous malignant melanoma metastases (CMMM) and benign melanocytic naevi (BMN) is limited. Patients with PCMM (n=9), CMMM (n=4) and BMN (n=8) were included in the study. Specimens were obtained during surgery from the center of the tumors (lesional). An exploratory microarray analysis was performed by miRNA expression profiling based on miRBase V.16. Additionally, the expression levels of selected miRNA candidates were confirmed by TaqMan real-time quantitative polymerase chain reaction (RT-PCR). New miRNA candidates previously not described to be associated with CMM were found to be potentially dysregulated in CMM.
2012-11-02 | GSE34460 | GEO
Project description:We performed microRNA sequencing of primary human FFPE Acral Melanoma (AM), Cutaneous Melanoma (CM), Acral Nevi (AN), and Cutaneous Nevi (CN). We found that previously identified ratios of microRNAs, particularly miR-21-5p and miR-211-5p, were able to accurately classify benign and malignant melanocytic neoplasia, both in non-acral cutaneous melanomas and nevi (CM vs CN), as well as matched acral melanoma and nevi (AM vs AN). Receiver operating characteristic area under the curve (AUC) of Ensemble models trained using these microRNA ratios demonstrated AUCs of 0.88-0.90 across these melanoma subtypes, suggesting the potential utility of these ratios as a biomarker of malignancy in melanocytic neoplasia.
2024-08-14 | GSE266413 | GEO
Project description:Perturbations in microRNA (miRNA) expression profiles has been reported for cutaneous malignant melanoma (CMM). With regards to a rapidly growing number of newly discovered miRNA sequences, the availability of up-to-date miRNA expression profiles for primary cutaneous malignant melanoma (PCMM), cutaneous malignant melanoma metastases (CMMM) and benign melanocytic naevi (BMN) is limited. Patients with PCMM (n=9), CMMM (n=4) and BMN (n=8) were included in the study. Specimens were obtained during surgery from the center of the tumors (lesional). An exploratory microarray analysis was performed by miRNA expression profiling based on miRBase V.16. Additionally, the expression levels of selected miRNA candidates were confirmed by TaqMan real-time quantitative polymerase chain reaction (RT-PCR). New miRNA candidates previously not described to be associated with CMM were found to be potentially dysregulated in CMM. Nine patients with PCMM (PCMM1-PCMM9), four patients with CMMM (CMMM1-CMMM4) and eight patients with BMN (BMN1-BMN8) were enrolled in the present study. All cutaneous specimens were harvested in the operating room, immediately stored in RNAlater (Quiagen, Hilden, Germany) and kept at - 80 M-BM-0C until RNA isolation. Total RNA including miRNAs was isolated using the miRNeasy Mini Kit (Quiagen, Hilden, Germany) according to the manufacturerM-bM-^@M-^Ys protocol. RNA concentration and purity was determined by NanoDrop ND-1000 spectral photometer (Peqlab, Erlangen, Germany). RNA integrity control (RIN) was determined by means of capillary electrophoresis with the 2100 Bioanalyzer and the RNA 6000 NanoLabCHip Kits (both Agilent Technologies, Santa Clara, USA). To be further considered for Microarray analysis a RIN M-bM-^IM-% 7.0 indicating medium to good RNA quality was defined as inclusion criteria. For assessment of labeling and hybridization efficiencies total RNA samples were spiked with in-vitro synthesized oligonucleotides by using the MicroRNA Spike-In Kit (Agilent Technologies, Santa Clara, USA). A total of 100 ng total RNA per sample were introduced into a labeling reaction. The spiked total RNA was treated with alkaline calf intestine phosphatase (CIP). The dephosphorylated RNA was labeled with the miRNA Complete Labeling and Hyb Kit (Agilent Technologies, Santa Clara, USA) according to the manufacturerM-BM-4s instructions using T4 RNA ligase, incorporating Cyanine 3-Cytidine biphosphate (pCp). The Cyanine-3-labeled miRNA samples were prepared for One-Color based hybridization with Complete miRNA Labeling and Hyb Kit (Agilent Technologies, Santa Clara, USA) according to the manufacturerM-BM-4s instructions. Labeled miRNA samples were hybridized at 55M-BM-0C for 20 hrs on separate Human miRNA Microarrays Release 16.0 (8x60K format, (Agilent Technologies, Santa Clara, USA). Afterwards, microarrays were washed with increasing stringency using Gene Expression Wash Buffers (Agilent Technologies, Santa Clara, USA) followed by drying with acetonitrile (Sigma-Aldich, St.Louis, USA). Fluorescent signal intensities were detected with Scan Control A.8.4.1 Software (Agilent Technologies, Santa Clara, USA) on the Agilent DNA Microarray Scanner and extracted from the images using Feature Extraction 10.7.3.1 Software (Agilent Technologies, Santa Clara, USA). All the steps described were carried out according to the manufacturerM-BM-4s instructions.
2012-11-02 | E-GEOD-34460 | biostudies-arrayexpress
Project description:Background: Timely diagnosis is important for successful treatment of cutaneous melanoma. Currently, Breslow tumor thickness and mitotic rate are used for malignant melanoma classification and prognosis, but these parameters can assess disease progression risk only to a certain degree. Therefore, there is a need for new melanoma protein biomarkers that would aid early and accurate diagnosis and prediction of their metastatic potential. Methodology and Findings: This retrospective case control study is based on proteomic profiling of formalin-fixed archival tissues of 31 early-stage head and neck cutaneous malignant melanoma samples using liquid chromatography / mass spectrometry. A melanoma proteomic profile was identified and protein expression levels were compared to the proteome profile of melanocytic naevi and correlated to established prognostic factors and disease-specific survival. In accordance with the American Joint Committee on Cancer guidelines, recursive partitioning multivariate analysis was used to identify potential biomarkers associated with metastatic potential of early-melanoma. Heterogeneous nuclear ribonucleoprotein M and heat shock protein 90 alpha were profiled as independent prognostic factors. Their elevated expression was clinically relevant for predicting an exceedingly high metastatic hazard ratio. These proteins were superior in estimating disease progression risk when compared to Breslow thickness and mitotic rate. Conclusions and Significance: Identification of biomarkers in early stage cutaneous head and neck melanoma is an important step towards predicting metastatic potential and prognosis of the disease. Clinical confirmation and further validation of the proteins identified in this study would provide a novel tool for identifying patients at risk for developing metastatic disease.
2019-11-27 | PXD015137 | Pride
Project description:The implication of epigenetic alterations in the pathogenesis of melanoma is increasingly recognized. Here we performed genome-wide DNA methylation analysis of primary cutaneous melanoma and benign melanocytic naevus interrogating 14,495 genes using beadchip technology. This first genome-wide view of promoter methylation in primary cutaneous melanoma revealed an array of recurrent DNA methylation alterations with potential diagnostic applications. Among 106 frequently hypermethylated genes there were many novel methylation targets and tumor suppressor genes. Highly recurrent methylation of the HOXA9, MAPK13, CDH11, PLEKHG6, PPP1R3C and CLDN11genes was established. Promoter methylation of MAPK13, encoding p38?, was present in 67% of primary and 85% of metastatic melanomas. Restoration of MAPK13 expression in melanoma cells exhibiting epigenetic silencing of this gene reduced proliferation, indicative of tumor suppressive functions. This study demonstrates that DNA methylation alterations are widespread in melanoma and suggests that epigenetic silencing of MAPK13 contributes to melanoma progression. Bisulphite converted genomic DNA from 5 fresh-frozen benign naevus and 24 fresh-frozen primary melanoma biopsy samples were hybridised to Illumina's Infinium HumanMethylation27 Beadchips
2013-04-24 | E-GEOD-45266 | biostudies-arrayexpress
Project description:Large Congenital Melanocytic Naevi have a higher propensity to malignant transformation compared to acquired naevi. They thus represent a good model for studying initial steps of melanocarcinogenesis. We have performed genotypic (karyotype, FISH and mutational analyses) and differential expression studies on a large cohort of medium (n=3) and large (n=24) congenital melanocytic naevi. Unlike malignant melanoma, chromosomal abnormalities were rare and single, a feature probably reflecting the benignity of these lesions. Mutational screening showed a high frequency of NRAS mutations in our series, while BRAF mutations were less common. Differential expression study between tumoral and normal melanocytes did not show significant alterations of cellular processes such as cell proliferation, cell migration/invasion, angiogenesis, apoptosis, and immune/inflammatory responses. However, significant down-regulation of genes involved in pigmentation and up-regulation of genes playing a role in DNA protection were observed. Lastly, our micro-arrays displayed up-regulation of genes mediating chemoresistance in cancer. As alteration of pigmentation mechanisms can trigger oxidative damage, increased expression of genes involved in maintenance of DNA integrity might reflect the ability of naevocytic cells to self protection against cellular stress. Furthermore, the observed alterations linked to chemoresistance might partially account for the well known inefficacy of chemotherapy in malignant melanoma. Keywords: cell type comparison
2008-07-01 | GSE8525 | GEO
Project description:The most common mutation in human melanoma, BRAF(V600E), activates the serine/threonine kinase BRAF and causes excessive activity in the mitogen-activated protein kinase pathway. BRAF(V600E) mutations are also present in benign melanocytic naevi, highlighting the importance of additional genetic alterations in the genesis of malignant tumours. Such changes include recurrent copy number variations that result in the amplification of oncogenes. For certain amplifications, the large number of genes in the interval has precluded an understanding of the cooperating oncogenic events. Here we have used a zebrafish melanoma model to test genes in a recurrently amplified region of chromosome 1 for the ability to cooperate with BRAF(V600E) and accelerate melanoma. SETDB1, an enzyme that methylates histone H3 on lysine 9 (H3K9), was found to accelerate melanoma formation significantly in zebrafish. Chromatin immunoprecipitation coupled with massively parallel DNA sequencing and gene expression analyses uncovered genes, including HOX genes, that are transcriptionally dysregulated in response to increased levels of SETDB1. Our studies establish SETDB1 as an oncogene in melanoma and underscore the role of chromatin factors in regulating tumorigenesis. ChIP was performed from short-term cultures of WM262 and WM451Lu cells.
2011-03-25 | E-GEOD-28170 | biostudies-arrayexpress
Project description:Human melanomas frequently harbor amplifications of EZH2. However, the oncogenic contribution of this methyltransferase to melanoma formation has remained elusive. Taking advantage of murine melanoma models, we now show that EZH2 drives tumorigenesis from benign BrafV600E or NrasQ61K-expressing melanocytes. EZH2 oncogenicity results from silencing of genes relevant for the integrity of the primary cilium, a signaling organelle projecting from the surface of vertebrate cells. Consequently, gain of EZH2 function promotes loss of primary cilia in benign melanocytic lesions. In contrast, blockade of EZH2 activity evokes ciliogenesis and cilia-dependent growth inhibition in malignant melanoma. Finally, we demonstrate that loss of cilia enhances pro-tumorigenic WNT/β-catenin signaling and is itself sufficient to drive metastatic melanoma in benign cells. Thus, primary cilia deconstruction is a key process in EZH2-driven melanomagenesis.
2019-04-04 | GSE112677 | GEO
Project description:The implication of epigenetic alterations in the pathogenesis of melanoma is increasingly recognized. Here we performed genome-wide DNA methylation analysis of primary cutaneous melanoma and benign melanocytic naevus interrogating 14,495 genes using beadchip technology. This first genome-wide view of promoter methylation in primary cutaneous melanoma revealed an array of recurrent DNA methylation alterations with potential diagnostic applications. Among 106 frequently hypermethylated genes there were many novel methylation targets and tumor suppressor genes. Highly recurrent methylation of the HOXA9, MAPK13, CDH11, PLEKHG6, PPP1R3C and CLDN11genes was established. Promoter methylation of MAPK13, encoding p38?, was present in 67% of primary and 85% of metastatic melanomas. Restoration of MAPK13 expression in melanoma cells exhibiting epigenetic silencing of this gene reduced proliferation, indicative of tumor suppressive functions. This study demonstrates that DNA methylation alterations are widespread in melanoma and suggests that epigenetic silencing of MAPK13 contributes to melanoma progression.
2013-04-24 | GSE45266 | GEO
Project description:To identify improved molecular markers to support histological examination we used microarray analysis of formalin-fixed and paraffin-embedded samples from different stages of melanomagenesis to identify differentially expressed microRNAs. Total RNA were obtained from isolated 19 human cell lines and 52 FFPE human samples. Cells include 2 immortalised melanocytes, 4 ovarian cancer cell lines and 13 melanoma cell lines. 61 FFPE samples include 11 benign naevi, 20 primary and 21 metastatic melanoma
2012-02-08 | E-GEOD-35579 | biostudies-arrayexpress