Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA169503 | ENA |
REPOSITORIES: ENA
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Project description:autologous pairs of cutaneous melanocyte and melanoma cell cultures
2015-07-28 | E-GEOD-38312 | ExpressionAtlas
Project description:Cisplatin treated melanoma and melanocyte cell lines
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Project description:To explore the roles of cell-type specific methylation QTL (meQTL) for melanoma GWAS annotation, we generated DNA methylation data from the same sample set as our previouse eQTL study including 106 primary melanocyte cultures. The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 480,000 CpGs in 106 primary melanocyte cultures. To be able to identify the DNA methylation probes whose methylation levels are correlated with germline genetic variants including the ones associated with melanoma, meQTL analysis was performed in these 106 primary melanocyte cultures using the same method as we did for eQTL study.
2021-10-01 | GSE166069 | GEO
Project description:Melanoblastoma-bearing Libechov minipigs (MeLiM) provide an animal model for the study of spontaneous cutaneous melanoma. We compared the serial analysis of gene expression (SAGE) profile between normal skin melanocytes and melanoma cells from a pulmonary metastasis of MeLiM. Keywords: disease state study To minimise the contribution of cells other than melanocytes, we constructed SAGE libraries from a primary culture of melanoma cells derived from a pulmonary melanoma metastasis of a young MeLiM and from a pigmented melanocyte cell line, PigMel, derived from the skin of a healthy Meishan pig.
2008-05-07 | E-GEOD-5982 | biostudies-arrayexpress
Project description:Expression data from human choroidal melanocyte cultures
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Project description:Gene expression data from melanoma cell lines and melanocyte controls
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Project description:Kynureninase is a member of a large family of catalytically diverse but structurally homologous pyridoxal 5'-phosphate (PLP) dependent enzymes known as the aspartate aminotransferase superfamily or alpha-family. The Homo sapiens and other eukaryotic constitutive kynureninases preferentially catalyze the hydrolytic cleavage of 3-hydroxy-l-kynurenine to produce 3-hydroxyanthranilate and l-alanine, while l-kynurenine is the substrate of many prokaryotic inducible kynureninases. The human enzyme was cloned with an N-terminal hexahistidine tag, expressed, and purified from a bacterial expression system using Ni metal ion affinity chromatography. Kinetic characterization of the recombinant enzyme reveals classic Michaelis-Menten behavior, with a Km of 28.3 +/- 1.9 microM and a specific activity of 1.75 micromol min-1 mg-1 for 3-hydroxy-dl-kynurenine. Crystals of recombinant kynureninase that diffracted to 2.0 A were obtained, and the atomic structure of the PLP-bound holoenzyme was determined by molecular replacement using the Pseudomonas fluorescens kynureninase structure (PDB entry 1qz9) as the phasing model. A structural superposition with the P. fluorescens kynureninase revealed that these two structures resemble the "open" and "closed" conformations of aspartate aminotransferase. The comparison illustrates the dynamic nature of these proteins' small domains and reveals a role for Arg-434 similar to its role in other AAT alpha-family members. Docking of 3-hydroxy-l-kynurenine into the human kynureninase active site suggests that Asn-333 and His-102 are involved in substrate binding and molecular discrimination between inducible and constitutive kynureninase substrates.
| S-EPMC2531291 | biostudies-literature
Project description:It is generally accepted that human cancers derive from a mutated single cell. However, the genetic steps characterizing various stages of progression remain unclear. Studying a unique case of metastatic melanoma, we observed that cell lines derived from metachronous metastases arising over a decade retained a central core of genetic stability in spite of divergent phenotypes. In the present study we expanded our previous observations comparing these autologous cell lines of clonal derivation with heterologous ones and correlated array Comparative Genomic Hybridization (aCGH) with gene expression profiling to determine their relative contribution to the dynamics of disease progression. aCGH and gene expression profiling were performed on autologous cell lines and heterologous melanoma cell lines originated from other patients. A striking correlation existed between total extent of genetic imbalances, global transcriptional patterns and cellular phenotypes; they did not follow a strict temporal progression but stemmed independently at various time points from a central core of genetic stability best explained according to the cancer stem cell hypothesis; although their contribution was intertwined, genomic imbalances detectable by aCGH contributed only 25% of the transcriptional traits determining autologous tumors distinctiveness. Our study provides important insights about the dynamics of cancer progression and supports the development of targeted anti-cancer therapies against stable genetic factors determining the individuality of each patientâs disease that are maintained throughout the end stage of disease. Keywords: genetic modification design PBMC from a female donor were Ficoll gradient separated and used throughout the study as reference.. Validation of array CGH accuracy was done by obtaining six additional PBMC from female donors and six PBMC from male donors to confirm stability of gene representation in autosomes and sex-determined imbalances within the X and Y chromosome regions. Five melanoma cell lines were generated from distinct cutaneous melanoma metastases that progressively appeared in patient 888. Other melanoma cell lines were generated from cutaneous melanoma metastases from other patients. The melanoma cell line A375 was purchased from the American Type Culture Collection. For each cell line arrayCGh has been performed.
2010-05-25 | E-GEOD-8777 | biostudies-arrayexpress
Project description:Cutaneous malignant melanoma (CMM) lacks targeted therapies beyond the oft-circumvented BRAF inhibitors. Part of the difficulty in treating melanomas has been attributed to a strong survival program controlled by melanocyte transcription factors such as MITF - a phenomenon first described in melanoma as “lineage dependency.” Recently, a highly selective covalent CDK7 inhibitor (THZ1) has been shown to potently suppress the growth of various cancers through the depletion of master transcription-regulating oncogenes and the disruption of their attendant super-enhancers. We now show that melanoma cells are highly sensitive to CDK7 inhibition and that a melanocyte “lineage cluster,” whose members are transcriptionally driven by super-enhancers, is also strongly suppressed by THZ1. These results point to CDK7 inhibition as a viable strategy to deprive oncogenic transcription and suppress tumor growth in melanoma.
2017-10-23 | GSE75814 | GEO
Project description:MeDIP for ten early passage melanoma cell cultures
| PRJNA248623 | ENA