Project description:To clarify the mechanism of cisplatin resistance in testicular germ cell tumor (TGCT), cisplatin-resistant TGCT cells (N8R and G9R) were generated from parental NEC8 cells (N8P) and TGCT patient-derived cells (TGCT-PDC)(G9P), respectively, by culture in medium containing cisplatin. We used microarrays to detail the global programme of gene expression underlying cisplatin resistance and identified up- and down-regulated genes during this process.
Project description:Normal, premalignant and various histological subtypes of testicular germ cell tumor (TGCT) tissues were hybridized against Universal Human Reference RNA (Stratagene) onto Agilent 60mer oligo microarrays (GEO accession no GPL885). In vitro time series of two TGCT cell lines, NTERA2 and 2102Ep, treated with retinoic acid for 0, 3, and 7 days were also included. The data set (30 hybridizations) is particularly useful for comparisons between various histological subtypes of TGCT versus each other or versus normal testis. Keywords = 2102Ep Keywords = Agilent oligo microarrays Keywords = carcinoma in situ Keywords = choriocarcinoma Keywords = development Keywords = developmental biology Keywords = differenciation Keywords = embryogenesis Keywords = embryonal carcinoma Keywords = homo sapiens Keywords = human Keywords = human development Keywords = intratubular germ cell tumor Keywords = nonseminoma Keywords = NTera2 Keywords = pluripotency Keywords = pluripotent Keywords = retinoic acid Keywords = seminoma Keywords = teratocarcinoma Keywords = teratoma Keywords = testis Keywords = testicular germ cell tumor Keywords = testicular neoplasm Keywords = totipotency Keywords = totipotent Keywords = undifferentiated Keywords = universal human reference RNA (Stratagene) Keywords = yolk sac tumor Keywords: other
Project description:RNA-seq analysis of two Testicular Germ Cell Cancers (TGCC) of patients with chemotherapy-resistant disease. Purpose of the study was to resolve the early development and progression of the disease by whole genome sequencing, RNA-seq and methylation profiling of the primary tumor, and the targeted sequencing of purified tumor components (embryonal carcinoma (EC), teratoma (TE), and yolk sac tumor (YST), precursor lesion (Germ Cell Neoplasia In Situ (GCNIS)), and metastases. Whole genome sequencing for the two patients, T6107 and T3209, have been deposited with the European Nucleotide Archive under project accession number PRJEB20644 / study accession ERP022815 ( http://www.ebi.ac.uk/ena/data/search?query=ERP022815 ).
Project description:Patient-derived cancer cells (PDCs) were established by three-dimensional (3D) spheroid culture from testicular germ cell tumor (GCT) specimens. Microarray expression analysis revealed that cancer stem-like cell-related genes were upregulated in 3D culture condition compared with two-dimensional (2D) culture condition.
Project description:Genomic screening was performed for one family containing MZ twins with testicular germ cell tumors, in order to define alterations associated with risk of tumor development.
Project description:To investigate the role of the testicular germ cell tumor cells in complex traits, we generated ATAC-seq and Promoter Focused Capture C to gain insight into the gene regulatory arcitecture contacting promoters in an testicular cell line NT2-D1 model of testicular cancer
Project description:To investigate the role of the testicular germ cell tumor cells in complex traits, we generated ATAC-seq and Promoter Focused Capture C to gain insight into the gene regulatory arcitecture contacting promoters in an ttesticular cell line NT2-D1 model of testicular cancer
Project description:Chromosome substitution strains (CSS or consomic strains) are useful for mapping phenotypes to chromosomes. However, huge efforts are needed to identify the gene(s) responsible for the phenotype in the complex context of the chromosome. Here, we report the identification of candidate disease genes from a CSS using a combination of genetic and genomic approaches as well as by using knowledge about the germ cell tumor disease etiology. We utilized the CSS, 129.MOLF-Chr 19 chromosome substitution strain (or M19), in which males develop germ cell tumors of the testes at an extremely high rate. We are able to identify 3 protein-coding genes and 1 microRNA on chromosome 19 that have previously not been implicated to be testicular tumor susceptibility genes. Our findings suggest that changes in gene expression levels in the gonadal tissues of multiple genes from Chr 19 likely contribute to the high TGCT incidence of the M19 strain. Our data advances the use of CSS to identify disease susceptibility genes and demonstrates that the 129.MOLF-Chr 19 strain serves as a useful model to elucidate the genetics and biology of germ cell transformation and tumor development.