Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA148563 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The genomic landscape of small intestine neuroendocrine tumors [CGH]
| PRJNA193189 | ENA
Project description:ScRNA-seq of Small Intestine Neuroendocrine Tumors
| PRJNA1237312 | ENA
Project description:The radiolabelled somatostatin analogue 177Lu-octreotate is a promising treatment option for malignant neuroendocrine tumors that overexpress somatostatin receptors. The human small intestine neuroendocrine tumor cell line GOT1 and Medullary thyroid carcinoma model GOT2 have shown promising treatment response to 177Lu-octreotate in xenografted mice. In clinical studies, however, only low cure rates have been achieved to date. In xenografted tumors, the human stromal components have been replaced with mouse stroma, which may have an impact in the treatment response of the xenografts.
2017-12-31 | GSE80021 | GEO
Project description:Small Bowel Neuroendocrine Tumors (Carcinoid Tumors)
| PRJNA185381 | ENA
Project description:Alternative poladenylation of tumor suppressor genes in small intestinal neuroendocrine tumors
| PRJNA244234 | ENA
Project description:Small cell lung carcinoma (SCLC) and large cell neuroendocrine carcinoma (LCNEC) are high-grade pulmonary neuroendocrine tumors. The neural basic helix-loop-helix (bHLH) transcription factors ASCL1 and NEUROD1 have been shown to play crucial roles in promoting the malignant behavior and survival of human SCLC cell lines. In this study, we find ASCL1 and NEUROD1 identify distinct neuroendocrine tumors, bind distinct genomic loci, and regulate mostly distinct genes. ASCL1 and NEUROD1 are often bound in super-enhancers that are associated with highly expressed genes in their respective SCLC cell lines suggesting different cell lineage of origin for these tumors. ASCL1 targets oncogenic genes such as MYCL1, RET, and NFIB, while NEUROD1 targets the oncogenic gene MYC. Although ASCL1 and NEUROD1 regulate different genes, many of these gene targets commonly contribute to neuroendocrine and cell migration function. ASCL1 in particular also regulates genes in the NOTCH pathway and genes important in cell-cycle dynamics. Finally, we demonstrate ASCL1 but not NEUROD1 is required for SCLC and LCNEC tumor formation in current in vivo genetic mouse models of pulmonary neuroendocrine tumors RNA-seq analysis performed on two ASCL1high and two NEUROD1high human SCLC cell lines to identify gene expression patterns in these cells. Also, we performed RNA-seq in mouse neuroendocrine lung tumors obtained from Trp53;Rb1;Rbl2 triple knockout model mice treated with Adeno-CMVCRE intratracheally.
2016-07-21 | E-GEOD-69393 | biostudies-arrayexpress
Project description:Small intestine neuroendocrine tumors are the commonest neuroendocrine tumors of the GI tract. Next gen sequencing of the whole exome was undertaken to identify SNPs and SCNA in these tumor samples. Subsequent bioinformatic anlaysis was done where the reads ratios of tumor/normal were log2 tranformed, segments indentified with DNAcopy (R package) and regions of SCNA were identified. Amplification of chr 4, 5, 14 and 20 was observed. The validation of these SCNAs was done with arrayCGH. The results of array CGH is in concordeance with the exome sequencing data.
2013-03-16 | GSE45190 | GEO
Project description:Small cell lung carcinoma (SCLC) and large cell neuroendocrine carcinoma (LCNEC) are high-grade pulmonary neuroendocrine tumors. The neural basic helix-loop-helix (bHLH) transcription factors ASCL1 and NEUROD1 have been shown to play crucial roles in promoting the malignant behavior and survival of human SCLC cell lines. In this study, we find ASCL1 and NEUROD1 identify distinct neuroendocrine tumors, bind distinct genomic loci, and regulate mostly distinct genes. ASCL1 and NEUROD1 are often bound in super-enhancers that are associated with highly expressed genes in their respective SCLC cell lines suggesting different cell lineage of origin for these tumors. ASCL1 targets oncogenic genes such as MYCL1, RET, and NFIB, while NEUROD1 targets the oncogenic gene MYC. Although ASCL1 and NEUROD1 regulate different genes, many of these gene targets commonly contribute to neuroendocrine and cell migration function. ASCL1 in particular also regulates genes in the NOTCH pathway and genes important in cell-cycle dynamics. Finally, we demonstrate ASCL1 but not NEUROD1 is required for SCLC and LCNEC tumor formation in current in vivo genetic mouse models of pulmonary neuroendocrine tumors ChIP-seq analysis performed on three ASCL1high and two NEUROD1high human SCLC cell lines to identify ASCL1 and/or NEUROD1 binding sites in these two types of cells. Also, we performed ChIP-seq for Ascl1 binding sites in mouse neuroendocrine lung tumors obtained from Trp53;Rb1;Rbl2 triple knockout model mice treated with Adeno-CMVCRE intratracheally.
2016-07-21 | E-GEOD-69394 | biostudies-arrayexpress
Project description:The management of neuroendocrine tumors (NETs) is very variable, depending on many specific aspects, such as the type of tumor, spread and patient general health. Several advances have been made with the newly developed somatostatin analogues to cure this type of malignancies. Somatostain analogues such as octreotide have been used in clinic to treat patients with neuroendocrine tumors (NETs). However, the molecular mechanism leading either to successful therapy or acquired resistance to the analogues is still to large extent unclear. Patients develop drugs resistance during a long term treatment. Therefore, to identify the pivotal regulatory genes involved in the development of drug resistance is an actual challenge. We studied five human neuroendocrine tumor cell lines, CNDT2.5, KRJ1, QGP-1, NCI H720 and NCI H727. We also investigated a long-term treated CNDT2.5 by using octreotide. We performed gene expression profiling in all the human neuroendocrine cell lines. Keywords: Gene Expression profiling, treatment comparison
2012-12-12 | GSE24358 | GEO
Project description:Small intestine neuroendocrine tumors are the commonest neuroendocrine tumors of the GI tract. Next gen sequencing of the whole exome was undertaken to identify SNPs and SCNA in these tumor samples. Subsequent bioinformatic anlaysis was done where the reads ratios of tumor/normal were log2 tranformed, segments indentified with DNAcopy (R package) and regions of SCNA were identified. Amplification of chr 4, 5, 14 and 20 was observed. The validation of these SCNAs was done with arrayCGH. The results of array CGH is in concordeance with the exome sequencing data. DNA from matched tumor and normal sample of SI-NETs was done by spin column method. Libraries were constructed and exome enriched for next gen sequencing. The same gDNA was hybridized with Cy5 and Cy3 and subsequent analysis was done. This study represents the CGH portion of the study.
2013-03-16 | E-GEOD-45190 | biostudies-arrayexpress