Mus musculus domesticus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA507341 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8271510.fastq.gz | Fastqsanger.gz | |||
| SRR8271510_1.fastq.gz | Fastqsanger.gz | |||
| SRR8271510_2.fastq.gz | Fastqsanger.gz | |||
| SRR8271511_1.fastq.gz | Fastqsanger.gz | |||
| SRR8271511_2.fastq.gz | Fastqsanger.gz |
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Project description:Small-cell lung carcinoma (SCLC) and large-cell neuroendocrine lung carcinoma (LCNEC) are high-grade lung neuroendocrine tumors (NET). However, comparative protein expression within SCLC and LCNEC remains unclear. Here, protein expression profiles were obtained via mass spectrometry-based proteomic analysis.
2019-05-14 | PXD013583 | JPOST Repository
Project description:Two prognostically significant subtypes of high-grade lung neuroendocrine tumors independent of small-cell and large-cell neuroendocrine carcinomas identified by gene expression profiles. BACKGROUND: Classification of high-grade neuroendocrine tumors (HGNT) of the lung currently recognises large-cell neuroendocrine carcinoma (LCNEC) and small-cell lung carcinoma (SCLC) as distinct groups. However, a similarity in histology for these two carcinomas and uncertain clinical course have led to suggestions that a single HGNT classification would be more appropriate. Gene expression profiling, which can reproduce histopathological classification, and often defines new subclasses with prognostic significance, can be used to resolve HGNT classification. METHODS: We used cDNA microarrays with 40386 elements to analyze the gene expression profiles of 38 surgically resected samples of lung neuroendocrine tumors and 11 SCLC cell lines. Samples of large-cell carcinoma, adenocarcinoma, and normal lung were also included to give a total of 105 samples analyzed. The data were subjected to filtering to yield informative genes before unsupervised hierarchical clustering that identified relatedness of tumor samples. FINDINGS: Distinct groups for carcinoids, large-cell carcinoma, adenocarcinoma, and normal lung were readily identified. However, we were unable to distinguish LCNEC from SCLC by gene expression profiling. Three independent rounds of unsupervised hierarchical clustering consistently divided SCLC samples into two main groups with LCNEC samples largely integrated with these groups. Furthermore, patients in one of the groups identified by clustering had a significantly better clinical outcome than the other (83% vs 12% survived for 5 years; p=0.0094. None of the highly proliferative SCLC cell lines subsequently analyzed clustered with this good-prognosis group. INTERPRETATION: Our findings show that HGNT of the lung can be classified into two groups independent of SCLC and LCNEC. To this end, we have identified many genes, some of which encode well-characterized markers of cancer that distinguish the HGNT groups. These results have implications for the diagnosis, classification, and treatment of lung neuroendocrine tumors, and provide important insights into their underlying biology. Keywords: other
2004-02-10 | E-GEOD-1037 | biostudies-arrayexpress
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 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:Two prognostically significant subtypes of high-grade lung neuroendocrine tumors independent of small-cell and large-cell neuroendocrine carcinomas identified by gene expression profiles. BACKGROUND: Classification of high-grade neuroendocrine tumors (HGNT) of the lung currently recognises large-cell neuroendocrine carcinoma (LCNEC) and small-cell lung carcinoma (SCLC) as distinct groups. However, a similarity in histology for these two carcinomas and uncertain clinical course have led to suggestions that a single HGNT classification would be more appropriate. Gene expression profiling, which can reproduce histopathological classification, and often defines new subclasses with prognostic significance, can be used to resolve HGNT classification. METHODS: We used cDNA microarrays with 40386 elements to analyze the gene expression profiles of 38 surgically resected samples of lung neuroendocrine tumors and 11 SCLC cell lines. Samples of large-cell carcinoma, adenocarcinoma, and normal lung were also included to give a total of 105 samples analyzed. The data were subjected to filtering to yield informative genes before unsupervised hierarchical clustering that identified relatedness of tumor samples. FINDINGS: Distinct groups for carcinoids, large-cell carcinoma, adenocarcinoma, and normal lung were readily identified. However, we were unable to distinguish LCNEC from SCLC by gene expression profiling. Three independent rounds of unsupervised hierarchical clustering consistently divided SCLC samples into two main groups with LCNEC samples largely integrated with these groups. Furthermore, patients in one of the groups identified by clustering had a significantly better clinical outcome than the other (83% vs 12% survived for 5 years; p=0.0094. None of the highly proliferative SCLC cell lines subsequently analyzed clustered with this good-prognosis group. INTERPRETATION: Our findings show that HGNT of the lung can be classified into two groups independent of SCLC and LCNEC. To this end, we have identified many genes, some of which encode well-characterized markers of cancer that distinguish the HGNT groups. These results have implications for the diagnosis, classification, and treatment of lung neuroendocrine tumors, and provide important insights into their underlying biology. Keywords: other
2004-02-11 | GSE1037 | GEO
Project description:Background Neuroendcrine carcinoma (NEC) of lung consists of small-cell lung carcinoma (SCLC) and large cell neuroendocrine carcinoma (LCNEC). Although long-term outcomes of SCLC patients are usually poor, a few patients achieve long-term survivals. Prognostic factors in SCLC have not been fully elucidated. microRNAs (miRNAs) are known to negatively regulate gene expression and to be relevant to tumorigenesis, tumor classification and prognosis. Methods 63 samples (46 neuroendocrine carcinoma including 35 SCLC and 11 LCNEC, 4 adenocarcinoma, 5 squamous cell carcinoma and 8 normal lung) were obtained through surgical resection. miRNA expression in each sample was comprehensively investigated using miRNA microarray. Results Unsupervised hierarchial clustering classified the all NEC into two subgroups, group 1 and 2. Group 1 was felt into an independent branch that consisted of only NEC, whereas group 2 was included in a branch that contained both NEC and non-NEC. Compared with SCLC of group 1 (SCLC 1), SCLC of group 2 (SCLC 2) was a distinct subgroup with surprisingly good prognosis (0% v 79% survived for 5 years; p=0.007). Serum proGRP level was significantly lower in SCLC 2 than in SCLC 1 despite of similar tumor stages between the two groups. Among 12 cases treated by presurgical chemotherapy, PR:NC ratio was 6:3 in SCLC 1 and 2:1 in SCLC 2, suggesting no apparent difference of chemosensitivity. Histologically, distinction between both groups was difficult. Cox regression analysis demonstrated that three miRNA signature was correlated with survival of SCLC patients. These prognostic miRNAs were differentially expressed between SCLC 1 and 2, which were validated by quantitative real time RT-PCR. Bioinformatics analysis predicted that these miRNAs targeted not only genes involving with tumorigenesis but also genes associated with neuroendocrine function. Conclusion miRNA expression profiling identified a distinct subgroup of SCLC with favorable prognosis. This subgroup might have less neuroendocrine character than usual SCLC. All samples were tissue samples obtained by surgical resection. 35 samples of small-cell lung cancer were investigated. 11 samples of larege cell neuroendocrine cancer, 4 samples of adenocarcinoma, 5 samples of squamous cell carcinoma and 8 samples of normal lung were also included as reference.
2013-01-31 | E-GEOD-19945 | biostudies-arrayexpress
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
2016-07-21 | GSE69394 | 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
2016-07-21 | GSE69393 | GEO
Project description:There is a clear need to expand the toolkit of adequate mouse models and cell lines available for preclinical studies of high-grade neuroendocrine lung carcinoma (Small Cell Lung Carcinoma, SCLC and Large Cell Neuroendocrine Carcinoma, LCNEC), two highly aggressive tumor types with dismal prognosis and few therapeutic options. Actually, paucity is extreme in the case of LCNEC. Given the lack of murine cell lines and transplant models of LCNEC the need is imperative/unmet. In this study, we have generated and examined new models of LCNEC and SCLC transplantable cell lines derived from our previously developed primary mouse LCNEC and SCLC tumors. RNA-seq analysis demonstrated that our cell lines and syngeneic tumors maintained the transcriptome program from the original transgenic primary tumor, and display strong similarities to human SCLC or LCNEC. Importantly, the SCLC transplanted cell lines show the ability of metastasize, mimicking this characteristic of the human condition. In summary, we have generated mouse cell line tools that allow further basic and translational research, as well as preclinical testing of new treatment strategies for SCLC and LCNEC, as they retain important features of their human counterparts and address the lack of LCNEC disease models.
2023-10-29 | GSE242422 | GEO
Project description:Lung cancer is the leading cause of cancer mortality and is classified by the World Health Organization into two broad histological subtypes. Non–small cell lung cancer (NSCLC), including adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, accounts for ~85% of all lung cancer cases, with the remaining 15% of cases being due to small cell lung cancer (SCLC), which arises from neuroendocrine cells in the lung. Although most SCLC tumors are initially responsive to chemotherapy and radiation, patients often experience relapse, with the tumor acquiring an aggressiveness and therapeutic resistance that lead to a poor clinical outcome. Improvement of overall survival in individuals with SCLC will require the identification of novel therapeutic targets based on a better understanding of the changes in intracellular signaling of aggressive SCLC cells. The malignant progression of SCLC often occurs concomitantly with the acquisition of chemoresistance, suggesting that phenotypic malignant change is related to adaptation to the stresses induced by chemotherapy. In order to analyze gene expression changes associated with malignant transformation in SCLC, we established a cisplatin-resistant SCLC cell line and performed RNA sequencing.
2021-03-04 | GSE168184 | GEO