180f0e08-bd99-4871-81a8-1c800e9124db - samples
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ABSTRACT:
PROVIDER: EGAD00001007587 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:In this prospective study, targeted deep sequencing was performed on a total of 160 primary tumors (474 regions) and 112 lymph nodes from 125 patients with stage I-III lung cancer (LuCaTH). Progressive evolution at clonal divergence scale was observed while specific driver events were positively selected for clonal sweeps during tumor development. Between-region genetic divergence (BRGD) of tumors were assessed and positively correlated with tumor differentiation. A machine learning algorithm was employed to evaluate clinicopathological and molecular parameters of primary tumors underlying lymph node metastasis. By analyzing clonal lineages and metastatic trajectories across multiple nodal stations, we unraveled a common sequential LNM seeding pattern but with divergent modes of clonal spread.
| EGAS00001005242 | EGA
Project description:Genomes of closely-related species or populations often display localized regions of enhanced relative sequence divergence, termed genomic islands. It has been proposed that these islands arise through selective sweeps and/or barriers to gene flow. Here, we genetically dissect a genomic island that controls flower color pattern differences between two subspecies of Antirrhinum, A.m.striatum and A.m.pseudomajus, and relate it to clinal variation across a natural hybrid zone. We show that selective sweeps likely raised relative divergence at two tightly-linked MYB-like transcription factors, leading to distinct flower patterns in the two subspecies. The two patterns provide alternate floral guides and create a strong barrier to gene flow where populations come into contact. This barrier affects the selected flower color genes and tightly linked loci, but does not extend outside of this domain, allowing gene flow to lower relative divergence for the rest of the chromosome. Thus, both selective sweeps and barriers to gene flow play a role in shaping genomic islands: sweeps cause elevation in relative divergence while heterogeneous gene flow flattens the surrounding “sea”, making the island of divergence stand out. By showing how selective sweeps establish alternative adaptive phenotypes that lead to barriers to gene flow, our study sheds light on possible mechanisms leading to reproductive isolation and speciation.
2018-08-18 | GSE118621 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE34280: Clonal Selection Drives Genetic Divergence of Metastatic Medulloblastoma [Affymetrix SNP6 Arrays] GSE34355: Clonal Selection Drives Genetic Divergence of Metastatic Medulloblastoma [Illumina Infinium HumanMethylation27 Beadchip v1.2] Refer to individual Series
2011-12-13 | E-GEOD-34356 | biostudies-arrayexpress
Project description:Poly I:C is a powerful immune adjuvant as a result of its agonist activities on TLR-3, MDA5 and RIG-I. Intratumoral administration is conceivably safer than systemic delivery and allows concentrate proinflammatory adjuvanticity in the tumor microenvironment and tumor-draining lymphoid tissue. BO-112 is a nanoplexed formulation of Poly I:C complexed with polyethylenimine that causes tumor cell apoptosis showing immunogenic cell death features and that upon intratumoral release results in more prominent tumor infiltration by T lymphocytes. Intratumoral treatment of subcutaneous tumors derived from MC38, 4T1 and B16F10 with BO-112 leads to remarkable local disease control mediated by CD8+ T lymphocytes, as concluded from selective depletion experiments. Some degree of control of non-injected tumor lesions upon BO-112 intratumoral treatment was found in mice bearing bilateral B16OVA melanomas, that was enhanced when co-treated with systemic anti-CD137 and anti-PD-L1 immunomodulatory mAbs. More abundant CD8+ T lymphocytes were found in tumor-draining lymph nodes and in the tumor microenvironment following intratumoral treatment with BO-112. Enhanced numbers of tumor-specific CTLs recognizing melanosomal antigens and ovalbumin were readily detected among them. Genome-wide transcriptome analyses of injected tumor lesions were consistent with a marked upregulation of the type-I interferon pathway. Intratumorally delivered BO-112 is being tested in cancer patients (NCT02828098) and our results in mice suggest prominent anti-tumor local control through its proimmune effects. To compare the in-vitro and in vivo transcriptional profile induced by BO-112, B16-OVA cell lines were incubated with BO-112 for 24h. BO-112 induces a specific transcriptional profile in B16-OVA cell cultures. Key immunoregulatory genes were found to be differentially expressed between BO-112 and Vehicle-incubated B16-OVA cells.
2019-05-15 | GSE116075 | GEO
Project description:A multicompartmental model consisting of four submodules: the lungs, the upper airways, and the corresponding lymph nodes for both submodules. The model is made up of 35 differential equations (including ODEs and DDEs) and 112 parameters.
2025-03-07 | MODEL2503040001 | BioModels
Project description:We used massively parallel tagging of progenitors to track clonal relationships and transcriptomic signatures during murine forebrain development. We found several examples of clonal divergence and convergence in both neurons and glia, and examined the processes that led to clonal divergence of GABAergic neurons. Immediately after exiting the cell-cycle, GABAergic neurons originating from the same mitotic progenitor diverged into different trajectories, suggesting that differentiation into subtypes is initiated as a lineage-dependent processes at the progenitor cell level.
2021-12-15 | GSE188528 | GEO
Project description:Poly I:C is a powerful immune adjuvant as a result of its agonist activities on TLR-3, MDA5 and RIG-I. Intratumoral administration is conceivably safer than systemic delivery and allows concentrate proinflammatory adjuvanticity in the tumor microenvironment and tumor-draining lymphoid tissue. BO-112 is a nanoplexed formulation of Poly I:C complexed with polyethylenimine that causes tumor cell apoptosis showing immunogenic cell death features and that upon intratumoral release results in more prominent tumor infiltration by T lymphocytes. Intratumoral treatment of subcutaneous tumors derived from MC38, 4T1 and B16F10 with BO-112 leads to remarkable local disease control mediated by CD8+ T lymphocytes, as concluded from selective depletion experiments. Some degree of control of non-injected tumor lesions upon BO-112 intratumoral treatment was found in mice bearing bilateral B16OVA melanomas, that was enhanced when co-treated with systemic anti-CD137 and anti-PD-L1 immunomodulatory mAbs. More abundant CD8+ T lymphocytes were found in tumor-draining lymph nodes and in the tumor microenvironment following intratumoral treatment with BO-112. Enhanced numbers of tumor-specific CTLs recognizing melanosomal antigens and ovalbumin were readily detected among them. Genome-wide transcriptome analyses of injected tumor lesions were consistent with a marked upregulation of the type-I interferon pathway. Intratumorally delivered BO-112 is being tested in cancer patients (NCT02828098) and our results in mice suggest prominent anti-tumor local control through its proimmune effects. Intratumoral administration of BO-112, a nanoplexed form of PolyI:C, triggers an efficacious antitumor response in different tumor models as a consequence of proimmflamatory activity and its direct effects in tumor cells. BO-112 local administration induces direct tumor cell death by apoptosis, showing signs of immunogenic cell death, and a strong release of IFNα/β and other proinflammatory mediators. As a result, a tumor-specific CD8+ immune response is mounted or augmented to the point of controlling tumor progression both in the locally injected lesion and to some extent on distantly implanted tumor nodules
2019-05-15 | GSE116074 | GEO
Project description:Purpose: Metastasis remains the primary cause of prostate cancer (CaP) related death. Here, we investigate the molecular, pathologic, and clinical outcome associations of EphA6 expression and its role in CaP progression and metastasis.Experimental Design: The gene expression profiling of Eph receptors (Ephs) and their ephrin ligands was performed in CaP cell lines by real-time RT-PCR. Metastatic potential of EphA6 gene was analyzed by RNAi approaches in a spontaneous CaP mouse model. The mRNA expression of EphA6 was measured in 58 benign prostate hyperplasia (BPH) and 112 CaP samples. Results: Among the tested Ephs and ligands, EphA6 is the only consistently overexpressed member in CaP lymph node metastatic cells. EphA6 knock-down (KD) in human PC-3M cells causes decreased invasion in vitro and reduced lung and lymph node metastasis in vivo. In addition, KD of EphA6 decreases tube formation in vitro and angiogenesis in vivo. Studies on the clinical samples demonstrate that EphA6 is overexpressed in the CaP tumor tissues compared with those from BPH patients. The correlation was identified between EphA6 expression and vascular invasion (P=0.004), neural invasion (P=0.002), PSA level (P=0.013), and TNM staging (P=0.021) in 112 CaP cases.Further, genome-wide gene expression analysis in KD of EphA6 cells identified a panel of genes, such as PIK3IPA, AKT1, and EIF5A2, which could be associated with EphA6-regulated cancer progression. Conclusions: These findings identify EphA6 as a potentially novel metastasis gene, and increased EphA6 mRNA expression positively correlates with CaP progression. The mechanisms to inhibit EphA6 expression might suppress CaP metastatic aggressiveness. Knock-down of EphA6 induced gene expression in human prostate cell:PC-3M/shEphA6-1, PC3M/shControl, CWR22rv1/shEphA6-1, and CWR22rv1/shControl cell line.
2015-02-27 | E-GEOD-66335 | biostudies-arrayexpress
Project description:Purpose: Metastasis remains the primary cause of prostate cancer (CaP) related death. Here, we investigate the molecular, pathologic, and clinical outcome associations of EphA6 expression and its role in CaP progression and metastasis.Experimental Design: The gene expression profiling of Eph receptors (Ephs) and their ephrin ligands was performed in CaP cell lines by real-time RT-PCR. Metastatic potential of EphA6 gene was analyzed by RNAi approaches in a spontaneous CaP mouse model. The mRNA expression of EphA6 was measured in 58 benign prostate hyperplasia (BPH) and 112 CaP samples. Results: Among the tested Ephs and ligands, EphA6 is the only consistently overexpressed member in CaP lymph node metastatic cells. EphA6 knock-down (KD) in human PC-3M cells causes decreased invasion in vitro and reduced lung and lymph node metastasis in vivo. In addition, KD of EphA6 decreases tube formation in vitro and angiogenesis in vivo. Studies on the clinical samples demonstrate that EphA6 is overexpressed in the CaP tumor tissues compared with those from BPH patients. The correlation was identified between EphA6 expression and vascular invasion (P=0.004), neural invasion (P=0.002), PSA level (P=0.013), and TNM staging (P=0.021) in 112 CaP cases.Further, genome-wide gene expression analysis in KD of EphA6 cells identified a panel of genes, such as PIK3IPA, AKT1, and EIF5A2, which could be associated with EphA6-regulated cancer progression. Conclusions: These findings identify EphA6 as a potentially novel metastasis gene, and increased EphA6 mRNA expression positively correlates with CaP progression. The mechanisms to inhibit EphA6 expression might suppress CaP metastatic aggressiveness.
2015-02-27 | GSE66335 | GEO
Project description:Divergence of K-562 genomes through in vitro clonal evolution revealed by comparing three sublines. Comparison of three K-562 sublines
2024-01-01 | GSE243782 | GEO