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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

ABSTRACT: Two percent of children with Neuroblastoma, a pediatric solid tumor of the peripheral nerve ganglia, develop Opsoclonus Myoclonus Ataxia Syndrome (OMAS), a paraneoplastic disease characterized by devastating cerebellar and brainstem-directed autoimmunity, but typically with outstanding cancer-related outcomes. Here, we compared tumor transcriptomes and tumor infiltrating T- and B-cell repertoires from a cohort of OMAS subjects with neuroblastoma to a set of controls from 13 low- and 13 high-risk non-OMAS associated neuroblastoma tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189367 | GEO | 2023/08/01

REPOSITORIES: GEO

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

Project description:Two percent of children with Neuroblastoma, a pediatric solid tumor of the peripheral nerve ganglia, develop Opsoclonus Myoclonus Ataxia Syndrome (OMAS), a paraneoplastic disease characterized by devastating cerebellar and brainstem-directed autoimmunity, but typically with outstanding cancer-related outcomes. Here, we compared tumor transcriptomes and tumor infiltrating T- and B-cell repertoires from a cohort of OMAS subjects with neuroblastoma to a set of controls from 13 low- and 13 high-risk non-OMAS associated neuroblastoma tumors.

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-01 | GSE189743 | GEO

Mechanistic characterization of a Drosophila model of paraneoplastic nephrotic syndrome

Project description:Purpose: Paraneoplastic syndromes occur in cancer patients and originate from dysfunction of organs at a distance from the tumor or its metastasis. In this study, using a Drosophila gut tumor model, we characterized a mechanism of tumor-induced kidney dysfunction. Methods: snRNA-seq analysis of MT samples with and without Yki gut tumors and snRNA-seq analysis of MT samples with kidney principal cell-specific disregulation of PDGF/VEGF signaling Results: we found that Pvf1, a PDGF/VEGF signaling ligand, secreted by gut tumors activates the PvR/JNK/Jra signaling pathway in the principal cells of the kidney, leading to mis-expression of renal genes and paraneoplastic renal syndrome-like phenotypes Conclusions: Our study describes a novel mechanism by which gut tumors perturb the function of the kidney, which might be of clinical relevance for the treatment of paraneoplastic syndromes.

2024-01-18 | GSE251715 | GEO

Next generation sequencing identifies paraneoplastic effects of tumor-derived FGF19 on murine liver transcriptomes

Project description:Purpose. Despite having excellent prognosis when detected early, colorectal cancer (CRC) remains a leading cause of cancer-related deaths globally. Barriers to screening reduces compliance and negatively impacts patient outcomes, necessitating alternatives. A blood-based approach provides a more convenient and accessible modality, but serum markers are lacking. Using a meta-transcriptomics approach, we identified Fibroblast Growth Factor 19 (FGF19), an enteroendocrine FGF responsible for bile acid (BA) homeostasis, as an attractive CRC marker. However, whether FGF19 is aberrantly secreted into blood by colorectal tumors or induces endocrine-like paraneoplastic effects is unknown. Methods. To test if colorectal tumors contribute FGF19 into blood, subcutaneous xenografts of HCT116 and Colo201 cells were established in four male and female NSG mice. Tumor volume, as well as serum and urine FGF19 were assessed over 36 days. Following euthanasia, murine liver was processed for downstream mRNA and bile acid quantification. To determine global paraneoplastic effects of malignant FGF19 on its primary target organ (liver), hepatic mRNA was isolated and subjected to RNA sequencing on an Illumina NovaSeq 6000 system. Reads were processed, aligned, mapped, and analyzed for differential expression and functional enrichment using an integrated informatics pipeline implemented in R. Results. Circulating FGF19 levels derived from subcutaneous xenografts of Colo201, but not HCT116, cells exerted paraneoplastic effects on liver including suppression of BA synthesis, dysregulation of cholesterol metabolism, and induction of pre-neoplasia. Conclusion. Here we report novel paraneoplastic effects of tumor derived FGF19 on liver tissue. Study limitations include in vivo experimentation using two different cell lines, and significant gender-related batch effects in RNA sequencing data.

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Paraneoplastic neuronal intermediate filament autoimmunity.

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| S-EPMC6207411 | biostudies-literature

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