Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma
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PROVIDER: PRJNA784301 | ENA |
REPOSITORIES: ENA
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Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]
| PRJNA784303 | ENA
Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]
| PRJNA782665 | ENA
Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]
| PRJNA784304 | ENA
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.
2023-08-01 | GSE189742 | GEO
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.
2023-08-01 | GSE189741 | GEO
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.
2023-08-01 | GSE189367 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-08-01 | GSE189743 | GEO
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
Project description:ObjectiveTo describe paraneoplastic neuronal intermediate filament (NIF) autoimmunity.MethodsArchived patient and control serum and CSF specimens were evaluated by tissue-based indirect immunofluorescence assay (IFA). Autoantigens were identified by Western blot and mass spectrometry. NIF specificity was confirmed by dual tissue section staining and 5 recombinant NIF-specific HEK293 cell-based assays (CBAs, for α-internexin, neurofilament light [NfL], neurofilament medium, or neurofilament heavy chain, and peripherin). NIF-immunoglobulin Gs (IgGs) were correlated with neurologic syndromes and cancers.ResultsAmong 65 patients, NIF-IgG-positive by IFA and CBAs, 33 were female (51%). Median symptom onset age was 62 years (range 18-88). Patients fell into 2 groups, defined by the presence of NfL-IgG (21 patients, who mostly had ≥4 NIF-IgGs detected) or its absence (44 patients, who mostly had ≤2 NIF-IgGs detected). Among NfL-IgG-positive patients, 19/21 had ≥1 subacute onset CNS disorders: cerebellar ataxia (11), encephalopathy (11), or myelopathy (2). Cancers were detected in 16 of 21 patients (77%): carcinomas of neuroendocrine lineage (10) being most common (small cell [5], Merkel cell [3], other neuroendocrine [2]). Two of 257 controls (0.8%, both with small cell carcinoma) were positive by both IFA and CBA. Five of 7 patients with immunotherapy data improved. By comparison, the 44 NfL-IgG-negative patients had findings of unclear significance: diverse nervous system disorders (p = 0.006), as well as limited (p = 0.003) and more diverse (p < 0.0001) cancer accompaniments.ConclusionsNIF-IgG detection by IFA, with confirmatory CBA testing that yields a profile including NfL-IgG, defines a paraneoplastic CNS disorder (usually ataxia or encephalopathy) accompanying neuroendocrine lineage neoplasia.
| S-EPMC6207411 | biostudies-literature
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.
2021-11-15 | GSE188745 | GEO