{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE295nnn/GSE295678/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE295678"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Sensory neurons drive pancreatic cancer progression through glutamatergic cancer-neuron pseudo-synapses.","description":"The results provide significant insights into the role of Grin2D in regulating the secretion of neurotrophic factors that promote neuritogenesis. Transcriptomic analysis of orthotopically transplanted PDAC cancer cells with a knockout of the NMDA receptor subunit Grin2D, along with dorsal root ganglia (T8–T12) innervating the pancreas, strongly supports this conclusion. Furthermore, RNA-Seq analysis of tumor and ganglion biopsies from PDAC patients was performed to validate the identified gene candidates in a human context. This study tested the hypothesis that neuronal glutamate drives pancreatic cancer progression via glutamate-mediated GluN2D signaling at the cancer-neuron pseudo-synapses.","dates":{"publication":"2026/06/01"},"accession":"GSE295678","cross_references":{"GSM":["GSM8954989","GSM8954988","GSM8954985","GSM8954984","GSM8954987","GSM8954986"],"GPL":["34284"],"GSE":["295678"],"taxon":["Homo sapiens"]}}