{"entity":{"id":"lepr","kind":"target","name":"LEPR","aka":["leptin receptor","Leptin receptor","CD295","LEP-R","OB-R"],"tldr":"LEPR (Leptin receptor) is a gene. The public catalogues list it as a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Meningioma.","summary":"Receptor for hormone LEP/leptin. On ligand binding, mediates LEP central and peripheral effects through the activation of different signalling pathways such as JAK2/STAT3 and MAPK cascade/FOS. In the hypothalamus, LEP acts as an appetite-regulating factor that induces a decrease in food intake and an increase in energy consumption by inducing anorexinogenic factors and suppressing orexigenic neuropeptides, also regulates bone mass and secretion of hypothalamo-pituitary-adrenal hormones.\n\nCIViC holds 1 clinical evidence item and 0 assertions across 1 variant.","asOf":"2026-09-23","links":[{"label":"HGNC HGNC:6554","url":"https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:6554"},{"label":"UniProt P48357","url":"https://www.uniprot.org/uniprotkb/P48357/entry"},{"label":"NCBI Gene 3953","url":"https://www.ncbi.nlm.nih.gov/gene/3953"},{"label":"Ensembl ENSG00000116678","url":"https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000116678"}],"tags":["cancer-genes-wave"],"related":["civic"],"cancers":["meningioma"],"sections":[],"technologies":[],"targets":[],"drugs":[],"companies":[],"institutions":[],"pathways":[],"terms":[],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":["Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: CIViC holds 1 clinical evidence items on its variants. Evidence tier \"clinical-evidence\" is the strongest of those signals.","Prevalence not recorded: none of the sources gives a positivity rate."],"provenance":{"editedBy":"scripts/fetch-cancer-genes.ts (CIViC, Open Targets, IntOGen, HGNC, UniProt)","editedOn":"2026-09-23"},"symbol":"LEPR","role":["biomarker"],"evidenceTier":"clinical-evidence","sources":[{"label":"HGNC HGNC:6554","url":"https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:6554","note":"approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)"},{"label":"UniProt P48357","url":"https://www.uniprot.org/uniprotkb/P48357/entry","note":"protein name, function text, keywords and locations (REST API)"},{"label":"CIViC gene LEPR","url":"https://civicdb.org/features/3274","note":"1 evidence items, 0 assertions, 1 variants; diseases: Meningioma (GraphQL API, CC0)"}],"distribution":"one-type","specificityNote":"Specificity not established: no corpus medicine is aimed at it and the catalogues give it only the role biomarker; HPA finds the RNA tissue enriched, which says where the protein sits but not whether the tumour differs from normal tissue. HPA LEPR: RNA tissue enriched (liver 122 nTPM); blood lineage lineage enriched (granulocytes 5 nTPM); high antibody staining in 1 normal tissue. Distribution: 1 cancer family in the corpus carries a prevalence row, label threshold or catalogue link for it (Brain and spinal cord tumours (all types)); Open Targets associates it with 0 specific cancer types at or above 0.5. (No rule of scripts/fetch-target-specificity.ts fired.)","specificitySources":[{"label":"Human Protein Atlas LEPR tissue","url":"https://www.proteinatlas.org/ENSG00000116678-LEPR/tissue","note":"RNA tissue and blood lineage specificity, normal tissue antibody staining (version 25.1, CC BY-SA 3.0)"},{"label":"Open Targets ENSG00000116678 associations","url":"https://platform.opentargets.org/target/ENSG00000116678/associations","note":"cancer associations at or above 0.5 (CC0)"}],"hgnc":"HGNC:6554","ensembl":"ENSG00000116678","uniprot":"P48357","entrez":"3953","firstDescribed":1995,"firstDescribedBasis":"sequence","firstDescribedNote":"Earliest sequence paper UniProt cites for the protein: Tartaglia L.A. et al, Cell, 1995, \"Identification and expression cloning of a leptin receptor, OB-R\".","firstDescribedSource":"https://pubmed.ncbi.nlm.nih.gov/8548812/","biology":"Receptor for hormone LEP/leptin. On ligand binding, mediates LEP central and peripheral effects through the activation of different signalling pathways such as JAK2/STAT3 and MAPK cascade/FOS. In the hypothalamus, LEP acts as an appetite-regulating factor that induces a decrease in food intake and an increase in energy consumption by inducing anorexinogenic factors and suppressing orexigenic neuropeptides, also regulates bone mass and secretion of hypothalamo-pituitary-adrenal hormones. In the periphery, increases basal metabolism, influences reproductive function, regulates pancreatic beta-cell function and insulin secretion, is pro-angiogenic and affects innate and adaptive immunity. Control of energy homeostasis and melanocortin production (stimulation of POMC and full repression of AgRP transcription) is mediated by STAT3 signalling, whereas distinct signals regulate NPY and the control of fertility, growth and glucose homeostasis. Involved in the regulation of counter-regulatory response to hypoglycemia by inhibiting neurons of the parabrachial nucleus. Location: Cell membrane; Basolateral cell membrane; Secreted (UniProt). Locus 1p31.3 (HGNC).","whereFound":["Meningioma: CIViC evidence names this disease"],"targetClass":"other","prevalence":[]},"route":"/targets/lepr/","neighbours":{"collection":[{"id":"civic","kind":"collection","name":"CIViC","route":"/collections/civic/"}],"cancer":[{"id":"meningioma","kind":"cancer","name":"Meningioma","route":"/cancers/meningioma/"}]}}