{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:21:05Z","timestamp":1784557265563,"version":"3.55.0"},"reference-count":29,"publisher":"Bioscientifica","issue":"10","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,8,14]]},"abstract":"<jats:p>\n                    Gastrointestinal stromal tumors (GISTs) are mesenchymal neoplasms, believed to originate from the interstitial cells of Cajal (ICC), often caused by overexpression of tyrosine kinase receptors (TKR) KIT or PDGFRA. Here, we present evidence that the embryonic stem cell factor\n                    <jats:italic>FOXD3<\/jats:italic>\n                    , first identified as \u2018Genesis\u2019 and involved in both gastrointestinal and neural crest cell development, is implicated in GIST pathogenesis; its involvement is investigated both\n                    <jats:italic>in vitro<\/jats:italic>\n                    and in zebrafish and a mouse model of FOXD3 deficiency. Samples from a total of 58 patients with wild-type GISTs were used for molecular analyses, including Sanger sequencing, comparative genomic hybridization, and methylation analysis. Immunohistochemistry and western blot evaluation were used to assess FOXD3 expression. Additionally, we conducted\n                    <jats:italic>in vitro<\/jats:italic>\n                    functional studies in tissue samples and in transfected cells to confirm the pathogenicity of the identified genetic variants. Germline partially inactivating\n                    <jats:italic>FOXD3<\/jats:italic>\n                    sequence variants (p.R54H and p.Ala88_Gly91del) were found in patients with isolated GISTs. Chromosome 1p loss was the most frequent chromosomal abnormality identified in tumors.\n                    <jats:italic>In vitro<\/jats:italic>\n                    experiments demonstrate the impairment of FOXD3 in the presence of those variants. Animal studies showed disruption of the GI neural network and changes in the number and distribution in the ICC. FOXD3 suppresses KIT expression in human cells; its inactivation led to an increase in ICC in zebrafish, as well as mice, providing evidence for a functional link between\n                    <jats:italic>FOXD3<\/jats:italic>\n                    defects and KIT overexpression leading to GIST formation.\n                  <\/jats:p>","DOI":"10.1530\/erc-23-0067","type":"journal-article","created":{"date-parts":[[2023,8,14]],"date-time":"2023-08-14T08:52:05Z","timestamp":1692003125000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-8","source":"Crossref","is-referenced-by-count":5,"title":["Embryonic stem cell factor FOXD3 (Genesis) defects in gastrointestinal stromal tumors"],"prefix":"10.1530","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7959-9842","authenticated-orcid":true,"given":"Fabio R","family":"Faucz","sequence":"first","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anelia D","family":"Horvath","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Physiology, School of Medicine and Health Sciences, The George Washington University, Washington, District of Columbia, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guillaume","family":"Assi\u00e9","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Cit\u00e9, CNRS UMR8104, INSERM U1016, Institut Cochin, Paris, France"},{"name":"Endocrine Department, Center for Rare Adrenal Diseases, AP-HP, H\u00f4pital Cochin, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madson Q","family":"Almeida","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"},{"name":"Adrenal Unit, Laboratory of Molecular and Cellular Endocrinology LIM\/25, Division of Endocrinology and Metabolism, University of Sao Paulo Medical School, S\u00e3o Paulo, Brasil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Szarek","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sosipatros","family":"Boikos","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Angelousi","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isaac","family":"Levy","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea G","family":"Maria","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ajay","family":"Chitnis","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Genetics, Section on Neural Developmental Dynamics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristina R","family":"Antonescu","sequence":"additional","affiliation":[{"name":"Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rainer","family":"Claus","sequence":"additional","affiliation":[{"name":"Hematology and Oncology, Medical Faculty, University of Augsburg, Augsburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00e9r\u00f4me","family":"Bertherat","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Cit\u00e9, CNRS UMR8104, INSERM U1016, Institut Cochin, Paris, France"},{"name":"Endocrine Department, Center for Rare Adrenal Diseases, AP-HP, H\u00f4pital Cochin, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2554-3952","authenticated-orcid":true,"given":"Christoph","family":"Plass","sequence":"additional","affiliation":[{"name":"Division of Cancer Epigenomics, German Cancer Research Center, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3693-5145","authenticated-orcid":true,"given":"Charis","family":"Eng","sequence":"additional","affiliation":[{"name":"Genomic Medicine Institute, Lerner Research Institute, and Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, United States of America"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4058-5520","authenticated-orcid":true,"given":"Constantine A","family":"Stratakis","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, Program on Developmental Endocrinology & Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America"},{"name":"Human Genetics & Precision Medicine, IMBB, Foundation for Research & Technology Hellas, Heraklion, Crete, Greece"},{"name":"Research Institute, ELPEN, Pikermi, Athens, Greece"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"American Journal of Human Genetics","first-page":"903","article-title":"SNP arrays in heterogeneous tissue: highly accurate collection of both germline and somatic genetic information from unpaired single tumor samples","volume":"82","author":"Assie","year":"2008","unstructured":"Assie GLaFramboise TPlatzer PBertherat JStratakis CA & Eng C2008SNP arrays in heterogeneous tissue: highly accurate collection of both germline and somatic genetic information from unpaired single tumor samples. American Journal of Human Genetics82903\u2013915. (https:\/\/doi.org\/10.1016\/j.ajhg.2008.01.012)"},{"key":"bib2","series-title":"JAMA Oncology","first-page":"922","article-title":"Molecular subtypes of KIT\/PDGFRA wild-type gastrointestinal stromal tumors: a report from the National Institutes of Health gastrointestinal stromal tumor clinic","volume":"2","author":"Boikos","year":"2016","unstructured":"Boikos SAPappo ASKillian JKLaQuaglia MPWeldon CBGeorge STrent JCvon Mehren MWright JASchiffman JD, 2016Molecular subtypes of KIT\/PDGFRA wild-type gastrointestinal stromal tumors: a report from the National Institutes of Health gastrointestinal stromal tumor clinic. JAMA Oncology2922\u2013928. (https:\/\/doi.org\/10.1001\/jamaoncol.2016.0256)"},{"key":"bib3","series-title":"Journal of Clinical Endocrinology and Metabolism","first-page":"3656","article-title":"Carney triad: a syndrome featuring paraganglionic, adrenocortical, and possibly other endocrine tumors","volume":"94","author":"Carney","year":"2009","unstructured":"Carney JA2009Carney triad: a syndrome featuring paraganglionic, adrenocortical, and possibly other endocrine tumors. Journal of Clinical Endocrinology and Metabolism943656\u20133662. (https:\/\/doi.org\/10.1210\/jc.2009-1156)"},{"key":"bib4","series-title":"Developmental Dynamics","first-page":"875","article-title":"Kit and foxd3 genetically interact to regulate melanophore survival in zebrafish","volume":"238","author":"Cooper","year":"2009","unstructured":"Cooper CDLinbo TH & Raible DW2009Kit and foxd3 genetically interact to regulate melanophore survival in zebrafish. Developmental Dynamics238875\u2013886. (https:\/\/doi.org\/10.1002\/dvdy.21910)"},{"key":"bib5","series-title":"Genes, Chromosomes and Cancer","first-page":"412","article-title":"FGFR2::TACC2 fusion as a novel KIT-independent mechanism of targeted therapy failure in a multidrug-resistant gastrointestinal stromal tumor","volume":"61","author":"Dermawan","year":"2022","unstructured":"Dermawan JKVanderbilt CMChang JCUntch BRSinger SChi PTap WD & Antonescu CR2022FGFR2::TACC2 fusion as a novel KIT-independent mechanism of targeted therapy failure in a multidrug-resistant gastrointestinal stromal tumor. Genes, Chromosomes and Cancer61412\u2013419. (https:\/\/doi.org\/10.1002\/gcc.23030)"},{"key":"bib6","series-title":"Cancer Genetics and Cytogenetics","first-page":"30","article-title":"Consistent DNA losses on the short arm of chromosome 1 in a series of malignant gastrointestinal stromal tumors","volume":"127","author":"Derre","year":"2001","unstructured":"Derre JLagace RTerrier PSastre X & Aurias A2001Consistent DNA losses on the short arm of chromosome 1 in a series of malignant gastrointestinal stromal tumors. Cancer Genetics and Cytogenetics12730\u201333. (https:\/\/doi.org\/10.1016\/s0165-4608(0000409-x)"},{"key":"bib7","series-title":"Proceedings of the National Academy of Sciences of the United States of America","first-page":"15785","article-title":"Quantitative high-throughput analysis of DNA methylation patterns by base-specific cleavage and mass spectrometry","volume":"102","author":"Ehrich","year":"2005","unstructured":"Ehrich MNelson MRStanssens PZabeau MLiloglou TXinarianos GCantor CRField JK & van den Boom D2005Quantitative high-throughput analysis of DNA methylation patterns by base-specific cleavage and mass spectrometry. Proceedings of the National Academy of Sciences of the United States of America10215785\u201315790. (https:\/\/doi.org\/10.1073\/pnas.0507816102)"},{"key":"bib8","series-title":"Cancer Research","first-page":"3899","article-title":"DNA sequence copy number changes in gastrointestinal stromal tumors: tumor progression and prognostic significance","volume":"60","author":"El-Rifai","year":"2000","unstructured":"El-Rifai WSarlomo-Rikala MAndersson LCKnuutila S & Miettinen M2000DNA sequence copy number changes in gastrointestinal stromal tumors: tumor progression and prognostic significance. Cancer Research603899\u20133903."},{"key":"bib9","series-title":"Journal of Clinical Endocrinology and Metabolism","first-page":"E135","article-title":"Phosphodiesterase 11A (PDE11A) genetic variants may increase susceptibility to prostatic cancer","volume":"96","author":"Faucz","year":"2011","unstructured":"Faucz FRHorvath ARothenbuhler AAlmeida MQLibe RRaffin-Sanson MLBertherat JCarraro DMSoares FAMolina Gde C, 2011Phosphodiesterase 11A (PDE11A) genetic variants may increase susceptibility to prostatic cancer. Journal of Clinical Endocrinology and Metabolism96E135\u2013E140. (https:\/\/doi.org\/10.1210\/jc.2010-1655)"},{"key":"bib10","series-title":"Endocrine-Related Cancer","first-page":"R49","article-title":"Classification of gastrointestinal stromal tumor syndromes","volume":"25","author":"Gopie","year":"2018","unstructured":"Gopie PMei LFaber ACGrossman SRSmith SC & Boikos SA2018Classification of gastrointestinal stromal tumor syndromes. Endocrine-Related Cancer25R49\u2013R58. (https:\/\/doi.org\/10.1530\/ERC-17-0329)"},{"key":"bib11","series-title":"Proceedings of the National Academy of Sciences of the United States of America","first-page":"3663","article-title":"The embryonic stem cell transcription factors Oct-4 and FoxD3 interact to regulate endodermal-specific promoter expression","volume":"99","author":"Guo","year":"2002","unstructured":"Guo YCosta RRamsey HStarnes TVance GRobertson KKelley MReinbold RScholer H & Hromas R2002The embryonic stem cell transcription factors Oct-4 and FoxD3 interact to regulate endodermal-specific promoter expression. Proceedings of the National Academy of Sciences of the United States of America993663\u20133667. (https:\/\/doi.org\/10.1073\/pnas.062041099)"},{"key":"bib12","series-title":"Genes and Development","first-page":"2650","article-title":"Requirement for Foxd3 in maintaining pluripotent cells of the early mouse embryo","volume":"16","author":"Hanna","year":"2002","unstructured":"Hanna LAForeman RKTarasenko IAKessler DS & Labosky PA2002Requirement for Foxd3 in maintaining pluripotent cells of the early mouse embryo. Genes and Development162650\u20132661. (https:\/\/doi.org\/10.1101\/gad.1020502)"},{"key":"bib13","series-title":"Experimental and Molecular Pathology","first-page":"374","article-title":"Hypermethylation of FOXD3 suppresses cell proliferation, invasion and metastasis in hepatocellular carcinoma","volume":"99","author":"He","year":"2015","unstructured":"He GHu SZhang DWu PZhu XXin SLu GDing Y & Liang L2015Hypermethylation of FOXD3 suppresses cell proliferation, invasion and metastasis in hepatocellular carcinoma. Experimental and Molecular Pathology99374\u2013382. (https:\/\/doi.org\/10.1016\/j.yexmp.2015.06.017)"},{"key":"bib14","series-title":"American Journal of Pathology","first-page":"1259","article-title":"Gastrointestinal pacemaker cell tumor (GIPACT): gastrointestinal stromal tumors show phenotypic characteristics of the interstitial cells of Cajal","volume":"152","author":"Kindblom","year":"1998","unstructured":"Kindblom LGRemotti HEAldenborg F & Meis-Kindblom JM1998Gastrointestinal pacemaker cell tumor (GIPACT): gastrointestinal stromal tumors show phenotypic characteristics of the interstitial cells of Cajal. American Journal of Pathology1521259\u20131269."},{"key":"bib15","series-title":"Developmental Cell","first-page":"608","article-title":"From pioneer to repressor: bimodal foxd3 activity dynamically remodels neural crest regulatory landscape in vivo","volume":"47","author":"Lukoseviciute","year":"2018","unstructured":"Lukoseviciute MGavriouchkina DWilliams RMHochgreb-Hagele TSenanayake UChong-Morrison VThongjuea SRepapi EMead A & Sauka-Spengler T2018From pioneer to repressor: bimodal foxd3 activity dynamically remodels neural crest regulatory landscape in vivo. Developmental Cell47608\u2013628.e606. (https:\/\/doi.org\/10.1016\/j.devcel.2018.11.009)"},{"key":"bib16","series-title":"Cancer Cell International","first-page":"44","article-title":"FOXD3 may be a new cellular target biomarker as a hypermethylation gene in human ovarian cancer","volume":"19","author":"Luo","year":"2019","unstructured":"Luo GFChen CYWang JYue HYTian YYang PLi YK & Li Y2019FOXD3 may be a new cellular target biomarker as a hypermethylation gene in human ovarian cancer. Cancer Cell International1944. (https:\/\/doi.org\/10.1186\/s12935-019-0755-8)"},{"key":"bib17","series-title":"Frontiers in Oncology","first-page":"884814","article-title":"Identification of a novel FGFR2-KIAA1217 fusion in esophageal gastrointestinal stromal tumours: a case report","volume":"12","author":"Luo","year":"2022","unstructured":"Luo YWu YChang XHuang BLuo DZhang JZhang PShi HFan J & Nie X2022Identification of a novel FGFR2-KIAA1217 fusion in esophageal gastrointestinal stromal tumours: a case report. Frontiers in Oncology12884814. (https:\/\/doi.org\/10.3389\/fonc.2022.884814)"},{"key":"bib18","series-title":"Journal of Clinical Endocrinology and Metabolism","first-page":"2938","article-title":"Genetics of carney triad: recurrent losses at chromosome 1 but lack of germline mutations in genes associated with paragangliomas and gastrointestinal stromal tumors","volume":"92","author":"Matyakhina","year":"2007","unstructured":"Matyakhina LBei TAMcWhinney SRPasini BCameron SGunawan BStergiopoulos SGBoikos SMuchow MDutra A, 2007Genetics of carney triad: recurrent losses at chromosome 1 but lack of germline mutations in genes associated with paragangliomas and gastrointestinal stromal tumors. Journal of Clinical Endocrinology and Metabolism922938\u20132943. (https:\/\/doi.org\/10.1210\/jc.2007-0797)"},{"key":"bib19","series-title":"New England Journal of Medicine","first-page":"1054","article-title":"Familial gastrointestinal stromal tumors and germ-line mutations","volume":"357","author":"McWhinney","year":"2007","unstructured":"McWhinney SRPasini BStratakis CA & International Carney Triad and Carney-Stratakis Syndrome Consortium2007Familial gastrointestinal stromal tumors and germ-line mutations. New England Journal of Medicine3571054\u20131056. (https:\/\/doi.org\/10.1056\/NEJMc071191)"},{"key":"bib20","series-title":"Archives of Pathology and Laboratory Medicine","first-page":"1466","article-title":"Gastrointestinal stromal tumors: review on morphology, molecular pathology, prognosis, and differential diagnosis","volume":"130","author":"Miettinen","year":"2006","unstructured":"Miettinen M & Lasota J2006Gastrointestinal stromal tumors: review on morphology, molecular pathology, prognosis, and differential diagnosis. Archives of Pathology and Laboratory Medicine1301466\u20131478. (https:\/\/doi.org\/10.5858\/2006-130-1466-GSTROM)"},{"key":"bib21","series-title":"Journal of Biological Chemistry","first-page":"1573","article-title":"Dual blockade of cyclic AMP response element- (CRE) and AP-1-directed transcription by CRE-transcription factor decoy oligonucleotide. gene-specific inhibition of tumor growth","volume":"274","author":"Park","year":"1999","unstructured":"Park YGNesterova MAgrawal S & Cho-Chung YS1999Dual blockade of cyclic AMP response element- (CRE) and AP-1-directed transcription by CRE-transcription factor decoy oligonucleotide. gene-specific inhibition of tumor growth. Journal of Biological Chemistry2741573\u20131580. (https:\/\/doi.org\/10.1074\/jbc.274.3.1573)"},{"key":"bib22","series-title":"Journal of Neuroscience Methods","first-page":"108720","article-title":"A new methodological approach for in vitro determination of the role of DNA methylation on transcription factor binding using AlphaScreen(R) analysis: focus on CREB1 binding at hBDNF promoter IV","volume":"341","author":"Sabatucci","year":"2020","unstructured":"Sabatucci ABerchet VBellia FMaccarrone MDainese ED'Addario C & Pucci M2020A new methodological approach for in vitro determination of the role of DNA methylation on transcription factor binding using AlphaScreen(R) analysis: focus on CREB1 binding at hBDNF promoter IV. Journal of Neuroscience Methods341108720. (https:\/\/doi.org\/10.1016\/j.jneumeth.2020.108720)"},{"key":"bib23","series-title":"BioTechniques","first-page":"374","article-title":"TM4: a free, open-source system for microarray data management and analysis","volume":"34","author":"Saeed","year":"2003","unstructured":"Saeed AISharov VWhite JLi JLiang WBhagabati NBraisted JKlapa MCurrier TThiagarajan M, 2003TM4: a free, open-source system for microarray data management and analysis. BioTechniques34374\u2013378. (https:\/\/doi.org\/10.2144\/03342mt01)"},{"key":"bib24","series-title":"Developmental Biology","first-page":"174","article-title":"Zebrafish foxd3 is selectively required for neural crest specification, migration and survival","volume":"292","author":"Stewart","year":"2006","unstructured":"Stewart RAArduini BLBerghmans SGeorge REKanki JPHenion PD & Look AT2006Zebrafish foxd3 is selectively required for neural crest specification, migration and survival. Developmental Biology292174\u2013188. (https:\/\/doi.org\/10.1016\/j.ydbio.2005.12.035)"},{"key":"bib25","series-title":"Journal of Physiology","first-page":"1185","article-title":"Hypothalamic input is required for development of normal numbers of thyrotrophs and gonadotrophs, but not other anterior pituitary cells in late gestation sheep","volume":"586","author":"Szarek","year":"2008","unstructured":"Szarek EFarrand KMcMillen ICYoung IRHoughton D & Schwartz J2008Hypothalamic input is required for development of normal numbers of thyrotrophs and gonadotrophs, but not other anterior pituitary cells in late gestation sheep. Journal of Physiology5861185\u20131194. (https:\/\/doi.org\/10.1113\/jphysiol.2007.141523)"},{"key":"bib26","series-title":"Development","first-page":"1615","article-title":"Requirement for Foxd3 in the maintenance of neural crest progenitors","volume":"135","author":"Teng","year":"2008","unstructured":"Teng LMundell NAFrist AYWang Q & Labosky PA2008Requirement for Foxd3 in the maintenance of neural crest progenitors. Development1351615\u20131624. (https:\/\/doi.org\/10.1242\/dev.012179)"},{"key":"bib27","series-title":"Experimental Biology and Medicine","doi-asserted-by":"crossref","first-page":"327","DOI":"10.1007\/978-981-13-1117-8","article-title":"FOXD3\/FOXD4 is required for the development of hindgut in the rat model of anorectal malformation","volume":"243","author":"Wang","year":"2018","unstructured":"Wang LJWang WLGao HBai YZ & Zhang SC2018FOXD3\/FOXD4 is required for the development of hindgut in the rat model of anorectal malformation. Experimental Biology and Medicine243327\u2013333. (https:\/\/doi.org\/10.1177\/1535370217751073)"},{"key":"bib28","series-title":"Biochimica et Biophysica Acta. Molecular Cell Research","first-page":"118531","article-title":"Tuning FOXD3 expression dose-dependently balances human embryonic stem cells between pluripotency and meso-endoderm fates","volume":"1866","author":"Xiao","year":"2019","unstructured":"Xiao LShan YMa LDunk CYu Y & Wei Y2019Tuning FOXD3 expression dose-dependently balances human embryonic stem cells between pluripotency and meso-endoderm fates. Biochimica et Biophysica Acta. Molecular Cell Research1866118531. (https:\/\/doi.org\/10.1016\/j.bbamcr.2019.118531)"},{"key":"bib29","series-title":"Carcinogenesis","first-page":"1253","article-title":"FOXD3, frequently methylated in colorectal cancer, acts as a tumor suppressor and induces tumor cell apoptosis under ER stress via p53","volume":"41","author":"Xu","year":"2019","unstructured":"Xu MZhu JLiu SWang CShi QKuang YFang X & Hu X2019FOXD3, frequently methylated in colorectal cancer, acts as a tumor suppressor and induces tumor cell apoptosis under ER stress via p53. Carcinogenesis411253\u20131262. (https:\/\/doi.org\/10.1093\/carcin\/bgz198)"}],"container-title":["Endocrine-Related Cancer"],"original-title":[],"link":[{"URL":"https:\/\/erc.bioscientifica.com\/view\/journals\/erc\/30\/10\/ERC-23-0067.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/erc.bioscientifica.com\/view\/journals\/erc\/30\/10\/ERC-23-0067.xml","content-type":"text\/html","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/erc.bioscientifica.com\/view\/journals\/erc\/30\/10\/ERC-23-0067.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:56:37Z","timestamp":1784555797000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/erc\/article\/25789"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2023,8,14]]},"references-count":29,"journal-issue":{"issue":"10"},"URL":"https:\/\/doi.org\/10.1530\/erc-23-0067","relation":{},"ISSN":["1351-0088","1479-6821"],"issn-type":[{"value":"1351-0088","type":"print"},{"value":"1479-6821","type":"electronic"}],"subject":[],"published":{"date-parts":[[2023,8,14]]}}}