[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100627449":3},{"organization":4,"armGroups":7,"interventions":7,"overallOfficials":7,"centralContacts":7,"locations":8,"responsibleParty":27,"collaborators":7,"id":30,"slug":7,"hasResults":31,"nctId":32,"briefTitle":33,"officialTitle":33,"acronym":34,"eligibilityCriteria":35,"healthyVolunteers":31,"sex":36,"minAge":37,"maxAge":38,"enrollmentInfo":39,"targetDuration":7,"studyType":42,"phases":7,"briefSummary":43,"conditions":44,"keywords":7,"overallStatus":10,"whyStopped":7,"lastUpdateSubmitDate":49,"lastUpdatePostDateStruct":50,"startDateStruct":53,"completionDateStruct":55,"leadSponsor":57,"locationsCount":58},{"fullName":5,"class":6},"Fondazione IRCCS Policlinico San Matteo di Pavia","OTHER",null,[9],{"facility":5,"status":10,"city":11,"state":12,"zip":13,"country":14,"cosmosGeoPoint":15,"geoPoint":20,"contacts":21},"RECRUITING","Pavia","PV","27100","Italy",{"type":16,"coordinates":17},"Point",[18,19],9.15917,45.19205,{"lat":19,"lon":18},[22],{"name":23,"role":24,"phone":25,"phoneExt":7,"email":26},"Alice Nevone, PhD","CONTACT","+390382502967","a.nevone@smatteo.pv.it",{"type":28,"investigatorFullName":29,"investigatorTitle":29,"investigatorAffiliation":5,"oldNameTitle":7,"oldOrganization":7},"PRINCIPAL_INVESTIGATOR","Alice Nevone","100627449",false,"NCT07448779","Investigating the Pathogenic Role of N-glycosylation in AL Amyloidosis: Molecular Bases, Diagnosis, and Treatment","GlycAL","Inclusion Criteria:\n\n* Diagnosis of monoclonal gammopathy (e.g. AL amyloidosis, MGUS, MM, others)\n* Planned peripheral blood sampling +\u002F- bone marrow aspiration\n* Age \\> 18 years\n* Willingness to allow use of clinical data and diagnostic leftovers of clinical specimens for research purposes through signing a written informed consent.\n\nExclusion Criteria:\n\n* Lack of monoclonal gammopathy\n* Patients fulfilling the criteria for complete hematologic response after anti-clonal therapy\n* Age \\\u003C18 years\n* Failure to show willingness to allow use of clinical data and diagnostic leftovers of clinical specimens for research purposes.","ALL","18 Years","99 Years",{"count":40,"type":41},100,"ESTIMATED","OBSERVATIONAL","Immunoglobulin light chain (AL) amyloidosis is caused by a typically small, minimally proliferating bone marrow plasma cell clone secreting a patient-unique, unstable, aggregation-prone, toxic light chain (LC). The amyloidogenicity of LCs is encrypted in their sequence, yet molecular determinants of LC pathogenicity remain obscure. N-glycosylation has been long suspected to be a determinant of LC amyloidogenicity based on anecdotal reports of individual AL patients with a clonal LC displaying this post-translational modification. It is hypothesized that N-glycosylation fundamentally contributes to determining the amyloidogenicity of immunoglobulin LCs in a subset of patients with AL and might influence its clinical phenotype. It is further proposed that the synthesis and secretion of unstable LCs that also have to be N-glycosylated might reverberate on the biology of the plasma cell clone, possibly modulating the sensitivity toward different drugs and might represent itself a therapeutic target.\n\nThe objective of our study is now to elucidate the molecular role of LC N-glycosylation in AL amyloidosis, exploit it for risk assessment, and define its potential impact on the biology of the underlying plasma cell clone and its drug sensitivity.",[45,46,47,48],"AL Amyloidosis","MGUS","Multiple Myeloma","Monoclonal Gammopathies","2026-02-25",{"date":51,"type":52},"2026-03-04","ACTUAL",{"date":54,"type":52},"2025-11-17",{"date":56,"type":41},"2027-05-30",{"name":5,"class":6},1]