[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100627449":3},{"organization":4,"armGroups":7,"interventions":7,"overallOfficials":7,"centralContacts":7,"locations":8,"responsibleParty":28,"collaborators":7,"id":31,"slug":32,"hasResults":33,"nctId":34,"briefTitle":35,"officialTitle":35,"acronym":36,"eligibilityCriteria":37,"healthyVolunteers":33,"sex":38,"minAge":39,"maxAge":40,"enrollmentInfo":41,"targetDuration":7,"studyType":44,"phases":7,"briefSummary":45,"conditions":46,"keywords":7,"overallStatus":10,"whyStopped":7,"lastUpdateSubmitDate":51,"lastUpdatePostDateStruct":52,"startDateStruct":55,"completionDateStruct":57,"leadSponsor":59,"locationsCount":60},{"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,"countryCode":15,"cosmosGeoPoint":16,"geoPoint":21,"contacts":22},"RECRUITING","Pavia","PV","27100","Italy","IT",{"type":17,"coordinates":18},"Point",[19,20],9.15917,45.19205,{"lat":20,"lon":19},[23],{"name":24,"role":25,"phone":26,"phoneExt":7,"email":27},"Alice Nevone, PhD","CONTACT","+390382502967","a.nevone@smatteo.pv.it",{"type":29,"investigatorFullName":30,"investigatorTitle":30,"investigatorAffiliation":5,"oldNameTitle":7,"oldOrganization":7},"PRINCIPAL_INVESTIGATOR","Alice Nevone","100627449","investigating-the-pathogenic-role-of-n-glycosylation-in-al-amyloidosis-molecular-bases-diagnosis-and-treatment-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":42,"type":43},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.",[47,48,49,50],"AL Amyloidosis","MGUS","Multiple Myeloma","Monoclonal Gammopathies","2026-02-25",{"date":53,"type":54},"2026-03-04","ACTUAL",{"date":56,"type":54},"2025-11-17",{"date":58,"type":43},"2027-05-30",{"name":5,"class":6},1]