dataesr/scientific-paragraphs-categorization huggingface dataset:
Pathway analyses To identify pathways the 126 biomarkers are involved in, we performed analyses based on KEGG, ClueGO, and ConsensusPathDB databases. The findings provided further support for the autoimmune component in dementias. KEGG and ClueGO analyses showed that the identified biomarkers increased MHC-II-mediated antigen presentation in several processes, HLA-DR expression across all hematopoietic cell lines, neuronal adhesion molecule CNTN2, and PD-L1 in T-cell-antigen interactions that reduces self-tolerance. The biomarkers also decreased barrier protecting IL-17F, self-tolerance increasing PDCD1 in T-cell-antigen interactions, and antiviral complement factor B and IFNAR1 (SFigures 4A-H and 5). ConsensusPathDB analyses showed that all of the 42 plasma proteins included in the 126 biomarkers had physical interactions with or were in a biological pathway within zero to two molecule distance from amyloid precursor protein, tau protein, or α-synuclein (SFigure 6A-R).
Inverse probability-weighted analyses To evaluate the autoimmune hypothesis in relation to modifiability and drug repurposing, we used inverse probability-weighted (IPW) analyses in FinnGen and studied whether commonly used antiinflammatory and immunosuppressive medications are likely to reduce the risk of dementias (Table  1 ). 5] [16] [17]  Supporting the autoimmune hypothesis, risk of dementiacausing diseases was reduced with methotrexate and TNF-α inhibitors. Methotrexate appeared to decrease risk only in those with above-average MR-based autoimmune PRS (50% cut-off). To identify rare medications not detectable in FinnGen with sufficient power, we additionally searched the OpenTargets database. This search identified 64 drugs that target 18 of the 126 proteins, suggesting that these may have potential for repurposing to treatment of dementias (SFile 2).
The identified 8 proteins with SNPs located near APOE gene were associated with increased BBB permeability, inflammation, neurotoxicity, and lipid transport disturbances,  42, 56, 69, [81] [82] [83] [84]  which are all processes linked to APOE in Alzheimer's disease. 85 Our results suggest that the 8 proteins may be linked to the effects of APOE. Another novel result was that higher levels of CD33, one of the top GWAS hits for Alzheimer's diseases  86  and target receptor on microglia for an ongoing trial (NCT03822208) including mild to moderate Alzheimer's diseases patients, increased the risk of disease even when expressed on peripheral leukocytes.
Strengths and limitations Our triangulation approach has several strengths. By using a broad set of immune system and BBB biomarkers we were able to study these systems comprehensively without restrictions to specific predefined hypotheses. Our findings are based on MR, a promising approach to examine causality,  12  and on analyses using plasma proteomics, PRS, HLA, pathway, and IPW analyses in two independent cohorts and a range of databases. Plasma protein analyses allowed us to adjust effect estimates for APOE which was not possible in Mendelian randomization analyses for some proteins. PRS and HLA analyses used data from the FinnGen study with a sample size of 340,000 providing sufficient statistical power for the identification of shared novel risk alleles between dementias and autoimmune disease.
We used ConsensusPathDB, which is one of the most comprehensive collection of databases on molecular pathways and interactions. 92 The medication analyses used IPW survival analysis that is suggested to provide more reliable causal estimates than traditional survival analyses of observational data. 93  study has also several limitations. Although we explored over 40,000 biomarkers related to the immune system and BBB, we may have missed some biomarkers due to limitations in search protocol or lack of SNPs. Our plasma protein analyses were limited by lack of data on dementia subtypes. The PRS and PheWAS analyses were done with samples with European ancestry and may not apply to non-European ancestries. Due to limited number of SNPs included in PRS, we may have missed important immune system and BBB related associations in our phenome-wide analyses.
Mendelian randomization The SNPs for biomarkers and outcomes were searched from MR-base database. 94 Immune system and BBB search terms were identified using identifiers of cell types, receptors, proteins, metabolites, and genes. The identifiers were searched from several publications  3, 4, 6, 23, 36, 38, 40, 95, 96  and from Uniprot  97  with search terms "immune" and "blood brain barrier". Outcomes included all cohorts with following diseases: all types of Alzheimer's disease, Parkinson's disease, vascular dementia, frontotemporal dementia, dementia in general, and progression of dementia. (SMethods). Poor cognitive performance was chosen as an intermediate outcome. Two sample MR was used to analyse associations between biomarkers and outcomes. 12 First analyses estimated effects with Wald ratio or inverse variance-weighted analyses.
Polygenic risk score and IPW analyses FinnGen Data Freeze 8 contains 339,233 individuals, and is a collection of prospective epidemiological and disease-based cohorts, and hospital biobank samples and links genotypes by the unique national personal identification numbers to nationwide health registries, including the national hospital discharge (available from 1968), death (1969-), cancer (1953-) and medication reimbursement (1964-) and purchase (1995-) registries. Genotyping and imputation is described in SMethods. PRS was constructed from SNPs that were associated with the 126 MR identified causal biomarkers for dementias. The SNPs were LD-pruned with clumping cut-off R 2 = 0. 01 in 500kb window with R package TwoSampleMR. The available SNPs were searched from FinnGen genotypes and the final scores were generated with PLINK v2.
00aLM3 by calculating the SNP-biomarker beta weighted sum of risk alleles for each SNP. The PRS was scaled to zero mean and unit variance, and we analysed its phenome-wide associations across 2401 disease endpoints. The association between PRS and endpoints were studied with logistic regression, adjusting for birth year, sex, and ten first principal components of ancestry. The IPW analyses  93  were done in FinnGen and included participants aged over 45 without any dementia-causing disease at baseline (N = 90,512). ATC codes for anti-inflammatory medication use were obtained from linkage to national medication purchase registry (data starts from 1995) and in each analyses we included only new medication users to simulate trial design. 106 A model including a range of baseline and time-varying variables and informative censoring estimated the weights (SMethods).
Data sharing Data, protocols, and other metadata of the Whitehall II and FinnGen studies are available according to the data sharing policies of these studies. Pre-existing data access policy for Whitehall II specify that research data requests can be submitted to each steering committee; these will be promptly reviewed for confidentiality or intellectual property restrictions and will not unreasonably be refused. Detailed information on data sharing can be found here: https://www. ucl. ac. uk/epidemiology-health-care/research/epidemiology-and-publichealth/research/whitehall-ii/data-sharing Individual-level patient or protein data may further be restricted by consent, confidentiality, or privacy laws/considerations. The FinnGen data may be accessed through Finnish Biobanks' FinBB portal (www.
Mendelian randomization analyses The SNPs for biomarkers and outcomes were searched from MR-base database. 1 Immune system and BBB search terms were identified using identifiers of cell types, receptors, proteins, and genes. The identifiers were searched from several publications  [2] [3] [4] [5] [6] [7] [8] [9] [10]  and from Uniprot  11  with search terms "immune" and "blood brain barrier". Outcomes included all cohorts with following dementiacausing diseases: all types of Alzheimer's disease, Parkinson's disease, vascular dementia, frontotemporal dementia, dementia in general, and progression of dementia. Poor cognitive performance was chosen as an intermediate outcome. Two sample Mendelian randomization was used to analyse associations between biomarkers and outcomes. 12 First analyses estimated effects with Wald ratio or inverse variance-weighted analyses.
Plasma proteins and Whitehall II study Plasma protein measurements in Whitehall II study were available for 6,235 individuals of whom 310 developed dementia. The participants are linked to the National Health Services (NHS) Hospital Episode Statistics (HES) database, and the British National mortality register using individual NHS identification numbers for linkage. 14 The NHS provides nearly complete health care coverage for all individuals legally resident in the UK. Incident dementia was defined using the WHO International Classification of Diseases, version 10 (ICD-10) codes F00, F01, F03, G30, and G31 and ICD-9 codes 290. 0-290. 4, 331. 0-331. 2, 331. 82, and 331. 9. We also conducted informant interviews and checked participants' medications at each screening (in 1996-1998, 2011-2013 and 2016-2017) for dementia-related medication.
Sensitivity and specificity of dementia assessment based on HES data is 0. 78 and 0. 92. 15 plasma proteins were measured using the SomaScan version 4. 0 and 4. 1 assays. 4, 16, 17 The assays were validated against external reference population and protein-specific conversion coefficients were used to balance the technical differences between versions 4. 0 and 4. 1. The analyses used plasma samples measured in 1995/1997 and stored in 0. 25 mL aliquots at -80•C. Earlier studies describe performance of the SomaScan assay and the modified aptamer binding in detail. 4, 16, 17 In brief, the assay uses a mix of thousands of slow off-rate modified aptamers (SOMAmers) that bind to proteins in participants' plasma samples where the specificity is ensured with two-step process analogous to a conventional immunoassay.
The specificity of the aptamer reagents is good and has been tested in several ways. 4, 18, 19 Median intra-and inter-assay coefficients of variation for SomaScan version 4 are ~5% and assay sensitivity is comparable to that of typical immunoassays, with a median lower limit of detection in the femtomolar range. In the Whitehall II study, standard self-administered questionnaires provided data on age and sex. Using DNA extracted from whole blood, a standard PCR assay determined APOE genotype using the salting out method. 20, 21 Two blinded independent observers read the genotype and any discrepancies were resolved by repeating the PCR analysis. In analyses, proteins were transformed to a normal distribution by inverse rank-based normal transformation. The follow-up ended at onset of dementia, death, or 1 st of October 2019, which ever occurred first.
Polygenic risk score and IPW analyses FinnGen Data Freeze 8 contains 339,233 individuals, and represents approximately 7% of Finnish adult population. FinnGen is a collection of prospective epidemiological and disease-based cohorts, and hospital biobank samples and links genotypes by the unique national personal identification numbers to nationwide health registries, including the national hospital discharge (available from 1968), death (1969-), cancer (1953-) and medication reimbursement (1964-) and purchase (1995-) registries. The registry-based follow-up ended on Dec 31, 2019. Alzheimer's disease was defined with ICD-10 codes under F00 and G30, ICD-9 codes under 3310, ICD-8 code under 29010, and medication purchase code N06D. Vascular dementia was defined with ICD-10 codes under F01 and ICD-9 codes under 4378.
Parkinson's disease was defined with ICD-10 codes under G20, ICD-9 codes under 3320A, ICD-8 code under 34200, and reimbursements code 110. FinnGen samples were genotyped with Illumina and Affymetrix arrays (Illumina Inc. , San Diego, and Thermo Fisher Scientific, Santa Clara, CA, USA), and genotype calls were made with the GenCall or zCall (for Illumina) and the AxiomGT1 algorithm for Affymetrix data. Individuals with ambiguous gender, high genotype missingness (>5%), excess heterozygosity (+-4SD) and non-Finnish ancestry were excluded, as well as all variants with high missingness (>2%), low Hardy-Weinberg equilibrium p-value (<1e-6) and minor allele count (MAC < 3). Array data pre-phasing was carried out with Eagle 2. 3. 5  23  with the number of conditioning haplotypes set to 20,000. Genotype imputation was done using the population-specific SISu v3 imputation reference with 3,775 high-coverage (25-30x) whole-genome sequences in Finns, described in detail at https://doi.
Pathway analyses KEGG pathway analysis was used for studying the effect of the biomarkers on validated pathways with Generally Applicable Gene-set Enrichment (GAGE),  26  using Mendelian randomization Wald ratios or inverse variance weight betas and p-values as input for expression ratios. GO term enrichment analyses were done with ClueGO version 2. 5. 8  27  in Cytoscape version 3. 7. 2. 28 The hypergeometric test used all the 76 plasma proteins or surface receptors of the 126 biomarkers as input and all immune system and BBB related proteins from Uniprot 11 as background, with correction for 5% FDR. The shortest interaction path analyses were done with ConsensusPathDB,  29  a web based analysis tool containing a range of biomedical databases. ConsensusPathDB was used to decipher the potential common pathways between the biomarkers and amyloid β, tau protein, and α-synuclein.
gov/search? id=%22NCT03597282%22 CHEMBL4297888 APX-005M  Unknown not recruiting https://clinicaltrials. gov/search?id=%22NCT03214250%22CHEMBL2109266 AVE-9633 Antibody CD33 binding agent Binding agent MONDO_0004643 myeloid leukemia 1 Terminated https://clinicaltrials. gov/search?id=%22NCT00543972%22CHEMBL3989989 AXICABTAGENE CILOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent EFO_0000616 neoplasm 3 http://www. whocc. no/atc_ddd_index/?code=L01XX70CHEMBL3989989 AXICABTAGENE CILOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent EFO_0011057 neurotoxicity 2 Recruiting https://clinicaltrials. gov/search?id=%22NCT04150913%22CHEMBL3989989 AXICABTAGENE CILOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent EFO_1001469 Mantle cell lymphoma 2 Active, not recruiting https://clinicaltrials.
gov/search?id=%22NCT02601313%22CHEMBL3989989 AXICABTAGENE CILOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent  EFO_0000096  neoplasm of mature B-cells 1 Active, not recruiting https://clinicaltrials. gov/search?id=%22NCT04314843%22,https://clinicaltrials. gov/search?id=%22NCHEMBL3989989 AXICABTAGENE CILOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent EFO_0000403 diffuse large B-cell lymphoma 1 Active, not recruiting https://clinicaltrials. gov/search?id=%22NCT02926833%22CHEMBL3989989 AXICABTAGENE CILOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent EFO_0000574 lymphoma 1 Recruiting https://clinicaltrials. gov/search?id=%22NCT04608487%22CHEMBL3989989 AXICABTAGENE CILOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent MONDO_0018906 follicular lymphoma 1 Active, not recruiting https://clinicaltrials.
gov/search?id=%22NCT02348216%22CHEMBL3989989 AXICABTAGENE CILOLEUCEL CD19 binding agent Binding agent MONDO_0044889 high grade B-cell lymphoma 1 Active, not recruiting https://clinicaltrials. gov/search?id=%22NCT02348216%22CHEMBL4594618 BREXUCABTAGENE AUTOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent EFO_1001469 Mantle cell lymphoma 2 Active, not recruiting https://clinicaltrials. gov/search?id=%22NCT02601313%22CHEMBL4594618 BREXUCABTAGENE AUTOLEUCEL Gene B-lymphocyte antigen CD19 binding agent Binding agent EFO_0000095 chronic lymphocytic leukemia 1 Active, not recruiting https://clinicaltrials. gov/search?id=%22NCT03624036%22CHEMBL4594618 BREXUCABTAGENE AUTOLEUCEL CD19 binding agent Binding agent EFO_0000220 acute lymphoblastic leukemia 1 Active, not recruiting https://clinicaltrials.
gov/search?id=%22NCT02614066%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0000540 immune system disease 4 http://www. whocc. no/atc_ddd_index/?code=L04AC08CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor Orphanet_208650 Cryopyrin-associated periodic syndrome 4 http://dailymed. nlm. nih. gov/dailymed/drugInfo. cfm?setid=7d271f3b-e4f9-4d80-8dcf-28d49123f80 CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0003106 pneumonia 3 Completed https://clinicaltrials. gov/search?id=%22NCT04362813%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0003914 atherosclerosis 3 Completed https://clinicaltrials. gov/search?id=%22NCT01327846%22CHEMBL1201834 CANAKINUMAB Antibody Terminated https://clinicaltrials.
gov/search?id=%22NCT00886769%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor Orphanet_1451 CINCA syndrome 3 Terminated https://clinicaltrials. gov/search?id=%22NCT00770601%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor DOID_13406 pulmonary sarcoidosis 2 Completed https://clinicaltrials. gov/search?id=%22NCT02888080%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor  EFO_0000275. gov/search?id=%22NCT00947427%22 CHEMBL1201834 CANAKINUMAB Antibody clinicaltrials. gov/search?id=%22NCT00900146%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0002506 osteoarthritis 2 Completed https://clinicaltrials. gov/search?id=%22NCT01160822%22CHEMBL1201834  CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0003780 Behcet 's syndrome 2 Completed https://clinicaltrials.
gov/search?id=%22NCT02756650%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0004214 Abdominal Aortic Aneurysm 2 Terminated https://clinicaltrials. gov/search?id=%22NCT02007252%22CHEMBL1201834 CANAKINUMAB Withdrawn https://clinicaltrials. gov/search?id=%22NCT02980263%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0004265 peripheral arterial disease 2 Terminated https://clinicaltrials. gov/search?id=%22NCT01731990%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0004274 gout 2 Completed https://clinicaltrials. gov/search?id=%22NCT00819585%22,https://clinicaltrials. gov/search?id=%22NCHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0005531 urticaria 2 Unknown status https://clinicaltrials.
gov/search?id=%22NCT01635127%22CHEMBL1201834 CANAKINUMAB 's disease 2 Terminated https://clinicaltrials. gov/search?id=%22NCT02204293%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0008518 polymyalgia rheumatica 2 Terminated https://clinicaltrials. gov/search?id=%22NCT01364389%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_1000906 dry eye syndrome 2 Completed https://clinicaltrials. gov/search?id=%22NCT01250171%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_1001165 Schnitzler syndrome 2 Completed https://clinicaltrials. gov/search?id=%22NCT01390350%22,https://clinicaltrials. gov/search?id=%22NCHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_1001345 Hepatitis, Alcoholic 2 Active, not recruiting https://clinicaltrials.
gov/search?id=%22NCT03775109%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor  HP_0000999 Pyoderma 2  Completed https://clinicaltrials. gov/search?id=%22NCT01302795%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor MONDO_0100096 COVID-19 2 Completed https://clinicaltrials. gov/search?id=%22NCT04365153%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor Orphanet_232 Sickle cell anemia 2 Completed https://clinicaltrials. gov/search?id=%22NCT02961218%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor Orphanet_309025 Mevalonate kinase deficiency 2 Completed https://clinicaltrials. gov/search?id=%22NCT01303380%22CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor Orphanet_342 Familial Mediterranean fever 2 Completed https://clinicaltrials.
gov/search?id=%22NCT01148797%22,https://clinicaltrials. gov/search?id=%22NCHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0000198 myelodysplastic syndrome 1 Recruiting https://clinicaltrials. gov/search?id=%22NCT04810611%22,https://clinicaltrials. gov/search?id=%22NCHEMBL1201834 CANAKINUMAB Antibody. gov/search?id=%22NCT00581945%22 CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor EFO_0000685 rheumatoid arthritis 1 Terminated https://clinicaltrials. gov/search?id=%22NCT00505089%22CHEMBL1201834 CANAKINUMAB macular degeneration 1 Completed https://clinicaltrials. gov/search?id=%22NCT00503022%22CHEMBL1201834 CANAKINUMAB inhibitor Inhibitor EFO_0002609 juvenile idiopathic arthritis 1 Completed https://clinicaltrials. gov/search?id=%22NCT00426218%22CHEMBL1201834 CANAKINUMAB.
gov/search?id=%22NCT01589029%22 CHEMBL1201834 CANAKINUMAB Antibody Interleukin-1 beta inhibitor Inhibitor HP_0001945 Fever 1 Unknown status https://clinicaltrials. gov/search?id=%22NCT02775994%22CHEMBL1201834 CANAKINUMAB Antibody binding agent Binding agent EFO_0000220 acute lymphoblastic leukemia 2 Terminated https://clinicaltrials. gov/search?id=%22NCT01440179%22CHEMBL2109286 COLTUXIMAB RAVTANSINE Antibody B-lymphocyte antigen CD19 binding agent Binding agent EFO_0000403 diffuse large B-cell lymphoma 2 Completed https://clinicaltrials. gov/search?id=%22NCT01472887%22,https://clinicaltrials. gov/search?id=%22NCHEMBL2109286 COLTUXIMAB RAVTANSINE Antibody B-lymphocyte antigen CD19 binding agent Binding agent EFO_0005952 non-Hodgkins lymphoma 1 Completed https://clinicaltrials. gov/search?id=%22NCT00796731%22,https://clinicaltrials.
CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent EFO_0005952 non-Hodgkins lymphoma 1 Terminated https://clinicaltrials. gov/search?id=%22NCT00089284%22 CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent EFO_0009441 Waldenstrom macroglobulinemia 1 Completed https://clinicaltrials. gov/search?id=%22NCT00438880%22,https://clinicaltrials. gov/search?id=%22N CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent EFO_1000550 Splenic Marginal Zone Lymphoma 1 Terminated https://clinicaltrials. gov/search?id=%22NCT00012298%22 CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent EFO_1001365 Lymphoma, AIDS-Related 1 Terminated https://clinicaltrials.
gov/search?id=%22NCT00036855%22 CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent EFO_1001469 Mantle cell lymphoma 1 Completed https://clinicaltrials. gov/search?id=%22NCT00438880%22 CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent MONDO_0000873 lymphoblastic lymphoma 1 Terminated https://clinicaltrials. gov/search?id=%22NCT00036855%22 CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent MONDO_0018906 follicular lymphoma 1 Completed https://clinicaltrials. gov/search?id=%22NCT00438880%22 CHEMBL1201606 IBRITUMOMAB TIUXETAN Antibody B-lymphocyte antigen CD20 binding agent Binding agent MONDO_0019088 post-transplant lymphoproliferative disease 1 Terminated https://clinicaltrials.