Neoplasia mieloproliferativa crônica caracterizada pela expressão do gene de fusão BCR-ABL1. Apresenta leucocitose neutrofílica. Pode aparecer em qualquer idade, mas afeta principalmente indivíduos de meia idade e mais velhos. Os pacientes geralmente apresentam fadiga, perda de peso, anemia, sudorese noturna e esplenomegalia. Se não for tratada, segue um curso natural bifásico ou trifásico; uma fase crônica indolente inicial que é seguida por uma fase acelerada, uma fase blástica ou ambas. O transplante alogênico de células-tronco e os inibidores da tirosina quinase atrasam a progressão da doença e prolongam a sobrevida global.
Introdução
O que você precisa saber de cara
Leucemia mielóide crônica é um câncer de crescimento lento do tecido formador de sangue (medula óssea). A medula óssea normal produz glóbulos vermelhos (eritrócitos) que transportam oxigênio, glóbulos brancos (leucócitos) que protegem o corpo contra infecções e plaquetas (trombócitos) que participam da coagulação sanguínea. Na leucemia mielóide crônica, a medula óssea produz glóbulos brancos em excesso. Inicialmente, essas células funcionam relativamente normalmente. No entanto, à medida que a condição progride, glóbulos brancos imaturos chamados mieloblastos (ou blastos) se acumulam no sangue e na medula óssea. O crescimento excessivo de mieloblastos prejudica o desenvolvimento de outras células sanguíneas, levando a uma escassez de glóbulos vermelhos (anemia) e de plaquetas.
A leucemia mielóide crônica geralmente começa após os 60 anos de idade. Características comuns incluem cansaço excessivo (fadiga), febre e perda de peso. Muitas pessoas com a condição desenvolvem um baço aumentado (esplenomegalia), o que pode causar sensação de plenitude no abdômen e perda de apetite. Cerca de metade das pessoas com leucemia mielóide crônica não apresentam inicialmente nenhum sinal ou sintoma e são diagnosticadas quando um exame de sangue é realizado por outro motivo.
A condição consiste em três fases: a fase crônica, a fase acelerada e a fase blast (ou crise blast). Na fase crônica, o número de glóbulos brancos maduros está elevado, e os mieloblastos representam menos de 10 % das células sanguíneas. Sinais e sintomas da condição durante essa fase são tipicamente leves ou ausentes e pioram lentamente. A fase crônica pode durar de meses a anos. Na fase acelerada, o número de mieloblastos é ligeiramente maior, representando de 10 a 29 % das células sanguíneas. Os sinais e sintomas continuam a piorar. A fase acelerada geralmente dura de 4 a 6 meses, embora seja pulada em algumas pessoas com a condição. Na crise blast, 30 % ou mais das células do sangue ou da medula óssea são mieloblastos. Sinais e sintomas são mais graves nessa fase, incluindo um baço massivamente aumentado, dor óssea e perda de peso. Infecções graves e sangramentos descontrolados podem ser ameaçadores à vida.
Fonte: MedlinePlus Genetics (NLM/NIH), traduzidoNeoplasia mieloproliferativa crônica caracterizada pela expressão do gene de fusão BCR-ABL1. Apresenta leucocitose neutrofílica. Pode aparecer em qualquer idade, mas afeta principalmente indivíduos de meia idade e mais velhos. Os pacientes geralmente apresentam fadiga, perda de peso, anemia, sudorese noturna e esplenomegalia. Se não for tratada, segue um curso natural bifásico ou trifásico; uma fase crônica indolente inicial que é seguida por uma fase acelerada, uma fase blástica ou ambas. O transplante alogênico de células-tronco e os inibidores da tirosina quinase atrasam a progressão da doença e prolongam a sobrevida global.
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Sinais e sintomas
O que aparece no corpo e com que frequência cada sintoma acontece
Partes do corpo afetadas
+ 8 sintomas em outras categorias
Características mais comuns
Os sintomas variam de pessoa para pessoa. Abaixo estão as 15 características clínicas mais associadas, ordenadas por frequência.
Linha do tempo da pesquisa
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Genética e causas
O que está alterado no DNA e como passa nas famílias
Genes associados
3 genes identificados com associação a esta condição. Padrão de herança: Not applicable.
Leukemia, chronic myeloid
A clonal myeloproliferative disorder of a pluripotent stem cell with a specific cytogenetic abnormality, the Philadelphia chromosome (Ph), involving myeloid, erythroid, megakaryocytic, B-lymphoid, and sometimes T-lymphoid cells, but not marrow fibroblasts.
Leukemia, chronic myeloid
A clonal myeloproliferative disorder of a pluripotent stem cell with a specific cytogenetic abnormality, the Philadelphia chromosome (Ph), involving myeloid, erythroid, megakaryocytic, B-lymphoid, and sometimes T-lymphoid cells, but not marrow fibroblasts.
Medicamentos aprovados (FDA)
2 medicamentos encontrados nos registros da FDA americana.
Variantes genéticas (ClinVar)
684 variantes patogênicas registradas no ClinVar.
Classificação de variantes (ClinVar)
Distribuição de 6 variantes classificadas pelo ClinVar.
Vias biológicas (Reactome)
41 vias biológicas associadas aos genes desta condição.
Diagnóstico
Os sinais que médicos procuram e os exames que confirmam
Tratamento e manejo
Remédios, cuidados de apoio e o que precisa acompanhar
Onde tratar no SUS
Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)
🇧🇷 Atendimento SUS — Leucemia mieloide crônica
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Publicações mais relevantes
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Cellular stresses regulate transcriptional readthrough, whereby RNA polymerase II elongates past a gene's polyadenylation cleavage site without RNA cleavage. Readthrough has been reported in several cancer types. Here, we use long-read sequencing of nascent RNA to quantify transcriptional readthrough in chronic myeloid leukemia (CML) cells and characterize early responses to the targeted therapeutic, imatinib. We show that the amount, length, and gene specificity of readthrough increase within 1 hour, before gene expression and alternative splicing alterations emerge. Notably, imatinib-dependent messenger RNA (mRNA) isoform changes involved "readthrough chimeras," in which exons from an upstream gene are alternatively spliced to exons in a downstream gene. Altered mRNA isoforms and chimera levels were detected in imatinib-resistant K562 cells as well as cells of patients with CML. Thus, imatinib can provoke a cascade of early changes to transcription and splicing fidelity that may lead to longer-term adjustments in gene expression, cancer cell differentiation, and the development of therapy resistance.
FBXO3-mediated DUSP9 ubiquitination promotes leukemia stem cell maintenance and tyrosine kinase inhibitor resistance in chronic myeloid leukemia.
Eradicating leukemia stem cells (LSCs) and overcoming tyrosine kinase inhibitor (TKI) resistance is urgent for chronic myeloid leukemia (CML) treatment. We find that F-box protein 3 (FBXO3) is highly upregulated in CD34+ CML stem cells from TKI-resistant patients and identify it as an innovative CML-LSC marker via single-cell RNA sequencing (scRNA-seq). FBXO3 deficiency induces apoptosis and reduces proliferation of CML cell lines and LSCs in vitro and in vivo, with minimal effects on normal CD34+ hematopoietic stem cells (HSCs). Mechanistically, FBXO3 interacts with DUSP9 to promote its ubiquitination and activate the MAPK pathway, critical for CML cell activity. DUSP9 knockdown partially reverses FBXO3-deficiency-mediated LSC elimination. Furthermore, FBXO3 inhibitor monotherapy or combination with imatinib effectively eradicates CML-LSCs, overcomes TKI resistance, and spares normal hematopoiesis. Collectively, our findings highlight FBXO3's role in CML progression and support combining FBXO3 inhibitors with TKIs for durable LSC elimination.
Nonclassical Philadelphia-positive FISH signal patterns in CML and seven cases with variant Philadelphia.
Chronic myeloid leukemia (CML) is characterized by the Philadelphia chromosome (Ph), which occurs as a result of t(9;22). In 5%-10% of CML cases, variant t(9;22)s are observed. Additionally, while t(9;22) is formed, deletions can be observed in chromosomes 9 and 22. These deletions are observed more frequently in variant t(9;22). There is conflicting information in the literature about the prognostic effects of variant t(9;22) and deletions of 9q and 22q. There is also limited information about the frequency and breakpoints of other chromosomes involved in the variant t(9;22). Signal patterns other than the classical signal pattern of FISH analysis indicate deletions and variant translocations. In this study, we aimed to investigate the clinical significance of nonclassical FISH signal patterns and to determine the frequency of variant translocations. Bone marrow samples from 231 newly diagnosed CML patients were analyzed by conventional cytogenetics and FISH. As a result of FISH analysis, nonclassical FISH signal patterns were detected in 49/231 cases, and variant t(9;22) was detected in seven cases by conventional cytogenetics. It was determined that chromosomes 1, 3, 5, 7, 8, and 21 were involved in variant t(9;22). When cases with classical and nonclassical signal patterns were compared in terms of 6th- and 12th-month treatment responses, survival times, and treatment changes, it was found that cases with classical signal patterns had significantly higher treatment responses at the 6th month (p < 0.001). Because variant translocations are extremely rare and involve many different chromosomal breaks, a large number of cases are needed to clearly understand their prognostic implications. Due to the limitations of conventional cytogenetic analyses, it should be considered in patient follow-up that nonclassical FISH signal patterns indicating deletions and/or variant translocations may cause a delay in obtaining a complete cytogenetic response at the 6th month.
From mutational signatures to practice: Artificial intelligence-guided repurposing for blast crisis chronic myeloid leukemia.
This article of discusses blast crisis chronic myeloid leukemia (CML), which is the most aggressive CML phase marked by rapid progression, substantial mutational complexity, and resistance to standard tyrosine kinase therapies. The methodology combines whole exome sequencing and machine learning to identify the molecular subtypes of blast crisis-CML and repurpose existing Food and Drug Administration-approved drugs on the basis of the Catalogue of Somatic Mutations in Cancer mutational patterns. In a pilot cohort (n = 7), three exploratory genomic clusters were identified: Breast cancer gene 2/tumor protein p53; isocitrate dehydrogenases (IDH) 1 and IDH 2 ten eleven translocation 2; and Janus kinase (JAK) 2/colony stimulating factor 3 receptor. The results present an opportunity to evaluate poly(ADP ribose) polymerase inhibitors (breast cancer gene 2/tumor protein p53), IDH inhibitors (IDH1/2 or ten eleven translocation 2), and JAK inhibitors (JAK2 or colony stimulating factor 3 receptor) as actionable therapeutics. Moreover, this e article presents as a strategic framework for mutation-targeted therapy targeting treatment-resistant leukemias, highlighting the potential of artificial intelligence-driven molecular stratification and uncovering clinically relevant therapeutic options for malignancies. However, limitations should be acknowledged, such as the limited cohort size and the necessity for validation in larger multicenter investigations. Prospective registries and trial enrollment should test signature-defined micro-cohorts with versioned and auditable reporting. These mappings are designed to provide hypotheses and depend on independent functional validation, prioritizing safety in combination methods with tyrosine kinase inhibitors, and allows for practical implementation in rapid turnaround environments.
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European journal of clinical pharmacologyDasatinib-Associated Recurrent Symptomatic Bilateral Pleural Effusions in an Elderly Patient With End-Stage Renal Disease on Maintenance Hemodialysis.
CureusOlverembatinib (HQP1351): a third-generation tyrosine kinase inhibitor in the treatment of hematologic and solid malignancies-a comprehensive review of clinical outcomes.
Discover oncologyA Framework for Locally Imputing and Predicting Biomarker Trajectories Under Irregular Monitoring: Application to Chronic Myeloid Leukemia.
Research squarePonatinib for CML patients in routine clinical practice: the PONDEROSA study.
Annals of hematologyModeling, analysis and numerical simulation of chronic myeloid leukemia.
Theory in biosciences = Theorie in den BiowissenschaftenAssessing trends in conditional survival for non-Hodgkin lymphoma and chronic myeloid leukemia via novel extensions to the joinpoint survival model.
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive OncologyAn Overview of Chronic Myeloid Leukemia Treatment: From Tyrosine Kinase Inhibitors to Novel and Emerging Therapies.
European journal of haematologyRandomized phase 3 trial of Ropeginterferon alfa-2b versus surveillance after tyrosine kinase inhibitor discontinuation in chronic myeloid leukemia (ENDURE/CML-IX).
Leukemia[Extramedullary blast crisis limited to the lymph nodes in chronic myeloid leukemia with a T/myeloid mixed phenotype].
[Rinsho ketsueki] The Japanese journal of clinical hematologyEvaluating the Safety of Combining Tyrosine Kinase Inhibitors with Anticoagulants in Chronic Myeloid Leukemia: A Systematic Review.
OncologyLeukemia epidemiology in China: Burden, trends, and determinants in the 21st century.
Chinese journal of cancer research = Chung-kuo yen cheng yen chiuImpact of Bone Marrow Fibrosis on the Outcome of Chronic Myeloid Leukemia Treated with Second Generation Tyrosine Kinase Inhibitors.
Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood TransfusionHypoxic conditions confer chemoresistance to crizotinib but not to imatinib in chronic myeloid leukemia cells.
Hematology, transfusion and cell therapyCorrigendum to "Aleukemic Chronic Myeloid Leukemia Without Neutrophilia and Thrombocytosis: A Report From the BCR::ABL1 Pathology Group" [Modern Pathology. 2024;37(2):100406].
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, IncA selenium-containing selective estrogen receptor modulator to overcome drug resistance of chronic myeloid leukemia.
Apoptosis : an international journal on programmed cell deathTrilineage Extramedullary Hematopoiesis in Pleural Effusion: A Rare Phenomenon.
Diagnostic cytopathologyReal-World Outcomes With Low-Dose Dasatinib (50 mg) in Imatinib-Resistant Chronic Myeloid Leukemia in Chronic Phase: A Retrospective Analysis of Efficacy and Safety.
Cancer reports (Hoboken, N.J.)[Total flavonoids from Sarcandra glabra promote apoptosis in leukemia K562 cells via sphingolipid metabolism and PI3K/Akt signaling pathway based on cellular metabolomics].
Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medicaBiological Features of KLC2 Mutations in Chronic Myeloid Leukemia and Their Contribution to Inducing Drug Resistance.
Oncology researchMPN-FIT: a randomized controlled pilot trial of supervised exercise in myeloproliferative neoplasms.
Blood advancesSpecifically targeting the ABL myristoyl pocket: STAMP inhibitors for chronic myeloid leukemia.
Expert review of hematologyAssociation of fibronectin 1 deregulation with tyrosine kinase inhibitor resistance in chronic myeloid leukemia.
Frontiers in cell and developmental biologyLigand Valency and Linker Design Dictate the Efficacy of CI-M6PR-Mediated Targeted Delivery of M6P-siRNA Conjugates.
ACS omega[Guideline for the diagnosis and treatment of chronic myeloid leukemia in China (2025)].
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhiCaffeic acid phenethyl ester induced apoptosis in chronic myeloid leukemia cells by inhibiting mitochondrial complex I.
Scientific reportsIntersection of Tyrosine Kinase Inhibition and Sepsis-Induced Cardiomyopathy.
Case reports in pathologyTyrosine Kinase Inhibitors as Risk Factors for Cerebral Vascular Disease: Report of Two Cases and Literature Review.
Case reports in neurological medicineBMP-7 Treatment Ameliorates PTEN-Akt Mediated Apoptosis and Adverse Cardiac Remodeling in Ponatinib-Induced Cardiotoxicity.
Pharmaceuticals (Basel, Switzerland)MUTATIONAL STATUS AND TREATMENT EFFICACY IN PATIENTS WITH CHRONIC MYELOID LEUKEMIA.
Problemy radiatsiinoi medytsyny ta radiobiolohiiBCR::ABL1 kinase domain mutations and their predictive value for treatment outcomes in patients with chronic myeloid leukemia treated with first-line imatinib in a low-income setting: Experience from Côte d'Ivoire.
Leukemia research reportsBone Marrow Edema and Tyrosine Kinase Inhibitors Treatment in Chronic Myeloid Leukemia.
Diagnostics (Basel, Switzerland)Early BCR::ABL1 Reduction as a Predictor of Deep Molecular Response in Pediatric Chronic-Phase Chronic Myeloid Leukemia.
CancersNeuropsychiatric Symptoms Mimicking Dementia in a Patient Treated With Imatinib.
Annals of clinical and translational neurologyWhat is the role of asciminib in chronic myeloid leukemia?
Clinical advances in hematology & oncology : H&OAddressing unmet needs in chronic myeloid leukemia in chronic phase treated with two or more tyrosine kinase inhibitors: insights from literature and Indian clinical practice.
Expert review of hematologyHsp70-Bim interaction mediated mitophagy as a potential therapeutic target for CML stem cells.
Stem cell reportsInterindividual variability in imatinib metabolism in human liver microsomes and primary human hepatocytes: Impact of CYP2C8 and CYP3A phenotypes.
Drug metabolism and disposition: the biological fate of chemicalsUSP8-EIF2S1 signaling enhances CML cell survival under TKI-induced stress.
The FEBS journalA Case of Synchronous Primary Pancreatic DLBCL and Incipient CML.
Journal of the Association of Genetic TechnologistsPrevalence of Chronic Myeloid Leukemia in the United States: A Cross-Sectional Study Using the SEER Database.
South Asian journal of cancerEfficacy and safety of flumatinib in adults with Ph-positive ALL: a prospective observational study.
Frontiers in oncologyIntestinal low-abundant bacteria drive MyD88/Trif-dependent CD8+ T cell exhaustion in chronic myeloid leukemia.
Cell reportsExtracellular vesicles-derived non-coding RNA in leukemias and pre-leukemic syndromes: a systematic review.
Journal of cancer research and clinical oncologyBehcet's disease in a patient with chronic myeloid leukemia.
Indian journal of sexually transmitted diseases and AIDSExosome and BCR-ABL mediated molecular alterations in endothelial cells in chronic myeloid leukemia: identification of seven genes and their regulatory network.
PeerJp38 MAPK-mediated suppression of Nrf2-MPC2 axis drives metabolic reprogramming which confers imatinib resistance in blast crisis phase of chronic myeloid leukemia.
Experimental cell researchExploring phytochemical inhibitors of fatty acid elongase ELOVL6 for targeted treatment of chronic myeloid leukemia: A comprehensive network-based drug discovery approach.
Computers in biology and medicineImmune Surveillance in Chronic Myeloid Leukemia: Tumor Antigen Expression and CD8+ T Cell Function in the Context of Treatment- Free Remission.
Archivum immunologiae et therapiae experimentalisTreatment expectations and goals among patients with chronic myeloid leukemia in Germany: a patient-centered perspective.
LeukemiaTargeting myeloid cell leukemia-1 protein to identify potential compounds for chronic myeloid leukemia treatment: Molecular docking and molecular dynamics simulation approaches.
Biochemical and biophysical research communicationsInnate CD8 T-cells as a potential predictive biomarker for deep molecular response in chronic myeloid leukemia patients.
Cancer immunology, immunotherapy : CIIIdentification of N-tert-butyloxycarbonyl protected amino acids as novel hydrophobic tags to induce targeted protein degradation.
European journal of medicinal chemistryReal-world efficacy and adverse events of frontline nilotinib in pediatric chronic myeloid leukemia in chronic phase: A prospective multicenter study from SCCCG[PLUS]-CML 2023.
CancerThe role of the bone marrow microenvironment in leukemic stem cell resistance: Pathways of persistence and selection.
Critical reviews in oncology/hematologyHigher HLA-DRB1 Evolutionary Divergence Is Associated with Reduced Relapse and Improved Survival after Matched Unrelated Hematopoietic Cell Transplantation.
Transplantation and cellular therapyAsciminib Demonstrates Superior Efficacy and Safety in Newly Diagnosed Chronic Myeloid Leukemia in the ASC4FIRST Trial.
BloodSingle-cell disentangled representations for perturbation modeling and treatment effect estimation.
bioRxiv : the preprint server for biologyReshape memory T cell landscape in CML patients' blood by tyrosine kinase inhibitors.
Caspian journal of internal medicineDiagnosis, treatment, and monitoring of cytomegalovirus pneumonia in a hematopoietic stem cell transplantation child.
Frontiers in cellular and infection microbiologySimultaneous chromatographic quantification of upadacitinib, nilotinib, and tryptophan decoding myeloid leukemia and liver cancer integrated with ELISA and Flow cytometry.
Journal of chromatography. B, Analytical technologies in the biomedical and life sciencesDevelopment of a blood test-based predictive scoring tool for treatment response in chronic myeloid leukemia.
International journal of hematologyDisarming the Hsp70-Bim Alliance: Small-Molecule and Peptidic Disruptors of a Chaperone-Apoptotic Switch in Cancer.
ChemistryOpenGenetic Variations in BCL3, MDM4, KLF14, and miR-146a and Their Associations with the Predisposition and Progression of Myeloproliferative Disorder and Chronic Myeloid Leukemia Patients.
Molecular syndromologyAtypical chronic myeloid leukemia: From diagnosis to molecular features and therapeutic options.
HemaSphereImproving quality of life for patients with chronic myeloid leukemia through supportive care, low-dose therapy, switching, and treatment-free remission.
HaematologicaIs there a best frontline therapy in chronic myeloid leukemia?
HaematologicaCombined asciminib and olverembatinib in blast-phase chronic myeloid leukemia.
HaematologicaNCIVISION: A Siamese Neural Network for Molecular Similarity Prediction MEP and RDG Images.
Molecules (Basel, Switzerland)Identification of a Novel miR-122-5p/CDC25A Axis and Potential Therapeutic Targets for Chronic Myeloid Leukemia.
International journal of molecular sciencesChronic Myeloid Leukemia and the T315I BCR::ABL1 Mutation.
International journal of molecular sciencesIdentification and characterization of peptidyl-prolyl isomerase Pin1 as a new regulatory component of BCR::ABL1 degradation.
Leukemia researchPeripheral blood CD26+ leukemic stem cells in chronic myeloid leukemia and tyrosine kinase inhibitor response: Questions remain!
CancerHeterocyclic Compounds as Bcr-Abl Tyrosine Kinase Inhibitors Against Chronic Myeloid Leukemia.
Medicinal chemistry (Shariqah (United Arab Emirates))Do genetic polymorphisms influence imatinib trough concentrations in patients with chronic myeloid leukemia? A systematic review and meta-analysis.
Expert review of anticancer therapyOlverembatinib for 8p11 myeloproliferative syndrome with a positive BCR-FGFR1 fusion gene: a case report.
Annals of hematologyInvestigating chronic myeloid leukemia therapeutics: AI-optimized design and synthesis of 4-methylthiazole-2-amine derivatives with translocation control activity.
RSC advancesOmics and artificial intelligence integration for stratifying blast crisis CML using COSMIC signatures and pan-cancer precision drug repurposing.
World journal of clinical oncologyAssociações
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Doença com base genética
Um médico geneticista pode ajudar no diagnóstico de Leucemia mieloide crônica e no aconselhamento genético da família.
Doenças relacionadas
Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico
Perguntas frequentes
O que as famílias mais perguntam sobre esta doença — cada resposta com a fonte de onde saiu
É uma neoplasia mieloproliferativa crônica caracterizada pela multiplicação descontrolada de glóbulos brancos. Ela se desenvolve a partir da presença do gene de fusão BCR-ABL1 no tecido formador do sangue.
Referências
Fontes citadas no texto, publicações do grafo e bases de dados usadas neste verbete
10 publicações do grafo RarasNet (PubMed) · 8 bases de dados. Títulos, periódicos e PMIDs vêm direto da fonte, sem intermediação de IA.
Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.
Citar este verbete
Raras. (s.d.). Leucemia mieloide crônica. Em Raras — Enciclopédia de Doenças Raras do Brasil. https://raras.org/doenca/leucemia-mieloide-cronica
Formato APA. Conteúdo sob CC BY 4.0 — reuso livre com atribuição.
Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar
Leucemia mieloide crônica
📋 Origem dos dados
Esta página agrega dados de fontes públicas e oficiais. Dados sobre cobertura no SUS (PCDT, CEAF) são verificados ativamente por agente proativo (ver badge no infobox). Demais dados têm atribuição de fonte + data da última sincronização — clique para abrir o original.
- Doença rara (ontologia)
- fonte: Orphanet
- Identificador unificado
- fonte: MONDO
- Genética mendeliana
- fonte: OMIM
- Codificação WHO/SUS
- fonte: WHO ICD-10 / DATASUS
- CID-11 (futuro)
- fonte: WHO ICD-11
- NIH/GARD
- fonte: GARD (NIH)
- Indexação biomédica
- fonte: MeSH (NLM)
- Dado público estruturado
- fonte: Wikidata
- Medicamentos aprovados FDA
- fonte: FDA OpenFDA
- Reposicionamento
- fonte: Drug Repurposing Hub
- Ensaios clínicos
- fonte: ClinicalTrials.gov
