ReviewHematology. American Society of Hematology. Education Program2017
AL amyloidosis: from molecular mechanisms to targeted therapies.
Review in Hematology. American Society of Hematology. Education Program, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
92 citing papers in PubMed, 3 syntheses or guidelines pooled it, 202 citations in OpenAlex.
- The clinical trials landscape in immunoglobulin light chain amyloidosis: a systematic review.Blood advances · 2024Pooled it
- Cardiac Toxicity in the Treatment of Light Chain Amyloidosis: Systematic Review of Clinical Studies.Current drug safety · 2024Pooled it
- The Heart of the Alzheimer's: A Mindful View of Heart Disease.Frontiers in physiology · 2020Pooled it
- A journey through the molecular networks of endomyocardial biopsies to explore ATTR and ALiScience · 2026Article
- Determinants of gastrointestinal disease burden and survival in systemic AL amyloidosis.Blood advances · 2026Article
- Article
- Diagnostic Journeys and Delays in AL Amyloidosis: Insights From a Cross-Sectional Patient Survey.Clinical lymphoma, myeloma & leukemia · 2026Article
- Cryo-EM of Cardiac AL-224L Amyloid Reveals Shared Structural Motifs and Mutation-induced Differences in λ6 Light Chain Fibrils.Journal of molecular biology · 2026Article
- Left ventricular posterior wall thickness independently predicts the possibility of light-chain cardiac amyloidosis in hospitalized heart failure patients with monoclonal gammopathies.Cardiology journal · 2026Article
- Development and characterization of chimeric antigen receptor macrophages for amyloid clearance.Frontiers in immunology · 2026Article
- Bridging the Gap in AL and ATTR Cardiac Amyloidosis: Integrating Histopathology, Biomarkers, and Multimodal Imaging for Subtype-Specific Diagnosis.Reviews in cardiovascular medicine · 2026Review
- Article
- Heavy Chains, Heavy Consequences: A Case of Concomitant Heavy Chain Amyloidosis and Heavy Chain Deposition Disease.Kidney medicine · 2025Article
- The Great Mimicker, a Rare Pleural Presentation.CHEST pulmonary · 2025Article
- B Cell-Derived and Non-B Cell-Derived Free Light Chains: From Generation to Biological and Pathophysiological Roles.International journal of molecular sciences · 2025Review
- Modeling immunoglobulin light chain amyloidosis in Caenorhabditis elegans.Disease models & mechanisms · 2025Article
- Localized Amyloidosis of the Oral Cavity: A Rare Clinical Entity.Clinical case reports · 2025Article
- Prevalence and Spectrum of Neuropathies in a Cohort of 585 Patients With Immunoglobulin A Monoclonal Gammopathy.European journal of neurology · 2025Article
- Antibody Aggregation: A Problem Within the Biopharmaceutical Industry and Its Role in AL Amyloidosis Disease.The protein journal · 2025Review
- Discovery of Potent and Selective Pyridone-Based Small Molecule Kinetic Stabilizers of Amyloidogenic Immunoglobulin Light Chains.Journal of medicinal chemistry · 2024Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic amyloidosis is caused by misfolding and extracellular deposition of circulating proteins as amyloid fibrils, resulting in the dysfunction of vital organs. The most common systemic amyloidosis, light-chain (AL) amyloidosis, is caused by misfolded light chains produced by a small, dangerous B-cell clone. The process of amyloid formation, organ targeting, and damage is multifaceted and, after disease initiation, the complexity of the downstream pathogenic cascade increases, rendering its control a challenge. Because of the progressive nature of the disease, early diagnosis to prevent end-stage organ damage is vital. Improving awareness and systematic use of biomarkers of organ damage in screening populations at risk may improve the still unsatisfactory diagnostic process. Amyloid imaging is now emerging as an important companion of biomarkers in formulating the diagnosis and prognosis and monitoring the effects of therapy. An accurate diagnosis is the basis for appropriate therapy that is risk-adapted and response-tailored. Effective treatments targeting the clone and rapidly and profoundly reducing the amyloid light chains have produced marked improvements in overall survival, making AL amyloidosis the most successful model of all amyloidoses. New therapies targeting the amyloid deposits are now under development, together with novel agents modulating light chain aggregation and proteotoxicity. The future of AL amyloidosis treatment is combination therapy and will require an innovative collaborative model for a rapid translation from bench to bedside with the ultimate aim of achieving a cure for this complex disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.