ReviewExperimental hematology & oncology2021
Genetic pathogenesis of immunoglobulin light chain amyloidosis: basic characteristics and clinical applications.
Review in Experimental hematology & oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Multiple Myeloma Concomitant with AL Amyloidosis: Histopathological Aspects of the Common Plasma Cell Spectrum.International journal of molecular sciences · 2026Article
- Case Report: Autologous stem cell transplantation in a patient diagnosed with AL amyloidosis in Kazakhstan.Frontiers in oncology · 2026Article
- Multi-omics profiling and AI-driven clinically deployable risk models in MGUS and smoldering myeloma.Clinical and experimental medicine · 2025Review
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- The molecular landscape of AL amyloidosis.British journal of haematology · 2025Review
- Association between CTX-1 and Fibulin-1 Serum Levels with Pathogenesis of Multiple Myeloma Cancer.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Characterization of N-Terminal Asparagine Deamidation and Clipping of a Monoclonal Antibody.Antibodies (Basel, Switzerland) · 2023Article
- Need for Early Recognition of Amyloidosis in Cases of Unexplained Heart Failure: A Case Report.Cureus · 2023Article
- Role of the mechanisms for antibody repertoire diversification in monoclonal light chain deposition disorders: when a friend becomes foe.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin light chain amyloidosis (AL) is an indolent plasma cell disorder characterized by free immunoglobulin light chain (FLC) misfolding and amyloid fibril deposition. The cytogenetic pattern of AL shows profound similarity with that of other plasma cell disorders but harbors distinct features. AL can be classified into two primary subtypes: non-hyperdiploidy and hyperdiploidy. Non-hyperdiploidy usually involves immunoglobulin heavy chain translocations, and t(11;14) is the hallmark of this disease. T(11;14) is associated with low plasma cell count but high FLC level and displays distinct response outcomes to different treatment modalities. Hyperdiploidy is associated with plasmacytosis and subclone formation, and it generally confers a neutral or inferior prognostic outcome. Other chromosome abnormalities and driver gene mutations are considered as secondary cytogenetic aberrations that occur during disease evolution. These genetic aberrations contribute to the proliferation of plasma cells, which secrete excess FLC for amyloid deposition. Other genetic factors, such as specific usage of immunoglobulin light chain germline genes and light chain somatic mutations, also play an essential role in amyloid fibril deposition in AL. This paper will propose a framework of AL classification based on genetic aberrations and discuss the amyloid formation of AL from a genetic aspect.
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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.