Evidence map›Paper›PMID 42279355›Full record

ReviewCancers2026

MAGa: Monoclonal Autoimmune Gammopathies.

Stephanie Torres, Sarah E Wheeler, Michael R Shurin

Abstract readReview
In one paragraph

Review in Cancers, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Stephanie TorresDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.ORCID 0000-0001-8016-3181
Sarah E WheelerDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.
Michael R ShurinDepartment of Pathology, University of Pittsburgh and University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.ORCID 0000-0002-6570-7395

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a growing recognition of bidirectional relationships between immune phenomena in plasma cell disorders, such as multiple myeloma and its precursor malignancies, including autoimmune phenomena that either precede or complicate the development of neoplasms. The development of specific autoimmune disorders is a well-known aspect of B-cell lymphoproliferative diseases. At the same time, the development of plasma cell dyscrasia in patients with autoimmune diseases is well established. This may suggest that some subclones of multiple myeloma and its precursor, monoclonal gammopathy of undetermined significance, originate in the setting of persistent autoimmune activation. Interestingly, monoclonal immunoglobulins, which are key biomarkers for characterizing and monitoring monoclonal gammopathies, have long been overlooked in clinical research because they are thought to have no significant antibody function. It is plausible that unusual clinical consequences may occur when monoclonal myeloma paraproteins bind to endogenous self-antigens. Published clinical data illustrate this possibility well. This review synthesizes published evidence demonstrating that many patients with multiple myeloma and related plasma cell dyscrasias exhibit specific clinical manifestations of antigen-antibody interactions between a monoclonal immunoglobulin produced by proliferating B-cell or plasma-cell clones and autologous antigens, including neural antigens, insulin, complement components, and others. We present pilot data showing antinuclear antibody reactivity in 38% of IgM monoclonal gammopathy sera. Numerous experimental and clinical data support the importance of identifying the target of the monoclonal immunoglobulins in monoclonal gammopathy of undetermined significance, smoldering multiple myeloma, and multiple myeloma. This approach not only aids in selecting an appropriate treatment strategy and predicting prognosis but may also guide the development of targeted therapies for managing monoclonal gammopathy cases that present with a paraprotein reactive against a known self-antigen. We propose the term monoclonal autoimmune gammopathies (MAGa) to describe this clinically distinct subset of plasma cell disorders characterized by pathogenic autoantibody activity of the monoclonal immunoglobulin.

Indexed as

autoantibodyautoinflammationmonoclonal gammopathyplasma cell disorders

Identifiers

PMID42279355
PMCPMC13255662

What Socratic holds

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Registered trials

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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 Socratic graph.