Evidence map›Paper›PMID 40119178›Full record

ArticleAnnals of hematology2025

Gain or amplification of 1q21 in systemic light chain amyloidosis is associated with advanced Mayo stage, plasma cell disease and worse overall survival.

Sara Oubari, Maria Papathanasiou, Lars Michel, Tienush Rassaf, Andreas Thimm, Tim Hagenacker, Daniela Ehling, Stefan Wieczorek, Eyad Naser, Ute Hegenbart and 4 more

Abstract read
In one paragraph

Article in Annals of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

14 authors.

Sara OubariDepartment of Hematology and Stem Cell Transplantation, West German Cancer Center, University Hospital Essen, University Duisburg-Essen, Hufelandstraße 55, Essen, 45147, Germany.
Maria PapathanasiouDepartment of Cardiology and Angiology, University Hospital Frankfurt, Frankfurt am Main, Germany.
Lars MichelInterdisciplinary Amyloidosis Network, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Tienush RassafInterdisciplinary Amyloidosis Network, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Andreas ThimmInterdisciplinary Amyloidosis Network, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Tim HagenackerInterdisciplinary Amyloidosis Network, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Daniela EhlingDepartment of Medical Genetics, MVZ Dr. Eberhard & Partner Dortmund, Dortmund, Germany.
Stefan WieczorekDepartment of Medical Genetics, MVZ Dr. Eberhard & Partner Dortmund, Dortmund, Germany.
Eyad NaserInstitute of Molecular Biology, University of Duisburg-Essen, Essen, Germany.
Ute HegenbartDepartment of Internal Medicine V, Amyloidosis Center Heidelberg, University Hospital Heidelberg, Heidelberg, Germany.
Stefan SchönlandDepartment of Internal Medicine V, Amyloidosis Center Heidelberg, University Hospital Heidelberg, Heidelberg, Germany.
Ulrich DührsenDepartment of Hematology and Stem Cell Transplantation, West German Cancer Center, University Hospital Essen, University Duisburg-Essen, Hufelandstraße 55, Essen, 45147, Germany.
Hans Christian ReinhardtDepartment of Hematology and Stem Cell Transplantation, West German Cancer Center, University Hospital Essen, University Duisburg-Essen, Hufelandstraße 55, Essen, 45147, Germany.
Alexander CarpinteiroDepartment of Hematology and Stem Cell Transplantation, West German Cancer Center, University Hospital Essen, University Duisburg-Essen, Hufelandstraße 55, Essen, 45147, Germany. alexander.carpinteiro@uk-essen.de.

Funding

Deutsche Forschungsgemeinschaft CA2420/2-1
6 · The paper itself

Abstract

Systemic light-chain amyloidosis (AL) is an acquired protein misfolding disease characterized by deposition of immunoglobulin light-chain fibrils most often secreted from clonal plasma cells. In this retrospective study we analyzed the impact of iFISH aberrations on clinical characteristics and outcomes in 175 AL patients presented between 2015 and 2024. The most common aberrations were t(11;14) (57%), deletion 13q14 (33%), +1q21 (21%), hyperdiploidy (21%) and deletion 16q23 (17%). Significant elevations in dFLC levels were observed in patients with + 1q21 (median 407 vs. 213 mg/l, p = 0.04) and deletion 16q23 (median 476 vs. 204, p = 0.006). Only + 1q21 was associated with increased levels of cardiac biomarkers NTproBNP (median 9945 vs. 3538 pg/ml, p = 0.002) and hsTnT (median 110 vs. 53 ng/l, p = 0.002). This resulted in an increased proportion of patients with Mayo stage IIIb (53% vs. 26%, p = 0.01). Patients with + 1q21 had more advanced plasma cell disease (p = 0.0004). Our study highlights for the first time + 1q21 as the key aberration associated with advanced cardiac and plasma cell disease. After 17 months of follow-up, overall survival was significantly worse in patients with + 1q21 treated with daratumumab (7.2 months vs. not reached, p = 0.006). Alternative therapeutic approaches such as CAR-T therapies or bispecific antibodies should be further investigated.

Indexed as

Chromosome AberrationsChromosomes, Human, Pair 1Immunoglobulin Light-chain AmyloidosisAdultAgedAged, 80 and overFemaleHumansMaleMiddle AgedPlasma CellsRetrospective StudiesSurvival Rate+1q21AL amyloidosisIFISHMayo stage

Identifiers

PMID40119178
PMCPMC12031875

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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 OpenQuestion graph.