Evidence map›Paper›PMID 36138464›Full record

ArticleBMC medical genomics2022

Correlation of plasma cell assessment by phenotypic methods and molecular profiles by NGS in patients with plasma cell dyscrasias.

Ekaterina Rebmann Chigrinova, Naomi A Porret, Martin Andres, Gertrud Wiedemann, Yara Banz, Myriam Legros, Matthias Pollak, Elisabeth Oppliger Leibundgut, Thomas Pabst, Ulrike Bacher

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC medical genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 39% of its field
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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
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

10 authors at 1 institution in 1 country.

Ekaterina Rebmann Chigrinova *Department of Hematology; Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. ekaterina.rebmann@insel.ch.ORCID 0000-0001-9478-4069
Naomi A Porret *Department of Hematology; Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Martin AndresDepartment of Hematology; Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Gertrud WiedemannDepartment of Hematology; Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Yara BanzInstitute of Pathology, University of Bern, Bern, Switzerland.
Myriam LegrosCenter for Laboratory Medicine (ZLM), Inselspital, University of Bern, Bern, Switzerland.
Matthias PollakDepartment of Hematology; Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Elisabeth Oppliger LeibundgutDepartment of Hematology; Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Thomas Pabst *Department of Medical Oncology, Inselspital, University of Bern, Bern, Switzerland.
Ulrike Bacher *Department of Hematology; Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNext-generation sequencing (NGS) detects somatic mutations in a high proportion of plasma cell dyscrasias (PCD), but is currently not integrated into diagnostic routine. We correlated NGS data with degree of bone marrow (BM) involvement by cytomorphology (BMC), histopathology (BMH), and multiparameter flow cytometry (MFC) in 90 PCD patients.

methodsOf the 90 patients the diagnoses comprised multiple myeloma (n = 77), MGUS (n = 7), AL-amyloidosis (n = 4) or solitary plasmocytoma (n = 2). The NGS panel included eight genes CCND1, DIS3, EGR1, FAM46C (TENT5C), FGFR3, PRDM1, TP53, TRAF3, and seven hotspots in BRAF, IDH1, IDH2, IRF4, KRAS, NRAS.

resultsMutations were detected in 64/90 (71%) of cases. KRAS (29%), NRAS (16%) and DIS3 (16%) were most frequently mutated. At least one mutation/sample corresponded to a higher degree of BM involvement with a mean of 11% pathologic PC by MFC (range, 0.002-62%), and ~ 50% (3-100%) as defined by both BMC and BMH.

conclusionsThe probability of detecting a mutation by NGS in the BM was highest in samples with > 10% clonal PC by MFC, or > 20% PC by BMC/ BMH. We propose further evaluation of these thresholds as a practical cut-off for processing of samples by NGS at initial PCD diagnosis.

Indexed as

ParaproteinemiasProto-Oncogene Proteins B-rafHigh-Throughput Nucleotide SequencingHumansMutationPlasma CellsProto-Oncogene Proteins p21(ras)TNF Receptor-Associated Factor 3Proto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)TNF Receptor-Associated Factor 3Bone marrow aspirateFlow cytometryHistopathologyMultiple myelomaNGSTrephine biopsy

Identifiers

PMID36138464
PMCPMC9503268
OpenAlexW4296793580

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.