Evidence map›Paper›PMID 36252999›Full record

ArticleJournal for immunotherapy of cancer2022

IgE type multiple myeloma exhibits hypermutated phenotype and tumor reactive T cells.

Niklas Kehl, Michael Kilian, Julius Michel, Tim R Wagner, Sebastian Uhrig, Alexander Brobeil, Lilli-Sophie Sester, Sven Blobner, Simon Steiger, Michael Hundemer and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Eosinophilia and elevated IgE serum levels: a red flag: when your diagnosis is not a common atopic eczema or common allergy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    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

20 authors at 3 institutions in 1 country.

Niklas KehlDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Michael KilianClinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Julius MichelDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Tim R WagnerDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Sebastian UhrigMolecular Precision Oncology Program, National Center for Tumor Diseases, Heidelberg, Germany.
Alexander BrobeilDepartment of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Lilli-Sophie SesterDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Sven BlobnerDepartment of Translational Oncology, National Center of Tumor Diseases (NCT) and German Cancer Consortium (DKTK), Heidelberg, Germany.
Simon SteigerDivision of Chromatin Networks, BioQuant Center and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Michael HundemerDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Niels WeinholdDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Karsten RippeDivision of Chromatin Networks, BioQuant Center and German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0001-9951-9395
Stefan FröhlingDepartment of Translational Oncology, National Center of Tumor Diseases (NCT) and German Cancer Consortium (DKTK), Heidelberg, Germany.
Stefan B EichmüllerGMP and Cell Therapy Group, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-3497-6904
Lukas BunseClinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Carsten Müller-TidowDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Hartmut GoldschmidtDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Michael PlattenClinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Marc-Steffen RaabDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany.
Mirco J FriedrichDepartment of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany mirco.friedrich@dkfz.de.
German Cancer Research Center · DEHeidelberg University · DENational Center for Tumor Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a hematological malignancy originating from malignant and clonally expanding plasma cells. MM can be molecularly stratified, and its clonal evolution deciphered based on the Ig heavy and light chains of the respective malignant plasma cell clone. Of all MM subtypes, IgE type MM accounts for only <0.1% of cases and is associated with an aggressive clinical course and consequentially dismal prognosis. In such malignancies, adoptive transfer of autologous lymphocytes specifically targeting presented (neo)epitopes encoded by either somatically mutated or specifically overexpressed genes has resulted in substantial objective clinical regressions even in relapsed/refractory disease. However, there are no data on the genetic and immunological characteristics of this rare and aggressive entity. Here, we comprehensively profiled IgE type kappa MM on a genomic and immune repertoire level by integrating DNA- and single-cell RNA sequencing and comparative profiling against non-IgE type MM samples. We demonstrate distinct pathophysiological mechanisms as well as novel opportunities for targeting IgE type MM. Our data further provides the rationale for patient-individualized neoepitope-targeting cell therapy in high tumor mutation burden MM.

Indexed as

Multiple MyelomaDNAEpitopesHumansPhenotypeT-LymphocytesDNAEpitopesadaptive immunityimmunity, cellularlymphocytes, tumor-infiltratingtumor microenvironment

Identifiers

PMID36252999
PMCPMC9577923
OpenAlexW4306411244

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.