Evidence map›Paper›PMID 24153012›Full record

ReviewLeukemia2014

Coinhibitory molecule PD-1 as a potential target for the immunotherapy of multiple myeloma.

D Atanackovic, T Luetkens, N Kröger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 98 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Monoclonal Antibodies: The Greatest Resource to Treat Multiple Myeloma.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Bone marrow-derived mesenchymal stem cells inhibit CD8Clinical and experimental immunology · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. The T-win® technology: immune-modulating vaccines.Seminars in immunopathology · 2019
    Review
  20. 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

3 authors at 1 institution in 1 country.

D AtanackovicDepartment of Oncology/Hematology/Bone Marrow Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
T LuetkensDepartment of Oncology/Hematology/Bone Marrow Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
N KrögerDepartment of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adaptive immune system is clearly capable of recognizing and attacking malignant plasma cells in patients with multiple myeloma (MM). However, MM patients evidence severe defects of humoral and cellular immunity, and it is likely that the profound immune dysregulation typical for this malignancy contributes to its eventual escape from natural immune control. One of the factors responsible for the immune dysfunction in MM might be the programmed death 1 (PD-1) protein. The physiological role of PD-1 is to guarantee T-cell homeostasis by limiting T-cell activation and proliferation. Accordingly, binding of the ligand PD-L1 to PD-1 expressed on the surface of activated T cells delivers an inhibitory signal, reducing cytokine production and proliferation. Using the same mechanism, PD-L1/PD-1 interactions have been shown in a number of animal models to confer tumor escape from immune control. Recently, clinical trials have suggested a significant therapeutic impact of PD-1/PD-L inhibition on a variety of solid tumors-for example, by the application of monoclonal antibodies. We show here that based on (1) the broad expression of PD-1 and its ligands in the microenvironment of myeloma, (2) data indicating an important role of the PD-1 pathway in the immune evasion by MM cells and (3) preclinical results providing a strong rationale for therapeutic PD-1/PD-L inhibition in this malignancy, MM may be very well suited for immunotherapy, for example, a monoclonal antibody, targeting PD-1 and/or its ligands.

Indexed as

ImmunotherapyAnimalsHumansLymphocyte ActivationMultiple MyelomaProgrammed Cell Death 1 ReceptorStem Cell TransplantationT-LymphocytesPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID24153012
OpenAlexW2105826859

What OpenQuestion holds

Textmetadata
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.