Evidence map›Paper›PMID 32149732›Full record

ReviewThe Journal of clinical investigation2020

Immunotherapy of multiple myeloma.

Simone A Minnie, Geoffrey R Hill

2 registry-linked trialsAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 134 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 3 pooled it
–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.

NCT06252792 recruitingnot on this mapstarted 2023, after this paper: background citation

Prospective, Multicenter, Open and Non-interference Observational Clinical Study of Daratumumab, Pomalidomide and Dexamethasone (Dara-PD) in the Treatment of Patients With First Relapse of Multiple Myeloma

TypeobservationalSponsorFengYan JinRan2023 to 2026Enrolled50ConditionsMultiple Myeloma, First Relapse
NCT06536413 phase1 / phase2recruitingnot on this mapstarted 2024, after this paper: background citation

Phase IB/II Study Combining All-Trans Retinoic Acid (ATRA) With Carfilzomib Based Therapy in Plasma Cell Myeloma Patients Refractory to Carfilzomib

TypeinterventionalSponsorThe Methodist Hospital Research InstituteRan2024 to 2030Enrolled42ConditionsMultiple MyelomaArmsAll-Trans Retinoic Acid (ATRA) Dose 0, All-Trans Retinoic Acid (ATRA) Dose -1, All-Trans Retinoic Acid (ATRA) Dose 1
3 · Its place in the literature

Who cites it

134 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  12. Selinexor potentiates NK cell activation against multiple myeloma.Clinical and experimental immunology · 2026
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74 more citing papers are in PubMed but not listed here.

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

2 authors.

Simone A MinnieClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Geoffrey R HillClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.

Funding

Preventing Myeloma Relapse after Autologous Stem Cell Transplantation with Decoy Resistant IL-18U01CA244291 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HILL, GEOFFREY ROGER · 2019 to 2022
$4.2M
NCI NIH HHS U01 CA244291
6 · The paper itself

Abstract

Multiple myeloma (MM), a bone marrow-resident hematological malignancy of plasma cells, has remained largely incurable despite dramatic improvements in patient outcomes in the era of myeloma-targeted and immunomodulatory agents. It has recently become clear that T cells from MM patients are able to recognize and eliminate myeloma, although this is subverted in the majority of patients who eventually succumb to progressive disease. T cell exhaustion and a suppressive bone marrow microenvironment have been implicated in disease progression, and once these are established, immunotherapy appears largely ineffective. Autologous stem cell transplantation (ASCT) is a standard of care in eligible patients and results in immune effects beyond cytoreduction, including lymphodepletion, T cell priming via immunogenic cell death, and inflammation; all occur within the context of a disrupted bone marrow microenvironment. Recent studies suggest that ASCT reestablishes immune equilibrium and thus represents a logical platform in which to intervene to prevent immune escape. New immunotherapies based on checkpoint inhibition targeting the immune receptor TIGIT and the deletion of suppressive myeloid populations appear attractive, particularly after ASCT. Finally, the immunologically favorable environment created after ASCT may also represent an opportunity for approaches utilizing bispecific antibodies or chimeric antigen receptor T cells.

Indexed as

Hematopoietic Stem Cell TransplantationImmunotherapyMultiple MyelomaHumansTransplantation, AutologousTumor Microenvironment

Identifiers

PMID32149732
PMCPMC7108923

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.