Evidence map›Paper›PMID 40136679›Full record

ReviewCells2025

Selinexor's Immunomodulatory Impact in Advancing Multiple Myeloma Treatment.

Kereshmeh Tasbihi, Heiko Bruns

Abstract readReview
In one paragraph

Review in Cells, 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

2 authors.

Kereshmeh TasbihiDepartment of Medicine 5-Hematology and Oncology, University Hospital Erlangen, 91054 Erlangen, Germany.
Heiko BrunsDepartment of Medicine 5-Hematology and Oncology, University Hospital Erlangen, 91054 Erlangen, Germany.

Funding

Interdisciplinary Center for Clinical Research, Faculty of Medicine, Friedrich-Alexander University Erlangen-Nürnberg None
6 · The paper itself

Abstract

Despite the major advancements in the repertoire for multiple myeloma (MM) treatment, this disease remains a chronically progressive plasma cell malignancy. Drug resistance and high relapse rates complicate the extended treatment strategies. However, the tumor microenvironment (TME) in MM is decisive for the success of a therapy or relapse. Aiming to improve the outcome of relapsed and refractory MM patients, Selinexor has entered the drug arsenal of myeloma therapy through the implementation of a novel therapeutic approach by selectively inhibiting the nuclear export receptor Exportin-1 (XPO1). Selinexor leads to the inactivation of cancer-related proteins and induces apoptosis by disrupting the nucleocytoplasmic flow in myeloma cells. While this drug is selectively cytotoxic to neoplastic cells, Selinexor's immunomodulatory impact on the TME is currently being investigated. The aim of this review was to elucidate Selinexor's capacity to influence the cell interaction network of the TME from an immunological perspective. Deciphering the complex interplay of highly plastic immune cells provides a contribution to the molecular-biological exploration of disease initiation and progression in MM. Unraveling the novel therapeutic targets of the immunological TME and evaluating the advanced immunotherapeutic regimens implementing Selinexor will shape the future directions of immune-oncotherapy in MM.

Indexed as

HydrazinesImmunomodulationMultiple MyelomaTriazolesAnimalsExportin 1 ProteinHumansReceptors, Cytoplasmic and NuclearTumor MicroenvironmentExportin 1 ProteinHydrazinesReceptors, Cytoplasmic and NuclearselinexorTriazolesExportin-1immunotherapymultiple myelomanuclear exportSelinexortumor microenvironmentXPO1XPOVIO

Identifiers

PMID40136679
PMCPMC11940887

What OpenQuestion holds

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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.