ArticleOncotarget2018
Selinexor synergizes with dexamethasone to repress mTORC1 signaling and induce multiple myeloma cell death.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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.
Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Trial
- Once weekly selinexor, carfilzomib and dexamethasone in carfilzomib non-refractory multiple myeloma patients.British journal of cancer · 2022Trial
- Selinexor, bortezomib, and dexamethasone versus bortezomib and dexamethasone in previously treated multiple myeloma: Outcomes by cytogenetic risk.American journal of hematology · 2021Trial
- Selinexor plus ruxolitinib in JAK inhibitor-naïve patients with myelofibrosis: a multicenter, open-label, phase 1 study.Blood advances · 2026Article
- Refining the role of selinexor in multiple myeloma: strategic use in a shifting treatment landscape.ESMO open · 2026Review
- Current Status of Molecularly Targeted Therapeutics in Blood Cancers.International journal of molecular sciences · 2025Review
- A phase IIb study of selinexor in combination with daratumumab in patients with daratumumab-refractory multiple myeloma.Haematologica · 2025Article
- Review
- Lowering the Selinexor Dose within the Pomalidomide and Dexamethasone Combination Regimen Elicits Fewer Side Effects While Comparable Efficacy Against Relapsed/Refractory Multiple Myeloma.OncoTargets and therapy · 2025Article
- The numerous facets of 1q21Oncology letters · 2024Review
- A novel application of XPO1 inhibition for the treatment of myelofibrosis.Blood neoplasia · 2024Review
- Treatment of multiple myeloma with selinexor: a review.Therapeutic advances in hematology · 2024Review
- Review
- Dual targeting of protein translation and nuclear protein export results in enhanced antimyeloma effects.Blood advances · 2023Article
- Selinexor-Bortezomib-Dexamethasone: A Review in Previously Treated Multiple Myeloma.Targeted oncology · 2023Review
- Relapsed/Refractory Multiple Myeloma: A Review of Available Therapies and Clinical Scenarios Encountered in Myeloma Relapse.Current oncology (Toronto, Ont.) · 2023Review
- Research progress in the role and mechanism of Leucine in regulating animal growth and development.Frontiers in physiology · 2023Review
- P2RY2-AKT activation is a therapeutically actionable consequence of XPO1 inhibition in acute myeloid leukemia.Nature cancer · 2022Article
- Selective inhibition of nuclear export: a promising approach in the shifting treatment paradigms for hematological neoplasms.Leukemia · 2022Review
- Selinexor inhibits growth of patient derived chordomasFrontiers in oncology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma (MM) is a plasma cell neoplasm that results in over 11,000 deaths in the United States annually. The backbone therapy for the treatment of MM patients almost always includes combinations with corticosteroids such as dexamethasone (DEX). We found that DEX in combination with selinexor, an inhibitor of exportin-1 (XPO1) activity, synergistically inhibits the mTOR pathway and subsequently promotes cell death in MM cells. Specifically, we show that selinexor induces the expression of the glucocorticoid receptor (GR) and when combined with dexamethasone increases GR transcriptional activity. Moreover, we found that key downstream targets of the mTOR pathway are deregulated by the combination and identified a mechanism in which GR enhances the expression of REDD1 in GR positive cells while suppressing mTOR activity and cell viability. While the single agent activity of selinexor in MM cells appears to be GR-independent, synergy with DEX depends on GR expression. These data suggest that patients with tumor cells that are GR positive will benefit substantially from the combination. The current findings are consistent with the beneficial therapeutic outcome in patients with MM when treated with the combination of selinexor and DEX. In addition, they provide a rationale for testing GR and REDD1 as predictive and prognostic markers of response, respectively, for patients treated with this beneficial combination.
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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.