Evidence map›Paper›PMID 28668761›Full record

ArticleTranslational oncology2017

Selinexor Overcomes Hypoxia-Induced Drug Resistance in Multiple Myeloma.

Barbara Muz, Feda Azab, Pilar de la Puente, Yosef Landesman, Abdel Kareem Azab

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  5. NAT10 MediatesJournal of Cancer · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Article
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  11. Therapeutics to harness the immune microenvironment in multiple myeloma.Cancer drug resistance (Alhambra, Calif.) · 2022
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Role of CD47 in Hematological Malignancies.Journal of hematology & oncology · 2020
    Review
  18. Review
  19. Review
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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

5 authors at 2 institutions in 1 country.

Barbara MuzDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, Saint Louis, MO 63108, USA.
Feda AzabDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, Saint Louis, MO 63108, USA.
Pilar de la PuenteDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, Saint Louis, MO 63108, USA.
Yosef LandesmanKaryopharm Therapeutics, Newton, MA 02459, USA.
Abdel Kareem AzabDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, Saint Louis, MO 63108, USA. Electronic address: kareem.azab@wustl.edu.
Washington University in St. Louis · USKaryopharm Therapeutics (United States) · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
Project 2 - Radiation-Induced Treatment of Multiple Myeloma using NanoparticlesU54CA199092 · NCI · WASHINGTON UNIVERSITY · PI ACHILEFU, SAMUEL · 2015 to 2019
$11.5M
NCI NIH HHS P30 CA091842NCI NIH HHS U54 CA199092
6 · The paper itself

Abstract

Increased levels of the nuclear export protein, exportin 1 (XPO1), were demonstrated in multiple myeloma (MM) patients. Targeting XPO1 with selinexor (the selective inhibitor of nuclear export; SINE compound KPT-330) demonstrates broad antitumor activity also in patient cells resistant to bortezomib; hence, it is a promising target in MM patients. Hypoxia is known to mediate tumor progression and drug resistance (including bortezomib resistance) in MM cells. In this study, we tested the effects of selinexor alone or in combination with bortezomib in normoxia and hypoxia on MM cell survival and apoptosis in vitro and in vivo. In vitro, selinexor alone decreased survival and increased apoptosis, resensitizing MM cells to bortezomib. In vivo, we examined the effects of selinexor alone on tumor initiation and tumor progression, as well as selinexor in combination with bortezomib, on tumor growth in a bortezomib-resistant MM xenograft mouse model. Selinexor, used as a single agent, delayed tumor initiation and tumor progression, prolonging mice survival. In bortezomib-resistant xenografts, selinexor overcame drug resistance, significantly decreasing tumor burden and extending mice survival when combined with bortezomib.

Identifiers

PMID28668761
PMCPMC5496204
OpenAlexW2730740345

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.