Evidence map›Paper›PMID 26399741›Full record

ArticleScientific reports2015

Longitudinal tracking of single live cancer cells to understand cell cycle effects of the nuclear export inhibitor, selinexor.

Joshua M Marcus, Russell T Burke, John A DeSisto, Yosef Landesman, James D Orth

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Article
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  8. Phase I Trial of Selinexor in Pediatric Recurrent/Refractory Solid and CNS Tumors (ADVL1414): A Children's Oncology Group Phase I Consortium Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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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.

Joshua M MarcusDepartment of Molecular, Cellular, and Developmental Biology, GOLD A240B, 347 UCB, University of Colorado-Boulder, Boulder, CO 80309 USA.
Russell T BurkeDepartment of Molecular, Cellular, and Developmental Biology, GOLD A240B, 347 UCB, University of Colorado-Boulder, Boulder, CO 80309 USA.
John A DeSistoDepartment of Molecular, Cellular, and Developmental Biology, GOLD A240B, 347 UCB, University of Colorado-Boulder, Boulder, CO 80309 USA.
Yosef LandesmanKaryopharm Therapeutics, Inc., 85 Wells Ave., Newton, MA 02459.
James D OrthDepartment of Molecular, Cellular, and Developmental Biology, GOLD A240B, 347 UCB, University of Colorado-Boulder, Boulder, CO 80309 USA.

Funding

TRAINING IN SIGNAL TRANSDUCTION &CELL CYCLE REGULATIONT32GM008759 · NIGMS · UNIVERSITY OF COLORADO AT BOULDER · PI AHN, NATALIE G. · 2000 to 2020
$5.9M
Training Program in Cell, Molecular, and Developmental BiologyT32GM008111 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 1985 to 2022
$5.4M
Predoctoral Training Program in Signaling and Cellular Regulation INCLUDE Down Syndrome SupplementT32GM142607 · NIGMS · UNIVERSITY OF COLORADO · PI Sabrina Leigh Spencer, Tin Tin Su · 2021 to 2026
$3.6M
NIGMS NIH HHS T32 GM008111NIGMS NIH HHS T32 GM008759NIGMS NIH HHS T32 GM08759NIGMS NIH HHS T32 GM142607
6 · The paper itself

Abstract

Longitudinal tracking is a powerful approach to understand the biology of single cells. In cancer therapy, outcome is determined at the molecular and cellular scale, yet relationships between cellular response and cell fate are often unknown. The selective inhibitor of nuclear export, selinexor, is in development for the treatment of various cancers. Selinexor covalently binds exportin-1, causing nuclear sequestration of cargo proteins, including key regulators of the cell cycle and apoptosis. The cell cycle effects of selinexor and the relationships between cell cycle effects and cell fates, has not been described for individual cells. Using fluorescent cell cycle indicators we report the majority of cell death after selinexor treatment occurs from a protracted G1-phase and early S-phase. G1- or early S-phase treated cells show the strongest response and either die or arrest, while those treated in late S- or G2-phase progress to mitosis and divide. Importantly, the progeny of cell divisions also die or arrest, mostly in the next G1-phase. Cells that survive selinexor are negative for multiple proliferation biomarkers, indicating a penetrant, arrested state. Selinexor acts quickly, shows strong cell cycle selectivity, and is highly effective at arresting cell growth and inducing death in cancer-derived cells.

Indexed as

Cell TrackingActive Transport, Cell NucleusAntineoplastic AgentsCell CycleCell Cycle CheckpointsCell DeathCell Line, TumorCell SurvivalFluorescent DyesHumansHydrazinesPhenotypeSingle-Cell AnalysisTriazolesAntineoplastic AgentsFluorescent DyesHydrazinesselinexorTriazoles

Identifiers

PMID26399741
PMCPMC4585873

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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.