Evidence map›Paper›PMID 28388555›Full record

ArticleOncotarget2017

Targeting mantle cell lymphoma metabolism and survival through simultaneous blockade of mTOR and nuclear transporter exportin-1.

Kazumasa Sekihara, Kaori Saitoh, Lina Han, Stefan Ciurea, Shinichi Yamamoto, Mika Kikkawa, Saiko Kazuno, Hikari Taka, Naoko Kaga, Hajime Arai and 4 more

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Metabolic Reprogramming and Potential Therapeutic Targets in Lymphoma.International journal of molecular sciences · 2023
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 2 countries.

Kazumasa SekiharaDepartment of Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Kaori SaitohDepartment of Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Lina HanSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Stefan CiureaSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Shinichi YamamotoDepartment of Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Mika KikkawaLaboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Saiko KazunoLaboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Hikari TakaLaboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Naoko KagaLaboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Hajime AraiLaboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Takashi MiidaDepartment of Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Michael AndreeffSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Marina KonoplevaSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Yoko TabeDepartment of Laboratory Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Juntendo University · JPThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KONOPLEVA, MARINA Y · 2003 to 2023
$43.7M
UNIVERSITY OF TEXAS MD ANDERSON SPORE IN OVARIAN CANCERP50CA083639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 1999 to 2015
$33.0M
THE THERAPY OF AMLP01CA055164 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMAS, MATTIE J · 1992 to 2011
$25.3M
UT M.D. Anderson Cancer Center Lymphoma SPOREP50CA136411 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BERRY, DONALD A · 2009 to 2011
$1.5M
NCI NIH HHS P01 CA055164NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA083639NCI NIH HHS P50 CA100632NCI NIH HHS P50 CA136411
6 · The paper itself

Abstract

Mantle cell lymphoma (MCL) is an aggressive B-cell lymphoma with poor prognosis, characterized by aberrant expression of growth-regulating and oncogenic effectors and requiring novel anticancer strategies. The nuclear transporter exportin-1 (XPO1) is highly expressed in MCL and is associated with its pathogenesis. mTOR signaling, a central regulator of cell metabolism, is frequently activated in MCL and is also an important therapeutic target in this cancer. This study investigated the antitumor effects and molecular/metabolic changes induced by the combination of the small-molecule selective inhibitor XPO1 inhibitor KPT-185 and the dual mTORC1/2 kinase inhibitor AZD-2014 on MCL cells. AZD-2014 enhanced the KPT-185-induced inhibition of cell growth and repression of cell viability. The combination of KPT-185 and AZD-2014 downregulated c-Myc and heat shock factor 1 (HSF1) with its target heat shock protein 70 (HSP70). As a consequence, the combination caused repression of ribosomal biogenesis demonstrated by iTRAQ proteomic analyses. Metabolite assay by CETOF-MS showed that AZD-2014 enhanced the KPT-185-induced repression of MCL cellular energy metabolism through the TCA (Krebs) cycle, and further repressed KPT-185-caused upregulation of glycolysis.Thus the simultaneous inhibition of XPO1 and mTOR signaling is a novel and promising strategy targeting prosurvival metabolism in MCL.

Indexed as

AcrylatesAntineoplastic Combined Chemotherapy ProtocolsBenzamidesCell Line, TumorCell ProliferationCell SurvivalEnergy MetabolismExportin 1 ProteinHumansKaryopherinsLymphoma, Mantle-CellMorpholinesProteomeProteomicsPyrimidinesReceptors, Cytoplasmic and NuclearAcrylatesBenzamidesExportin 1 ProteinKaryopherinsKPT-185MorpholinesMTOR protein, humanProteomePyrimidinesReceptors, Cytoplasmic and NuclearTOR Serine-Threonine KinasesTriazolesvistusertibmantle cell lymphomametabolismmTORC1/2selective inhibitor of nuclear exportXPO1

Identifiers

PMID28388555
PMCPMC5470990
OpenAlexW2599260063

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.