Evidence map›Paper›PMID 24696041›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2014

Preclinical characterization of signal transducer and activator of transcription 3 small molecule inhibitors for primary and metastatic brain cancer therapy.

Hikmat H Assi, Chris Paran, Nathan VanderVeen, Jonathan Savakus, Robert Doherty, Emanuele Petruzzella, James D Hoeschele, Henry Appelman, Leda Raptis, Tom Mikkelsen and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Article
  7. Targeting gliomas with STAT3-silencing nanoparticles.Molecular & cellular oncology · 2021
    Article
  8. Review
  9. Article
  10. Review
  11. Effect of caveolin-1 on Stat3-ptyr705 levels in breast and lung carcinoma cells.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2019
    Article
  12. STAT3-induced SMYD3 transcription enhances chronic lymphocytic leukemia cell growth in vitro and in vivo.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  13. Targeting STAT3 signaling in kidney disease.American journal of physiology. Renal physiology · 2019
    Review
  14. Article
  15. Article
  16. Article
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  19. Article
  20. Review
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

12 authors at 5 institutions in 2 countries.

Hikmat H AssiDepartment of Neurosurgery and Department of Cell and Developmental Biology, University of Michigan School of Medicine, Ann Arbor, Michigan (H.H.A., C.P., N.V., J.S., R.D., P.R.L., M.G.C.); Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California (H.H.A.); Department of Chemistry, Eastern Michigan University, Ypsilanti, Michigan (E.P., J.D.H.); Department of Pathology, University of Michigan School of Medicine, University Hospital, Ann Arbor, Michigan (H.A.); Department of Biomedical and Molecular Sciences, Queen's University School of Medicine, Kingston, Ontario, Canada (L.R.); and Department of Neurology, Henry Ford Hospital, Detroit, Michigan (T.M.).
Chris Paran
Nathan VanderVeen
Jonathan Savakus
Robert Doherty
Emanuele Petruzzella
James D Hoeschele
Henry Appelman
Leda Raptis
Tom Mikkelsen
Pedro R Lowenstein
Maria G Castro
University of Michigan–Ann Arbor · USEastern Michigan University · USUniversity of California, Los Angeles · USHenry Ford Hospital · USQueen's University · CA

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
MICHIGAN INSTITUTE FOR CLINICAL AND HEALTH RESEARCH (MICHR) (UL1): (BPCA)UL1RR024986 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHANLEY, THOMAS P. · 2007 to 2011
$51.2M
Michigan Institute for Clinical and Health Research (MCHR)UL1TR000433 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MASHOUR, GEORGE ALEXANDER · 2012 to 2016
$49.9M
MICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3M
TRAINING IN CLINICAL AND BASIC NEUROSCIENCET32NS007222 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Henry L Paulson · 1985 to 2026
$8.0M
Training Program in Tumor MicroenvironmentT32CA009676 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Maria G Castro, Analisa Virginia DiFeo · 1992 to 2026
$7.3M
Gutless Adenovirus Mediated Gene Therapy for GliomaU01NS052465 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTRO, MARIA G · 2007 to 2011
$3.1M
Engineering the Brain Immune System for Tumor TherapyR01NS057711 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTRO, MARIA G · 2009 to 2013
$2.0M
Crosstalk between glioma cells & immune cells in the tumor microenvironment: TherR01NS074387 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTRO, MARIA G · 2011 to 2015
$1.9M
Brain immune responses:Cellular & Molecular MechanismsR01NS061107 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOWENSTEIN, PEDRO R. · 2008 to 2012
$1.7M
Mechanisms of glioma growth and invasion novel therapeutic strategiesR01NS082311 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOWENSTEIN, PEDRO R. · 2013 to 2017
$1.7M
Gene Therapy and the Brain: Neuroimmune InteractionsR01NS054193 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOWENSTEIN, PEDRO R. · 2007 to 2011
$1.6M
NCATS NIH HHS UL1 TR000433NCATS NIH HHS UL1-TR000433NCI NIH HHS P30 CA046592NCI NIH HHS P30-CA046592NCI NIH HHS T32 CA009676NCI NIH HHS T32-CA009676NCRR NIH HHS UL1 RR024986NIGMS NIH HHS T32 GM007863NIGMS NIH HHS T32-GM007863NINDS NIH HHS R01 NS054193NINDS NIH HHS R01-NS054193NINDS NIH HHS R01 NS057711NINDS NIH HHS R01-NS057711NINDS NIH HHS R01 NS061107NINDS NIH HHS R01-NS061107NINDS NIH HHS R01 NS074387NINDS NIH HHS R01-NS074387NINDS NIH HHS R01 NS082311NINDS NIH HHS R01-NS082311NINDS NIH HHS R21 NS084275NINDS NIH HHS R21-NS084275NINDS NIH HHS T32 NS007222NINDS NIH HHS T32-NS007222NINDS NIH HHS U01 NS052465NINDS NIH HHS U01-NS052465NINDS NIH HHS U01-NS052465-S1PHS HHS U042841
6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (STAT3) has been implicated as a hub for multiple oncogenic pathways. The constitutive activation of STAT3 is present in several cancers, including gliomas (GBMs), and is associated with poor therapeutic responses. Phosphorylation of STAT3 triggers its dimerization and nuclear transport, where it promotes the transcription of genes that stimulate tumor growth. In light of this role, inhibitors of the STAT3 pathway are attractive therapeutic targets for cancer. To this end, we evaluated the STAT3-inhibitory activities of three compounds (CPA-7 [trichloronitritodiammineplatinum(IV)], WP1066 [(S,E)-3-(6-bromopyridin-2-yl)-2-cyano-N-(1-phenylethyl)acrylamide, C17H14BrN3O], and ML116 [4-benzyl-1-{thieno[2,3-d]pyrimidin-4-yl}piperidine, C18H19N3S]) in cultured rodent and human glioma cells, including GBM cancer stem cells. Our results demonstrate a potent induction of growth arrest in GBM cells after drug treatment with a concomitant induction of cell death. Although these compounds were effective at inhibiting STAT3 phosphorylation, they also displayed variable dose-dependent inhibition of STAT1, STAT5, and nuclear factor κ light-chain enhancer of activated B cells. The therapeutic efficacy of these compounds was further evaluated in peripheral and intracranial mouse tumor models. Whereas CPA-7 elicited regression of peripheral tumors, both melanoma and GBM, its efficacy was not evident when the tumors were implanted within the brain. Our data suggest poor permeability of this compound to tumors located within the central nervous system. WP1066 and ML116 exhibited poor in vivo efficacy. In summary, CPA-7 constitutes a powerful anticancer agent in models of peripheral solid cancers. Our data strongly support further development of CPA-7-derived compounds with increased permeability to enhance their efficacy in primary and metastatic brain tumors.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBlood-Brain BarrierBrain NeoplasmsCell Line, TumorCell ProliferationChlorine CompoundsDrug Screening Assays, AntitumorGliomaHEK293 CellsHeterocyclic Compounds, 2-RingHumansMelanoma, ExperimentalMicePiperidines4-benzyl-1-(thieno(2,3-d)pyrimidin-4-yl)piperidineAntineoplastic AgentsChlorine CompoundsHeterocyclic Compounds, 2-RingPiperidinesPlatinum CompoundsPyridinesSmall Molecule LibrariesSTAT3 Transcription Factortrichloronitritodiammineplatinum(IV)TyrphostinsWP1066

Identifiers

PMID24696041
PMCPMC4019317
OpenAlexW1971358650

What OpenQuestion holds

Textmetadata
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.