Evidence map›Paper›PMID 11426647›Full record

ReviewOncogene2000

STAT proteins: novel molecular targets for cancer drug discovery.

J Turkson, R Jove

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 251 papers.

0numbers the graph read from it
0cells of the map it votes in
251citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

251 citing papers in PubMed, 648 citations in OpenAlex.

  1. Review
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  7. Article
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  10. Review
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  14. Article
  15. The STAT3-Regulated Autophagy Pathway in Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  16. Review
  17. Roles of STAT3 in the pathogenesis and treatment of glioblastoma.Frontiers in cell and developmental biology · 2023
    Review
  18. Review
  19. Review
  20. Article

191 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

J TurksonH. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.
R Jove
Moffitt Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal Transducers and Activators of Transcription (STATs) are a family of cytoplasmic proteins with roles as signal messengers and transcription factors that participate in normal cellular responses to cytokines and growth factors. Frequently, however, abnormal activity of certain STAT family members, particularly Stat3 and Stat5, is associated with a wide variety of human malignancies, including hematologic, breast, head and neck, and prostate cancers. Application of molecular biology and pharmacology tools in disease-relevant models has confirmed Stat3 as having a causal role in oncogenesis, and provided validation of Stat3 as a target for cancer drug discovery and therapeutic intervention. Furthermore, a constitutively-active mutant form of Stat3 is sufficient to induce oncogenic transformation of cells, which form tumors in vivo. Constitutive activation of Stat3 signaling is accompanied by upregulation of cyclin D1, c-Myc, and Bcl-x, changes consistent with subversion of normal cellular growth and survival control mechanisms. Block of constitutive Stat3 signaling results in growth inhibition and apoptosis of Stat3-positive tumor cells in vitro and in vivo. The observed dependence of certain tumors on constitutive Stat3 signaling for growth and survival has wide implications for cancer therapy, offering the potential for preferential tumor cell killing. This review evaluates constitutive Stat3 activation as a 'cancer-causing' factor, and proposes a number of molecular strategies for targeting Stat3 signaling for therapeutic intervention.

Indexed as

Milk ProteinsAntineoplastic AgentsDNA-Binding ProteinsDrug Delivery SystemsDrug DesignEnzyme InhibitorsHumansImmunologic Deficiency SyndromesModels, BiologicalNeoplasmsOligodeoxyribonucleotides, AntisensePhosphoprotein PhosphatasesProtein Kinase InhibitorsReceptors, Cell SurfaceSignal TransductionSTAT3 Transcription FactorAntineoplastic AgentsDNA-Binding ProteinsEnzyme InhibitorsMilk ProteinsOligodeoxyribonucleotides, AntisensePhosphoprotein PhosphatasesProtein Kinase InhibitorsReceptors, Cell SurfaceSTAT3 protein, humanSTAT3 Transcription FactorSTAT5 Transcription FactorTrans-Activators

Identifiers

PMID11426647
OpenAlexW2056961869

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.