Evidence map›Paper›PMID 31671769›Full record

ReviewCancers2019

Targeting STAT3 in Cancer with Nucleotide Therapeutics.

Yue-Ting K Lau, Malini Ramaiyer, Daniel E Johnson, Jennifer R Grandis

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. 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
3.2field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
  3. Article
  4. The Role of Pomegranate (Food science & nutrition · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Chemotherapy: a double-edged sword in cancer treatment.Cancer immunology, immunotherapy : CII · 2022
    Review
  18. Article
  19. Review
  20. Article
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

4 authors at 1 institution in 1 country.

Yue-Ting K LauDepartment Otolaryngology-Head and Neck Surgery, University of California at San Francisco, 1450 3rd Street, Room HD268, Box 3111, San Francisco, CA 94143, USA. Kara.Lau@ucsf.edu.
Malini RamaiyerDepartment Otolaryngology-Head and Neck Surgery, University of California at San Francisco, 1450 3rd Street, Room HD268, Box 3111, San Francisco, CA 94143, USA. malinisramaiyer@gmail.com.
Daniel E JohnsonDepartment Otolaryngology-Head and Neck Surgery, University of California at San Francisco, 1450 3rd Street, Room HD268, Box 3111, San Francisco, CA 94143, USA. daniel.johnson@ucsf.edu.
Jennifer R GrandisDepartment Otolaryngology-Head and Neck Surgery, University of California at San Francisco, 1450 3rd Street, Room HD268, Box 3111, San Francisco, CA 94143, USA. jennifer.grandis@ucsf.edu.
University of California, San Francisco · US

Funding

WILD TYPE P53-BASED ADJUVANT IMMUNOTHERAPY FOR SCCHNP50CA097190 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Heath Devin Skinner · 2004 to 2026
$49.6M
Integrating genomics and the protein interactome for HPV+ head and neck cancer therapyR35CA231998 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRANDIS, JENNIFER RUBIN · 2018 to 2024
$6.2M
Implications of Procaspase-8 Mutations in Oral Squamous Cell CarcinomaR01DE024728 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHNSON, DANIEL E · 2016 to 2020
$2.0M
NCI NIH HHS P50 CA097190NCI NIH HHS R35 CA231998NIDCR NIH HHS R01 DE024728NIH HHS CA097190 (JRG)NIH HHS CA231998NIH HHS DE024728 (DEJ)
6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (STAT3) plays a critical role in promoting the proliferation and survival of tumor cells. As a ubiquitously-expressed transcription factor, STAT3 has commonly been considered an "undruggable" target for therapy; thus, much research has focused on targeting upstream pathways to reduce the expression or phosphorylation/activation of STAT3 in tumor cells. Recently, however, novel approaches have been developed to directly inhibit STAT3 in human cancers, in the hope of reducing the survival and proliferation of tumor cells. Several of these agents are nucleic acid-based, including the antisense molecule AZD9150, CpG-coupled STAT3 siRNA, G-quartet oligodeoxynucleotides (GQ-ODNs), and STAT3 decoys. While the AZD9150 and CpG-STAT3 siRNA interfere with STAT3 expression, STAT3 decoys and GQ-ODNs target constitutively activated STAT3 and modulate its ability to bind to target genes. Both STAT3 decoy and AZD9150 have advanced to clinical testing in humans. Here we will review the current understanding of the structures, mechanisms, and potential clinical utilities of the nucleic acid-based STAT3 inhibitors.

Indexed as

dynamic programminghedgingpost-decision state variablerisk managementtransaction costs

Identifiers

PMID31671769
PMCPMC6896109
OpenAlexW2982637596

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.