Evidence map›Paper›PMID 33203730›Full record

ReviewMolecular cancer therapeutics2021

Targeting STAT3 with Proteolysis Targeting Chimeras and Next-Generation Antisense Oligonucleotides.

Jamie V Shiah, Jennifer R Grandis, Daniel E Johnson

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cancer therapeutics, 2021. 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
0.9field-weighted citation impact, top 22% 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, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Psoralen and Isopsoralen fromPharmaceuticals (Basel, Switzerland) · 2026
    Article
  4. Review
  5. Sphingolipid Metabolism in the Pathogenesis of Hashimoto's Thyroiditis.International journal of molecular sciences · 2025
    Review
  6. STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
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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

3 authors at 1 institution in 1 country.

Jamie V ShiahDepartment of Otolaryngology - Head and Neck Surgery, University of California at San Francisco, San Francisco, California.
Jennifer R GrandisDepartment of Otolaryngology - Head and Neck Surgery, University of California at San Francisco, San Francisco, California.
Daniel E JohnsonDepartment of Otolaryngology - Head and Neck Surgery, University of California at San Francisco, San Francisco, California. daniel.johnson@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
Targeting STAT3 to enhance anti-tumor immunityR01DE028289 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRANDIS, JENNIFER RUBIN, JOHNSON, DANIEL E · 2019 to 2023
$3.2M
NCI NIH HHS P50 CA097190NCI NIH HHS R35 CA231998NIDCR NIH HHS R01 DE028289
6 · The paper itself

Abstract

STAT3 has been recognized for its key role in the progression of cancer, where it is frequently upregulated or constitutively hyperactivated, contributing to tumor cell proliferation, survival, and migration, as well as angiogenesis and suppression of antitumor immunity. Given the ubiquity of dysregulated STAT3 activity in cancer, it has long been considered a highly attractive target for the development of anticancer therapies. Efforts to target STAT3, however, have proven to be especially challenging, perhaps owing to the fact that transcription factors lack targetable enzymatic activity and have historically been considered "undruggable." Small-molecule inhibitors targeting STAT3 have been limited by insufficient selectivity and potency. More recently, therapeutic approaches that selectively target STAT3 protein for degradation have been developed, offering novel strategies that do not rely on inhibition of upstream pathways or direct competitive inhibition of the STAT3 protein. Here, we review these emerging approaches, including the development of STAT3 proteolysis targeting chimera agents, as well as preclinical and clinical studies of chemically stabilized antisense molecules, such as the clinical agent AZD9150. These therapeutic strategies may robustly reduce the cellular activity of oncogenic STAT3 and overcome the historical limitations of less selective small molecules.

Indexed as

ChimeraHumansOligonucleotides, AntisenseProteolysisSTAT3 Transcription FactorOligonucleotides, AntisenseSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID33203730
PMCPMC7888537
OpenAlexW3101466413

What OpenQuestion holds

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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.