Evidence map›Paper›PMID 28214929›Full record

ReviewCancer immunology, immunotherapy : CII2017

Myeloid cells as a target for oligonucleotide therapeutics: turning obstacles into opportunities.

Marcin Kortylewski, Dayson Moreira

Open access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Clinical applications of oligonucleotides for cancer therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Monocyte regulation by gut microbial signals.Trends in microbiology · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Tumor-Mediated Neutrophil Polarization and Therapeutic Implications.International journal of molecular sciences · 2022
    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

2 authors at 1 institution in 1 country.

Marcin KortylewskiDepartment of Immuno-Oncology at Beckman Research Institute, City of Hope National Medical Center, 1500 East Duarte Rd., Duarte, CA, 91010, USA. mkortylewski@coh.org.ORCID http://orcid.org/0000-0002-6003-1816
Dayson MoreiraDepartment of Immuno-Oncology at Beckman Research Institute, City of Hope National Medical Center, 1500 East Duarte Rd., Duarte, CA, 91010, USA.
City Of Hope National Medical Center · US

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI John Charles Williams · 1985 to 2026
$86.3M
Transplant for Lymphoma:Therapy-Related LeukemiaP50CA107399 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI FORMAN, STEPHEN J, KWAK, LARRY W · 2004 to 2022
$35.5M
CpG-siRNA Conjugates to Target Acute Myeloid LeukemiaR01CA155367 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI KORTYLEWSKI, MARCIN · 2011 to 2015
$1.7M
NCI NIH HHS P30 CA033572NCI NIH HHS P50 CA107399NCI NIH HHS R01 CA155367
6 · The paper itself

Abstract

Immunotherapies emerged as an alternative for cancer treatment, yet their clinical efficacies are still limited, especially in case of solid tumors. Myeloid immune cells, such as macrophages and myeloid-derived suppressor cells (MDSCs), are often hijacked by tumors and become pivotal inhibitors of antitumor immunity. Immunosuppressive functions of tumor-associated myeloid cells result from the activity of Signal Transducer and Activator of Transcription 3 (STAT3), a transcription factor with well-defined tumorigenic and tolerogenic roles in human cancers. To overcome challenges in the development of pharmacological STAT3 inhibitors, we recently developed oligonucleotide-based strategies for cell-selective, in vivo STAT3 targeting. Conjugation of a STAT3siRNA or decoy STAT3 inhibitors to synthetic Toll-like Receptor 9 (TLR9) agonists, CpG oligonucleotides, allowed for selective delivery into TLR9-positive cells. Cellular target for CpG-STAT3 inhibitors include non-malignant, tumor-associated myeloid cells, such as polymorphonuclear MDSCs, as well as cancer cells in acute myeloid leukemia, B cell lymphoma and in certain solid tumors. The chemically modified CpG-STAT3 inhibitors resist serum nucleases and thus can be administered intravenously. Their potency relies on the intracellular gain-of-function effect: release of the central immune checkpoint regulator (STAT3) to unleash proinflammatory signaling (CpG/TLR9) in the same antigen-presenting cell. At the cellular level, CpG-STAT3 inhibitors exert two-pronged effect by rescuing T cells from the immune checkpoint control while decreasing survival of cancer cells. In this article, we review the preclinical data on CpG-STAT3 inhibitors and discuss perspectives of using TLR9-targeted delivery of oligonucleotide therapeutics for the generation of novel, more effective and safer cancer immunotherapies.

Indexed as

AnimalsCpG IslandsHumansImmunotherapyLeukemia, Myeloid, AcuteMolecular Targeted TherapyMyeloid-Derived Suppressor CellsOligonucleotidesSTAT3 Transcription FactorToll-Like Receptor 9OligonucleotidesSTAT3 Transcription FactorToll-Like Receptor 9CpGMDSCOligonucleotidesRegulatory myeloid suppressor cellsSTAT3TLR9

Identifiers

PMID28214929
PMCPMC5522630
OpenAlexW2587880360

What OpenQuestion holds

Textmetadata
LicenceTDM
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.