Evidence map›Paper›PMID 29807457›Full record

ReviewImmunotherapy2018

Regulation of innate and adaptive antitumor immunity by IAP antagonists.

Stephanie K Dougan, Michael Dougan

Open access · hybridAbstract readReview
In one paragraph

Review in Immunotherapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.4field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Second Mitochondrial Activator of Caspases Mimetics Accelerate Progression of Locally Advanced Head and Neck Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025
    Article
  7. Article
  8. Early-Phase Trial of IAP Antagonist Tolinapant and Definitive Radiation in Cisplatin-Ineligible Patients with Advanced Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  9. Article
  10. Cytokines in cancer.Cancer cell · 2025
    Review
  11. Article
  12. 3D Tumor Model to Study Immune Cell Infiltration.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. cIAP1/2 Antagonism Induces Antigen-Specific T Cell-Dependent Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2023
    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

2 authors at 2 institutions in 1 country.

Stephanie K DouganDepartment of Cancer Immunology & Virology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Michael DouganHarvard Medical School, Boston, MA 02115, USA.
Dana-Farber Cancer Institute · USMassachusetts General Hospital · US

Funding

Regulation of brown fat metabolism by the immune receptor PD-L1K08DK114563 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI DOUGAN, MICHAEL LAWRENCE · 2017 to 2021
$868k
NIDDK NIH HHS K08 DK114563
6 · The paper itself

Abstract

Inhibition of the T-cell co-inhibitory checkpoint receptors or their ligands CTLA-4, PD-1 and PD-L1 using monoclonal antibodies has proven to be highly effective against many cancers. Yet many cancers remain resistant to checkpoint blockade, and durable remissions occur in only a minority of patients. Novel approaches to enhancing antitumor responses are thus necessary in order to expand the reach of these treatments. The inhibitor of apoptosis (IAP) protein family comprises a diverse group of proteins, many of which have immunoregulatory roles. Small molecule IAP antagonists have been developed and are undergoing early phase clinical testing. These drugs were initially developed to promote tumor cell apoptosis; however, a considerable body of work now indicates that IAP antagonists induce antitumor activity through modulation of innate and adaptive immunity. Primarily through inhibition of cellular (c)-IAP1 and c-IAP2, IAP antagonists can activate alternative NF-κB signaling, promoting B-cell survival, activation of dendritic cells and delivering a broad co-stimulatory signal to T cells. At the same time, IAP antagonists can promote tumor cell intrinsic sensitization to innate immune signals, and enhance tumor cell killing by inflammatory cytokines and phagocytic macrophages. These drugs thus represent an attractive investigational approach to immunotherapy, providing a positive signaling counterpart to the relief of signal inhibition conferred by checkpoint blockade.

Indexed as

Adaptive ImmunityAnimalsAntineoplastic AgentsApoptosis Regulatory ProteinsBaculoviral IAP Repeat-Containing 3 ProteinBiomimeticsClinical Trials as TopicDisease Models, AnimalHumansImmunity, InnateImmunotherapyIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsNeoplasmsNF-kappa BSignal TransductionAntineoplastic AgentsApoptosis Regulatory ProteinsBaculoviral IAP Repeat-Containing 3 ProteinDIABLO protein, humanIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsNF-kappa BTNF protein, humanTumor Necrosis Factor-alphac-IAP1/c-IAP2IAP antagonistsinhibitor of apoptosis proteinsSMAC mimeticstumor immunotherapy

Identifiers

PMID29807457
PMCPMC6462841
OpenAlexW2805076370

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.