Evidence map›Paper›PMID 25667985›Full record

ReviewmAbs2015

Macrophages are critical effectors of antibody therapies for cancer.

Kipp Weiskopf, Irving L Weissman

Open access · goldAbstract readReview
In one paragraph

Review in mAbs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed
11.2field-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

171 citing papers in PubMed, 282 citations in OpenAlex.

  1. Trial
  2. Inhibitory Fc Receptor sets a time limit on macrophage response to IgG.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Advances in immunotherapies in ovarian cancer.Journal for immunotherapy of cancer · 2026
    Review
  7. Review
  8. Hyperactive Rac converts sublethal to lethal trogocytosis in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Hyperactive Rac converts sublethal nibbling to lethal phagocytosisbioRxiv : the preprint server for biology · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

111 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 2 institutions in 2 countries.

Kipp Weiskopfa Institute for Stem Cell Biology and Regenerative Medicine ; Stanford University School of Medicine ; Stanford , CA USA.
Irving L Weissman
Cancer Institute (WIA) · INStanford University · US

Funding

EVOLVING HIGH AFFINITY SIRPa MUTANTS TO STIMULATE PHAGOCYTOSIS OF TUMOR CELLSF30CA168059 · NCI · STANFORD UNIVERSITY · PI WEISKOPF, KIPP A · 2012 to 2014
$142k
NCI NIH HHS F30CA168059
6 · The paper itself

Abstract

Macrophages are innate immune cells that derive from circulating monocytes, reside in all tissues, and participate in many states of pathology. Macrophages play a dichotomous role in cancer, where they promote tumor growth but also serve as critical immune effectors of therapeutic antibodies. Macrophages express all classes of Fcγ receptors, and they have immense potential to destroy tumors via the process of antibody-dependent phagocytosis. A number of studies have demonstrated that macrophage phagocytosis is a major mechanism of action of many antibodies approved to treat cancer. Consequently, a number of approaches to augment macrophage responses to therapeutic antibodies are under investigation, including the exploration of new targets and development of antibodies with enhanced functions. For example, the interaction of CD47 with signal-regulatory protein α (SIRPα) serves as a myeloid-specific immune checkpoint that limits the response of macrophages to antibody therapies, and CD47-blocking agents overcome this barrier to augment phagocytosis. The response of macrophages to antibody therapies can also be enhanced with engineered Fc variants, bispecific antibodies, or antibody-drug conjugates. Macrophages have demonstrated success as effectors of cancer immunotherapy, and further investigation will unlock their full potential for the benefit of patients.

Indexed as

Antibodies, NeoplasmNeoplasmsAnimalsHumansMacrophagesPhagocytosisReceptors, IgGAntibodies, NeoplasmReceptors, IgGADC, antibody-drug conjugateADCC, antibody-dependent cell-mediated cytotoxicityADCPADCP, antibody-dependent cellular phagocytosisAML, acute myelogenous leukemiaantibodiesBTK, Bruton's tyrosine kinasecancerCD47CD, cluster of differentiationCLL, chronic lymphocytic leukemiaEGFR, epidermal growth factor receptorFc, fragment crystallizableFc receptorFcγR, Fcγ receptorsGM-CSF, granulocyte-macrophage colony stimulating factorHER2, human epidermal growth factor receptor 2HSC, haematopoietic stem cellIgG, immunoglobulin Gimmune checkpointimmunotherapyITAM, immunoreceptor tyrosine-based activation motifITIM, immunoreceptor tyrosine-based inhibitory motifmacrophagesM-CSF, macrophage colony stimulating factorNK, natural killerphagocytosisSHP, Src homology 2 domain-containing phosphataseSIRPαSIRPα, signal-regulatory protein α

Identifiers

PMID25667985
PMCPMC4622600
OpenAlexW1934768104

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.