Evidence map›Paper›PMID 26915293›Full record

ReviewCell death and differentiation2016

Phosphatidylserine is a global immunosuppressive signal in efferocytosis, infectious disease, and cancer.

R B Birge, S Boeltz, S Kumar, J Carlson, J Wanderley, D Calianese, M Barcinski, R A Brekken, X Huang, J T Hutchins and 6 more

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04150900 (1922GCCC), which is not on this map. Cited by 421 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
421citing papers in PubMed, 1 pooled it
24.9field-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.

NCT04150900 phase2active not recruitingnot on this mapstarted 2020, after this paper: background citation

1922gccc: phase 2 study of pembrolizumab and bavituximab for progressive recurrent/metastatic squamous cell carcinoma of the head and neck

TypeinterventionalSponsorUniversity of Maryland, BaltimoreRan2020 to 2027Enrolled7ConditionsSquamous Cell CarcinomaArmsBavituximab, Pembrolizumab
3 · Its place in the literature

Who cites it

421 citing papers in PubMed, 1 synthesis or guideline pooled it, 712 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

361 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

16 authors at 8 institutions in 4 countries.

R B BirgeDepartment of Microbiology, Biochemistry and Molecular Genetics, Cancer Center, Rutgers New Jersey Medical School, 205 South Orange Ave, Newark, NJ 07103, USA.
S BoeltzDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), University Hospital Erlangen, 91054 Erlangen, Germany.ORCID 0000-0001-5227-8707
S KumarDepartment of Microbiology, Biochemistry and Molecular Genetics, Cancer Center, Rutgers New Jersey Medical School, 205 South Orange Ave, Newark, NJ 07103, USA.
J CarlsonPeregrine Pharmaceuticals, 14282 Franklin Avenue, Tustin, CA 92780, USA.
J WanderleyUniversidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.ORCID 0000-0002-9707-6284
D CalianeseDepartment of Microbiology, Biochemistry and Molecular Genetics, Cancer Center, Rutgers New Jersey Medical School, 205 South Orange Ave, Newark, NJ 07103, USA.
M BarcinskiLaboratório de Biologia Celular, Instituto Oswaldo Cruz, Rio de Janeiro, Brazil.
R A BrekkenDivision of Surgical Oncology, Department of Surgery, Hamon Center for Therapeutic Oncology Research, Dallas, TX 75390-8593, USA.
X HuangDivision of Surgical Oncology, Department of Surgery, Hamon Center for Therapeutic Oncology Research, Dallas, TX 75390-8593, USA.
J T HutchinsPeregrine Pharmaceuticals, 14282 Franklin Avenue, Tustin, CA 92780, USA.
B FreimarkPeregrine Pharmaceuticals, 14282 Franklin Avenue, Tustin, CA 92780, USA.
C EmpigPeregrine Pharmaceuticals, 14282 Franklin Avenue, Tustin, CA 92780, USA.
J MercerMedical Research Council Laboratory for Molecular Cell Biology, University College London, Gower Street, London WC1E 6BT, UK.
A J SchroitSimmons Cancer Center and the Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390 USA.
G SchettDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), University Hospital Erlangen, 91054 Erlangen, Germany.
M HerrmannDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), University Hospital Erlangen, 91054 Erlangen, Germany.
Avid Bioservices (United States) · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DERutgers, The State University of New Jersey · USTexas Oncology · USFundação Oswaldo Cruz · BRMRC Laboratory for Molecular Cell Biology · GBThe University of Texas Southwestern Medical Center · USUniversidade Federal do Rio de Janeiro · BR

Funding

Non-canonical Signal Pathway for Crk in Breast CancerR01CA165077 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI BIRGE, RAYMOND B. · 2012 to 2016
$1.7M
Medical Research Council MC_UU_12018/7NCI NIH HHS R01 CA165077
6 · The paper itself

Abstract

Apoptosis is an evolutionarily conserved and tightly regulated cell death modality. It serves important roles in physiology by sculpting complex tissues during embryogenesis and by removing effete cells that have reached advanced age or whose genomes have been irreparably damaged. Apoptosis culminates in the rapid and decisive removal of cell corpses by efferocytosis, a term used to distinguish the engulfment of apoptotic cells from other phagocytic processes. Over the past decades, the molecular and cell biological events associated with efferocytosis have been rigorously studied, and many eat-me signals and receptors have been identified. The externalization of phosphatidylserine (PS) is arguably the most emblematic eat-me signal that is in turn bound by a large number of serum proteins and opsonins that facilitate efferocytosis. Under physiological conditions, externalized PS functions as a dominant and evolutionarily conserved immunosuppressive signal that promotes tolerance and prevents local and systemic immune activation. Pathologically, the innate immunosuppressive effect of externalized PS has been hijacked by numerous viruses, microorganisms, and parasites to facilitate infection, and in many cases, establish infection latency. PS is also profoundly dysregulated in the tumor microenvironment and antagonizes the development of tumor immunity. In this review, we discuss the biology of PS with respect to its role as a global immunosuppressive signal and how PS is exploited to drive diverse pathological processes such as infection and cancer. Finally, we outline the rationale that agents targeting PS could have significant value in cancer and infectious disease therapeutics.

Indexed as

AnimalsAntibodiesApoptosisApoptosis Regulatory ProteinsAutoimmunityCommunicable DiseasesHumansMembrane GlycoproteinsNeoplasmsPhosphatidylserinesReceptors, Cell SurfaceSignal TransductionAntibodiesApoptosis Regulatory ProteinsMembrane Glycoproteinsphosphatidylserine receptorPhosphatidylserinesReceptors, Cell Surface

Identifiers

PMID26915293
PMCPMC4987730
OpenAlexW2285852644

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.