Evidence map›Paper›PMID 27822406›Full record

ReviewAmerican journal of cancer research2016

PD-1 inhibition and treatment of advanced melanoma-role of pembrolizumab.

Ali R Jazirehi, Alexandra Lim, Tam Dinh

Abstract readReview
In one paragraph

Review in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Review
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  4. Review
  5. Article
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  9. Review
  10. Re-introducing immunotherapy in patients surviving immune checkpoint inhibitors-mediated myocarditis.Clinical research in cardiology : official journal of the German Cardiac Society · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Monoclonal Antibodies for the Treatment of Multiple Myeloma: An Update.International journal of molecular sciences · 2018
    Review
  16. Article
  17. Review
  18. Review
  19. Photodynamic Therapy for Metastatic Melanoma Treatment: A Review.Technology in cancer research & treatment · 2018
    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

3 authors.

Ali R JazirehiDivision of Surgical Oncology, Department of Surgery, The Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, University of California at Los Angeles Los Angeles, California 90095, USA.
Alexandra LimDivision of Surgical Oncology, Department of Surgery, The Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, University of California at Los Angeles Los Angeles, California 90095, USA.
Tam DinhDivision of Surgical Oncology, Department of Surgery, The Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, University of California at Los Angeles Los Angeles, California 90095, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Remarkable clinical responses have been seen in patients with metastatic melanoma with targeted therapy (BRAFi vemurafenib, MEKi) and with modern immune cell-based approaches such as TCR engineered adoptive cell transfer (ACT) and earlier experiences with high-dose IL-2. The proximal mediators of these immune therapies are tumor-reactive CTL. Various mechanisms of resistance to immune-mediated apoptotic signals have been described, including phenotypic changes, effector cell exhaustion, functional tolerance, deficiencies in Ag processing and presentation, and mutation or down-regulation of antigenic epitopes. The immune system and drugs eradicate tumors via apoptosis. Therefore, tumors' resistance to apoptosis may be a determining factor that limits the efficacy of immunotherapies. It is predicted that these therapies have limited efficacy in patients whose melanomas have developed resistance to targeted therapy such as vemurafenib. Upregulation of the immune checkpoint molecule CTLA-4 on activated T cells and its interaction with CD80/86 blocks T cell activation. The fully humanized mAb ipilimumab blocks this interaction, resulting in sustained T cell stimulation. Likewise, the programmed death receptor 1 (PD-1) is another member of the B7:CD28 family of costimulatory molecules that regulates T cell activation, whose ligand (PD-L1) is expressed on melanomas. The human anti-PD-1 mAb, Pembrolizumab, overcomes tolerance, has a favorable pharmacokinetics profile with minimal undesired toxic side effects and has shown remarkable improvement in melanoma therapy. This review focuses on recent advances in the development of various anti-PD-1 checkpoint blockade antibodies and will summarize recent clinical data using immune checkpoint blocking antibodies.

Indexed as

apoptosisCTLA-4immunotherapyipilimumabMED14736melanomanivolumabPD-1PD-L1PembrolizumabTCRtremelimumab

Identifiers

PMID27822406
PMCPMC5088280

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.