Evidence map›Paper›PMID 19551381›Full record

ReviewCancer immunology, immunotherapy : CII2009

Treatment combinations targeting apoptosis to improve immunotherapy of melanoma.

Peter Hersey, Xu Dong Zhang

Open access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Multidrug Resistance: Are We Still Afraid of the Big Bad Wolf.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Role of Apollon in human melanoma resistance to antitumor agents that activate the intrinsic or the extrinsic apoptosis pathways.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Article
  17. Article
  18. Article
  19. Article
  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.

Peter HerseyOncology and Immunology Unit, Calvary Mater Newcastle Hospital, Room 443, David Maddison Clinical Sciences Building, Cnr. King and Watt Streets, Newcastle, NSW 2300, Australia. peter.hersey@newcastle.edu.au
Xu Dong Zhang
Calvary Mater Newcastle Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunotherapy based on T cell responses to the tumor is believed to involve killing of cancer cells by induction of apoptosis. The predominant mechanisms are death ligand-induced signaling mainly by TNF-related apoptosis-inducing ligand (TRAIL) mediated by CD4 T cells, monocytes and dendritic cells, and perforin/granzyme mediated apoptosis mediated by CD8 T cells and NK cells. Resistance against TRAIL involves loss of TRAIL death receptors and/or activation of the MEK and/or Akt signal pathways. Resistance to CD8 CTL responses also involves activation of the MEK and/or Akt pathways. Apoptosis induced by immune responses is regulated by the Bcl-2 family of proteins. Many reagents have been developed against the Bcl-2 antiapoptotic proteins and clinical trials combining them with immunotherapy are awaited. The second group of agents that regulate the Bcl-2 family of proteins are the signal pathway inhibitors. Clinical trials with inhibitors of RAS, RAF or MEK are in progress and would appear an exciting combination with immunotherapy. One of the main drivers of resistance to apoptosis are adaptive mechanisms that allow cancer cells to overcome endoplasmic reticulum (ER) stress. These adaptive mechanisms inhibit practically all known apoptotic pathways and create an acidic environment that may reduce infiltration of lymphocytes against the tumor. The signal pathway inhibitors may be effective against these adaptive processes but additional agents that target ER stress pathways are in development. In conclusion, combination of immunotherapy with agents that target antiapoptotic mechanisms in cancer cells offers a new approach that requires evaluation in clinical trials.

Indexed as

ImmunotherapyApoptosisEndoplasmic ReticulumHumansMelanomaMitogen-Activated Protein Kinase KinasesMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2Receptors, TNF-Related Apoptosis-Inducing LigandSignal TransductionT-Lymphocytes, CytotoxicTNF-Related Apoptosis-Inducing LigandMitogen-Activated Protein Kinase KinasesMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2Receptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID19551381
PMCPMC11030855
OpenAlexW2072642762

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.