Evidence map›Paper›PMID 27622058›Full record

ArticleOncoimmunology2016

Suppressive effects of tumor cell-derived 5'-deoxy-5'-methylthioadenosine on human T cells.

Frederik C Henrich, Katrin Singer, Kerstin Poller, Luise Bernhardt, Carolin D Strobl, Katharina Limm, Axel P Ritter, Eva Gottfried, Simon Völkl, Benedikt Jacobs and 8 more

Abstract read
In one paragraph

Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed.

  1. Review
  2. Article
  3. Presenting features and outcomes to standard systemic therapies in patients with MTAP-deleted advanced non-small cell lung cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. 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

18 authors.

Frederik C HenrichDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.
Katrin SingerDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen, Erlangen, Germany; Department of Internal Medicine 3 - Hematology and Oncology, University Hospital of Regensburg, Regensburg, Germany.
Kerstin PollerDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.
Luise BernhardtDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.
Carolin D StroblDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.
Katharina LimmInstitute of Biochemistry - Emil-Fischer-Zentrum, Friedrich-Alexander University of Erlangen-Nuremberg , Erlangen, Germany.
Axel P RitterInstitute of Functional Genomics, University of Regensburg , Regensburg, Germany.
Eva GottfriedDepartment of Internal Medicine 3 - Hematology and Oncology, University Hospital of Regensburg , Regensburg, Germany.
Simon VölklDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.
Benedikt JacobsDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen, Erlangen, Germany; Department of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Radiumhospital, Oslo, Norway; The KG Jebsen Center for Cancer Immunotherapy, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Katrin PeterDepartment of Internal Medicine 3 - Hematology and Oncology, University Hospital of Regensburg , Regensburg, Germany.
Dimitrios MougiakakosDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.
Katja DettmerInstitute of Functional Genomics, University of Regensburg , Regensburg, Germany.
Peter J OefnerInstitute of Functional Genomics, University of Regensburg , Regensburg, Germany.
Anja-Katrin BosserhoffInstitute of Biochemistry - Emil-Fischer-Zentrum, Friedrich-Alexander University of Erlangen-Nuremberg , Erlangen, Germany.
Marina P KreutzDepartment of Internal Medicine 3 - Hematology and Oncology, University Hospital of Regensburg , Regensburg, Germany.
Michael AignerDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.
Andreas MackensenDepartment of Internal Medicine 5 - Hematology and Oncology, University Hospital of Erlangen , Erlangen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immunosuppressive tumor microenvironment represents one of the main obstacles for immunotherapy of cancer. The tumor milieu is among others shaped by tumor metabolites such as 5'-deoxy-5'-methylthioadenosine (MTA). Increased intratumoral MTA levels result from a lack of the MTA-catabolizing enzyme methylthioadenosine phosphorylase (MTAP) in tumor cells and are found in various tumor entities. Here, we demonstrate that MTA suppresses proliferation, activation, differentiation, and effector function of antigen-specific T cells without eliciting cell death. Conversely, if MTA is added to highly activated T cells, MTA exerts cytotoxic effects on T cells. We identified the Akt pathway, a critical signal pathway for T cell activation, as a target of MTA, while, for example, p38 remained unaffected. Next, we provide evidence that MTA exerts its immunosuppressive effects by interfering with protein methylation in T cells. To confirm the relevance of the suppressive effects of exogenously added MTA on human T cells, we used an MTAP-deficient tumor cell-line that was stably transfected with the MTAP-coding sequence. We observed that T cells stimulated with MTAP-transfected tumor cells revealed a higher proliferative capacity compared to T cells stimulated with Mock-transfected cells. In conclusion, our findings reveal a novel immune evasion strategy of human tumor cells that could be of interest for therapeutic targeting.

Indexed as

Antitumor immune responsecell signalingimmunosuppressionMTAMTAPprotein methylationT cellstumor metabolism

Identifiers

PMID27622058
PMCPMC5007975

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.