Evidence map›Paper›PMID 30056600›Full record

ArticleCancer immunology, immunotherapy : CII2018

Cytotoxic activity of effector T cells against cholangiocarcinoma is enhanced by self-differentiated monocyte-derived dendritic cells.

Aussara Panya, Chutamas Thepmalee, Nunghathai Sawasdee, Jatuporn Sujjitjoon, Nattaporn Phanthaphol, Mutita Junking, Sopit Wongkham, Pa-Thai Yenchitsomanus

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  8. Dense GM-CSFRPeerJ · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. The role of tumor-infiltrating lymphocytes in cholangiocarcinoma.Journal of experimental & clinical cancer research : CR · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Cellular based immunotherapy for primary liver cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
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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

8 authors at 3 institutions in 1 country.

Aussara PanyaDepartment of Biology, Faculty of Science, Chiang Mai University, Chiang Mai, Thailand.
Chutamas ThepmaleeSiriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), 4th Floor Siriraj Medical Research Center (SiMR), Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Nunghathai SawasdeeSiriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), 4th Floor Siriraj Medical Research Center (SiMR), Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Jatuporn SujjitjoonSiriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), 4th Floor Siriraj Medical Research Center (SiMR), Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Nattaporn PhanthapholSiriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), 4th Floor Siriraj Medical Research Center (SiMR), Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Mutita JunkingSiriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), 4th Floor Siriraj Medical Research Center (SiMR), Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand.
Sopit WongkhamDepartment of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Pa-Thai YenchitsomanusSiriraj Center of Research Excellence for Cancer Immunotherapy (SiCORE-CIT), 4th Floor Siriraj Medical Research Center (SiMR), Faculty of Medicine Siriraj Hospital, Mahidol University, 2 Wanglang Road, Bangkoknoi, Bangkok, 10700, Thailand. pathai.yen@mahidol.ac.th.
Siriraj Hospital · THKhon Kaen University · THMahidol University · TH

Funding

International Research Network (IRN) under Thailand Research Fund (TRF) IRN58W0001Mahidol University R016010006Thailand Research Fund (TRF) IRG5980006TRF Grant for New Researcher TRG5780173TRF-IRN Scholarship IRN5801PHDW03TRF-Royal Golden Jubilee (RGJ)-Ph.D. Scholarship PHD/0044/2556
6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is a cancer of the bile ducts that is associated with poor prognosis and poor treatment outcome. Approximately one-third of CCA patients can undergo surgery, but the recurrence rate is high and chemotherapy often cannot satisfactorily prolong survival. Cellular immunotherapy based on adoptive T-cell transfer is a potential treatment for CCA; however, the development of this technology and the search for an appropriate tumor-associated antigen are still ongoing. To enhance the cytotoxic activity of effector T cells against CCA, we developed self-differentiated monocyte-derived dendritic cells (SD-DC) presenting cAMP-dependent protein kinase type I-alpha regulatory subunit (PRKAR1A), which is an overexpressed protein that plays a role in the regulation of tumor growth to activate T cells for CCA cell killing. Dendritic cells (DCs) transduced with lentivirus harboring tri-cistronic cDNA sequences (SD-DC-PR) could produce granulocyte-macrophage colony-stimulating factor, interleukin-4, and PRKAR1A. SD-DC showed similar phenotypes to those of DCs derived by conventional method. Autologous effector T cells (CD3+, CD8+) activated by SD-DC-PR exhibited greater cytotoxic activity against CCA than those activated by conventionally-derived DCs. Effector T cells activated by SD-DC-PR killed 60% of CCA cells at an effector-to-target ratio of 15:1, which is approximately twofold greater than the cell killing performance of those stimulated with control DC. The cytotoxic activities of effector T cells activated by SD-DC-PR against CCA cells were significantly associated with the expression levels of PRKR1A in CCA cells. This finding that SD-DC-PR effectively stimulated autologous effector T cells to kill CCA cells may help to accelerate the development of novel therapies for treating CCA.

Indexed as

ImmunotherapyBile Duct NeoplasmsCell DifferentiationCells, CulturedCholangiocarcinomaCyclic AMP-Dependent Protein Kinase RIalpha SubunitDendritic CellsGenetic VectorsHumansMonocytesT-Lymphocytes, CytotoxicCyclic AMP-Dependent Protein Kinase RIalpha SubunitPRKAR1A protein, humanCellular immunotherapyCholangiocarcinomaCytotoxic T cellsDendritic cellsSelf-differentiated monocyte-derived dendritic cells

Identifiers

PMID30056600
PMCPMC11028072
OpenAlexW2883727752

What OpenQuestion holds

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Registered trials

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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.