Evidence map›Paper›PMID 26928306›Full record

ArticleJournal of leukocyte biology2016

Tumor-reactive immune cells protect against metastatic tumor and induce immunoediting of indolent but not quiescent tumor cells.

Kyle K Payne, Rebecca C Keim, Laura Graham, Michael O Idowu, Wen Wan, Xiang-Yang Wang, Amir A Toor, Harry D Bear, Masoud H Manjili

Open access · hybridAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-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

35 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Anti-Tumour Immunity Relies on Targeting Tissue Homeostasis Through Monocyte-Driven Responses Rather Than Direct Tumour Cytotoxicity.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  3. Review
  4. Review
  5. Butyrophilins: Dynamic Regulators of Protective T Cell Immunity in Cancer.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Put in a "CaCells · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. The force awakens: metastatic dormant cancer cells.Experimental & molecular medicine · 2020
    Review
  19. Mechanisms of Metastatic Tumor Dormancy and Implications for Cancer Therapy.International journal of molecular sciences · 2019
    Review
  20. Review
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

9 authors at 1 institution in 1 country.

Kyle K PayneDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Massey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; The Wistar Institute, Philadelphia, Pennsylvania, USA kpayne@wistar.org.
Rebecca C KeimDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Massey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA;
Laura GrahamMassey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Department of Surgery, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA;
Michael O IdowuMassey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Department of Pathology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA;
Wen WanMassey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Department of Biostatistics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA;
Xiang-Yang WangMassey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Department of Human and Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA;
Amir A ToorMassey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Department of Internal Medicine, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; and.
Harry D BearMassey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Department of Surgery, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA;
Masoud H ManjiliDepartment of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; Massey Cancer Center, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA; masoud.manjili@vcuhealth.org.
Virginia Commonwealth University · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Keri R Maher · 1985 to 2026
$51.0M
Host-tumor interactions and cancer relapse after radiation therapyR01CA175033 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI WANG, XIANG-YANG SHAWN · 2014 to 2018
$1.6M
Large Stress Proteins in Biology and MedicineR01CA154708 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI WANG, XIANG-YANG SHAWN · 2011 to 2015
$1.5M
NCI NIH HHS P30 CA016059NCI NIH HHS R01 CA154708NCI NIH HHS R01 CA175033
6 · The paper itself

Abstract

Two major barriers to cancer immunotherapy include tumor-induced immune suppression mediated by myeloid-derived suppressor cells and poor immunogenicity of the tumor-expressing self-antigens. To overcome these barriers, we reprogrammed tumor-immune cell cross-talk by combined use of decitabine and adoptive immunotherapy, containing tumor-sensitized T cells and CD25(+) NKT cells. Decitabine functioned to induce the expression of highly immunogenic cancer testis antigens in the tumor, while also reducing the frequency of myeloid-derived suppressor cells and the presence of CD25(+) NKT cells rendered T cells, resistant to remaining myeloid-derived suppressor cells. This combinatorial therapy significantly prolonged survival of animals bearing metastatic tumor cells. Adoptive immunotherapy also induced tumor immunoediting, resulting in tumor escape and associated disease-related mortality. To identify a tumor target that is incapable of escape from the immune response, we used dormant tumor cells. We used Adriamycin chemotherapy or radiation therapy, which simultaneously induce tumor cell death and tumor dormancy. Resultant dormant cells became refractory to additional doses of Adriamycin or radiation therapy, but they remained sensitive to tumor-reactive immune cells. Importantly, we discovered that dormant tumor cells contained indolent cells that expressed low levels of Ki67 and quiescent cells that were Ki67 negative. Whereas the former were prone to tumor immunoediting and escape, the latter did not demonstrate immunoediting. Our results suggest that immunotherapy could be highly effective against quiescent dormant tumor cells. The challenge is to develop combinatorial therapies that could establish a quiescent type of tumor dormancy, which would be the best target for immunotherapy.

Indexed as

Immunotherapy, AdoptiveAnimalsCells, CulturedFemaleLung NeoplasmsMammary Neoplasms, ExperimentalMice, TransgenicMyeloid-Derived Suppressor CellsNatural Killer T-CellsTumor EscapeTumor Microenvironmentadoptive immunotherapybreast cancerdormancyescaperelapse

Identifiers

PMID26928306
PMCPMC4982610
OpenAlexW2305226887

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.