Evidence map›Paper›PMID 29699516›Full record

ArticleBMC cancer2018

Reduction of MHC-I expression limits T-lymphocyte-mediated killing of Cancer-initiating cells.

Brian J Morrison, Jason C Steel, John C Morris

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

77 citing papers in PubMed, 130 citations in OpenAlex.

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17 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 2 countries.

Brian J MorrisonViral and Rickettsial Diseases Department, Infectious Diseases Directorate, Naval Medical Research Center, Silver Spring, Maryland, 20910, USA. brian.j.morrison18.mil@mail.mil.ORCID 0000-0003-4649-6999
Jason C SteelFaculty of Medicine, The University of Queensland, Brisbane, Queensland, Australia.
John C MorrisDivision of Hematology-Oncology, University of Cincinnati Cancer Institute, University of Cincinnati, Cincinnati, Ohio, 45267, USA.
Naval Medical Research Command · USThe University of Queensland · AUUniversity of Cincinnati · US

Funding

Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
NCI NIH HHS T32 CA117846NIH T32 Ruth L. Kirschstein National Research Service Award 2T32CA117846-06A1
6 · The paper itself

Abstract

backgroundIt has been proposed that cancer establishment, maintenance, and recurrence may be attributed to a unique population of tumor cells termed cancer-initiating cells (CICs) that may include characteristics of putative cancer stem cell-like cells. Studies in lung cancer have shown that such cells can be enriched and propagated in vitro by culturing tumor cells in serum-free suspension as tumorspheres. CICs have been characterized for their phenotype, stem cell-like qualities, and their role in establishing tumor and maintaining tumor growth. Less is known about the interaction of CICs with the immune system.

methodsWe established CIC-enriched tumorspheres from murine TC-1 lung cancer cells, expressing human papillomavirus 16 (HPV-16) E6/E7 antigens, and evaluated their susceptibility to antitumor immune responses both in vitro and in vivo.

resultsTC-1 CICs demonstrated reduced expression of surface major histocompatibility complex (MHC)-I molecules compared to non-CICs. We similarly determined decreased MHC-I expression in five of six human lung cancer cell lines cultured under conditions enriching for CICs. In vivo, TC-1 cells enriched for CICs were resistant to human papillomavirus 16 E6/E7 peptide vaccine-mediated killing. We found that vaccinated mice challenged with CIC enriched tumorspheres demonstrated shorter survivals and showed significantly fewer CD8

conclusionsThese results suggest that the attenuated expression of MHC-I molecules by CICs represents a potential strategy of CICs to escape immune recognition, and that the development of successful immunotherapy strategies targeting CICs may decrease their resistance to T cell-mediated immune detection by enhancing CIC MHC-I expression.

Indexed as

Cytotoxicity, ImmunologicAnimalsBiomarkersCancer VaccinesCell Line, TumorCoculture TechniquesFemaleHistocompatibility Antigens Class IHumansInterferon-gammaKiller Cells, NaturalLung NeoplasmsLymphocytes, Tumor-InfiltratingMiceNeoplasmsNeoplastic Stem CellsBiomarkersCancer VaccinesE6 protein, Human papillomavirus type 16Histocompatibility Antigens Class IInterferon-gammaOncogene Proteins, ViralRepressor ProteinsAnimal modelsCancer-initiating cellsCancer stem cellsCytotoxic T lymphocytesInterferon-gammaLung cancerMajor histocompatibility complex-I

Identifiers

PMID29699516
PMCPMC5918869
OpenAlexW2805429168

What OpenQuestion holds

Textmetadata
LicenceCC0
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.