Evidence map›Paper›PMID 29434605›Full record

ArticleFrontiers in immunology2018

MHC Intratumoral Heterogeneity May Predict Cancer Progression and Response to Immunotherapy.

Irene Romero, Cristina Garrido, Ignacio Algarra, Virginia Chamorro, Antonia Collado, Federico Garrido, Angel M Garcia-Lora

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  5. KIR2DL2/DL3+NKs and Helios+Tregs in Peripheral Blood Predict Nivolumab Response in Patients with Metastatic Renal Cell Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
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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

7 authors at 5 institutions in 1 country.

Irene RomeroUGC Laboratorios, Complejo Hospitalario de Jaén, Jaén, Spain.
Cristina GarridoDepartamento de Bioquímica, Biología Molecular e Inmunología III, Universidad de Granada, Granada, Spain.
Ignacio AlgarraDepartamento de Ciencias de la Salud, Universidad de Jaén, Jaén, Spain.
Virginia ChamorroServicio de Análisis Clínicos e Inmunología, UGC Laboratorio Clínico, Hospital Universitario Virgen de las Nieves, Instituto de Investigación Biosanitaria ibs.Granada, Granada, Spain.
Antonia ColladoUnidad de Biobanco, Hospital Universitario Virgen de las Nieves, Instituto de Investigación Biosanitaria ibs.Granada, Granada, Spain.
Federico GarridoDepartamento de Bioquímica, Biología Molecular e Inmunología III, Universidad de Granada, Granada, Spain.
Angel M Garcia-LoraServicio de Análisis Clínicos e Inmunología, UGC Laboratorio Clínico, Hospital Universitario Virgen de las Nieves, Instituto de Investigación Biosanitaria ibs.Granada, Granada, Spain.
Hospital Universitario Virgen de las Nieves · ESInstituto de Investigación Biosanitaria de Granada · ESComplejo Hospitalario de Jaén · ESUniversidad de Granada · ESUniversidad de Jaén · ES

Funding

Worldwide Cancer Research 15-1166
6 · The paper itself

Abstract

An individual tumor can present intratumoral phenotypic heterogeneity, containing tumor cells with different phenotypes that do not present irreversible genetic alterations. We have developed a mouse cancer model, named GR9, derived from a methylcholanthrene-induced fibrosarcoma that was adapted to tissue culture and cloned into different tumor cell lines. The clones showed diverse MHC-I phenotypes, ranging from highly positive to weakly positive MHC-I expression. These MHC-I alterations are due to reversible molecular mechanisms, because surface MHC-I could be recovered by IFN-γ treatment. Cell clones with high MHC-I expression demonstrated low local oncogenicity and high spontaneous metastatic capacity, whereas MHC-I-low clones showed high local oncogenicity and no spontaneous metastatic capacity. Although MHC-I-low clones did not metastasize, they produced MHC-I-positive dormant micrometastases controlled by the host immune system, i.e., in a state of immunodormancy. The metastatic capacity of each clone was directly correlated with the host T-cell subpopulations; thus, a strong decrease in cytotoxic and helper T lymphocytes was observed in mice with numerous metastases derived from MHC-I positive tumor clones but a strong increase was observed in those with dormant micrometastases. Immunotherapy was administered to the hosts after excision of the primary tumor, producing a recovery in their immune status and leading to the complete eradication of overt spontaneous metastases or their decrease. According to these findings, the combination of MHC-I surface expression in primary tumor and metastases with host T-cell subsets may be a decisive indicator of the clinical outcome and response to immunotherapy in metastatic disease, allowing the identification of responders to this approach.

Indexed as

FibrosarcomaImmunotherapyAnimalsCell Line, TumorDisease Models, AnimalDocetaxelHistocompatibility Antigens Class IMaleMethylcholanthreneMice, Inbred BALB COligodeoxyribonucleotidesPolysaccharidesCpG ODN 1826DocetaxelHistocompatibility Antigens Class IMethylcholanthreneOligodeoxyribonucleotidesPolysaccharidesimmunotherapyintratumoral heterogeneitymetastasesMHCT lymphocytes

Identifiers

PMID29434605
PMCPMC5796886
OpenAlexW2793355209

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.