Evidence map›Paper›PMID 31509607›Full record

ReviewImmunology2019

Cancer immune escape: MHC expression in primary tumours versus metastases.

Federico Garrido, Natalia Aptsiauri

Open access · bronzeAbstract readComparative StudyReview
In one paragraph

Review in Immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 2 pooled it
6.9field-weighted citation impact, top 2% 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

105 citing papers in PubMed, 2 syntheses or guidelines pooled it, 176 citations in OpenAlex.

  1. Pooled it
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  13. The impact of aspirin on PD-L1 expression and alteration of M2 polarization in non-small cell lung cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  17. B4GALT5 inhibits CD8Journal for immunotherapy of cancer · 2025
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45 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

2 authors at 2 institutions in 1 country.

Federico GarridoServicio de Analisis Clínicos e Inmunología, UGC Laboratorio Clínico, Hospital Universitario Virgen de las Nieves, Granada, Spain.
Natalia AptsiauriInstituto de Investigación Biosanitaria ibs (A-08), Granada, Spain.
Hospital Universitario Virgen de las Nieves · ESUniversidad de Granada · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumours can escape T-cell responses by losing major histocompatibility complex (MHC)/ human leucocyte antigen (HLA) class I molecules. In the early stages of cancer development, primary tumours are composed of homogeneous HLA class I-positive cancer cells. Subsequently, infiltration of the tumour by T cells generates a vast diversity of tumour clones with different MHC class I expressions. A Darwinian type of T-cell-mediated immune selection results in a tumour composed solely of MHC class I-negative cells. Metastatic colonization is a highly complex phenomenon in which T lymphocytes and natural killer cells play a major role. We have obtained evidence that the MHC class I phenotype of metastatic colonies can be highly diverse and is not necessarily the same as that of the primary tumour. The molecular mechanisms responsible for MHC/HLA class I alterations are an important determinant of the clinical response to cancer immunotherapy. Hence, immunotherapy can successfully up-regulate MHC/HLA class I expression if the alteration is reversible ('soft'), leading to T-cell-mediated tumour regression. In contrast, it cannot recover this expression if the alteration is irreversible ('hard'), when tumour cells escape T-cell-mediated destruction with subsequent cancer progression. This review summarizes clinical and experimental data on the complexity of immune escape mechanisms used by tumour cells to avoid T and natural killer cell responses. We also provide in-depth analysis of the nature of MHC/HLA class I changes during metastatic colonization and contribute evidence of the enormous diversity of MHC/HLA class I phenotypes that can be produced by tumour cells during this process.

Indexed as

Tumor EscapeAnimalsGene Expression RegulationHistocompatibility Antigens Class IHumansImmunotherapyKiller Cells, NaturalNeoplasm MetastasisNeoplasmsT-LymphocytesHistocompatibility Antigens Class Iantigen presentation/processingcancerCD8 cellcytotoxicityimmunotherapy

Identifiers

PMID31509607
PMCPMC6856929
OpenAlexW2972412203

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.