Evidence map›Paper›PMID 29209560›Full record

ArticleOncoimmunology

PD-L1 and epithelial-mesenchymal transition in circulating tumor cells from non-small cell lung cancer patients: A molecular shield to evade immune system

Cristina Raimondi, Guido Carpino, Chiara Nicolazzo, Angela Gradilone, Walter Gianni, Alain Gelibter, Eugenio Gaudio, Enrico Cortesi, Paola Gazzaniga

Abstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

64 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  11. Is cancer an intelligent species?Cancer metastasis reviews · 2023
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4 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

9 authors.

Cristina RaimondiDipartimento di Medicina Molecolare, Sapienza Università di Roma Roma, Italia.
Guido CarpinoDipartimento di Anatomia, Istologia, Medicina Forense e Scienze Ortopediche, Sapienza Università di Roma, Roma, Italia.
Chiara NicolazzoDipartimento di Medicina Molecolare, Sapienza Università di Roma Roma, Italia.
Angela GradiloneDipartimento di Medicina Molecolare, Sapienza Università di Roma Roma, Italia.
Walter GianniPoliclinico Umberto I, II Clinica Medica, Sapienza Università di Roma, Roma, Italia.
Alain GelibterDipartimento di Scienze Radiologiche, Oncologiche ed Anatomopatologiche, Sapienza Università di Roma, Roma, Italia.
Eugenio GaudioDipartimento di Anatomia, Istologia, Medicina Forense e Scienze Ortopediche, Sapienza Università di Roma, Roma, Italia.
Enrico CortesiDipartimento di Scienze Radiologiche, Oncologiche ed Anatomopatologiche, Sapienza Università di Roma, Roma, Italia.
Paola GazzanigaDipartimento di Medicina Molecolare, Sapienza Università di Roma Roma, Italia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The programmed cell death 1 (PD-1)/PD-1 ligand 1 (PD-L1) pathway has emerged as a critical inhibitory pathway regulating T-cell response in non-small-cell lung cancer (NSCLC), and the development of PD-1/PD-L1 inhibitors has changed the landscape of NSCLC therapy. Nevertheless, the high degree of non-responders demonstrates that we are still far from completely understanding the events underlying tumor immune resistance. Although the expression of PD-L1 in tumor tissue has been correlated with clinical response to anti PD-1 inhibitors, the ability of this marker to discriminate the subgroup of patients who derive benefit from immunotherapy is suboptimal. Circulating tumor cells (CTCs), as an accessible source of tumor for biologic characterization that can be serially obtained with minimally invasive procedure, hold significant promise to facilitate treatment-specific biomarkers discovery. We recently demonstrated that the presence of PD-L1 on CTCs apparently predicts resistance to the anti-PD-1 Nivolumab in metastatic NSCLC patients and that PD-L1 positive CTCs usually have an elongated morphology that can be ascribed to epithelial-mesenchymal transition (EMT). We here demonstrate for the first time that PD-L1 positive CTCs isolated from NSCLC patients are characterized by partial EMT phenotype, and hypothesize that the co-expression of PD-L1 and EMT markers might represent for these cells a possible molecular background for immune escape.

Indexed as

Circulating tumor cellsepithelial mesenchymal transitionlung cancerPD-L1

Identifiers

PMID29209560
PMCPMC5706610

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.