Evidence map›Paper›PMID 35742933›Full record

ReviewInternational journal of molecular sciences2022

EGFR-Mutated Non-Small Cell Lung Cancer and Resistance to Immunotherapy: Role of the Tumor Microenvironment.

Clelia Madeddu, Clelia Donisi, Nicole Liscia, Eleonora Lai, Mario Scartozzi, Antonio Macciò

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 3 pooled it
12.8field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 3 syntheses or guidelines pooled it, 130 citations in OpenAlex.

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47 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

6 authors at 1 institution in 1 country.

Clelia MadedduDepartment of Medical Sciences and Public Health, Medical Oncology Unit, "Azienda Ospedaliero Universitaria" of Cagliari, University of Cagliari, 09100 Cagliari, Italy.ORCID 0000-0001-8940-6987
Clelia DonisiDepartment of Medical Sciences and Public Health, Medical Oncology Unit, "Azienda Ospedaliero Universitaria" of Cagliari, University of Cagliari, 09100 Cagliari, Italy.
Nicole LisciaDepartment of Medical Sciences and Public Health, Medical Oncology Unit, "Azienda Ospedaliero Universitaria" of Cagliari, University of Cagliari, 09100 Cagliari, Italy.
Eleonora LaiDepartment of Medical Sciences and Public Health, Medical Oncology Unit, "Azienda Ospedaliero Universitaria" of Cagliari, University of Cagliari, 09100 Cagliari, Italy.ORCID 0000-0002-0275-8187
Mario ScartozziDepartment of Medical Sciences and Public Health, Medical Oncology Unit, "Azienda Ospedaliero Universitaria" of Cagliari, University of Cagliari, 09100 Cagliari, Italy.ORCID 0000-0001-5977-5546
Antonio MacciòGynecologic Oncology Unit, ARNAS G. Brotzu, Department of Surgical Sciences, University of Cagliari, 09100 Cagliari, Italy.
University of Cagliari · IT

Funding

Fondazione di Sardegna grant number 2021.1517
6 · The paper itself

Abstract

Lung cancer is a leading cause of cancer-related deaths worldwide. About 10-30% of patients with non-small cell lung cancer (NSCLC) harbor mutations of the EGFR gene. The Tumor Microenvironment (TME) of patients with NSCLC harboring EGFR mutations displays peculiar characteristics and may modulate the antitumor immune response. EGFR activation increases PD-L1 expression in tumor cells, inducing T cell apoptosis and immune escape. EGFR-Tyrosine Kinase Inhibitors (TKIs) strengthen MHC class I and II antigen presentation in response to IFN-γ, boost CD8+ T-cells levels and DCs, eliminate FOXP3+ Tregs, inhibit macrophage polarization into the M2 phenotype, and decrease PD-L1 expression in cancer cells. Thus, targeted therapy blocks specific signaling pathways, whereas immunotherapy stimulates the immune system to attack tumor cells evading immune surveillance. A combination of TKIs and immunotherapy may have suboptimal synergistic effects. However, data are controversial because activated EGFR signaling allows NSCLC cells to use multiple strategies to create an immunosuppressive TME, including recruitment of Tumor-Associated Macrophages and Tregs and the production of inhibitory cytokines and metabolites. Therefore, these mechanisms should be characterized and targeted by a combined pharmacological approach that also concerns disease stage, cancer-related inflammation with related systemic symptoms, and the general status of the patients to overcome the single-drug resistance development.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsB7-H1 AntigenErbB ReceptorsHumansImmunotherapyMutationProtein Kinase InhibitorsTumor MicroenvironmentB7-H1 AntigenEGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsEGFR mutationsimmunotherapy resistancenon-small cell lung cancertumor-associated macrophagestumor microenvironmenttyrosine kinase inhibitor

Identifiers

PMID35742933
PMCPMC9224267
OpenAlexW4281641667

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.