Evidence map›Paper›PMID 39856479›Full record

ReviewCancer metastasis reviews2025

Cellular plasticity and non-small cell lung cancer: role of T and NK cell immune evasion and acquisition of resistance to immunotherapies.

Sarra Mestiri, Ana Sami, Naresh Sah, Dina Moustafa Abo El-Ella, Sabiha Khatoon, Khadija Shafique, Afsheen Raza, Darin Mansor Mathkor, Shafiul Haque

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer metastasis reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–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

14 citing papers in PubMed.

  1. Risk prediction of non-small cell lung cancer in patients with pulmonary nodules: a single-center cohort study based on six machine learning algorithms.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

9 authors.

Sarra MestiriQatar Biomedical Research Institute, Hamad Bin Khalifa University, Qatar Foundation, Doha, Qatar.
Ana SamiQueen Mary University of London, London, UK.
Naresh SahDepartment of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, USA.
Dina Moustafa Abo El-EllaTranslational Cancer Research Facility, National Center for Cancer Care and Research/Translational Research Institute, Hamad Medical Corporation, Doha, Qatar.
Sabiha KhatoonDepartment of Physiology and Biochemistry, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Khadija ShafiqueDepartment of Genetics and Genomics, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE.
Afsheen RazaDepartment of Biomedical Sciences, College of Health Sciences, Abu Dhabi University, Abu Dhabi, UAE. raza.afsheen@adu.ac.ae.
Darin Mansor MathkorResearch and Scientific Studies Unit, College of Nursing and Health Sciences, Jazan University, Jazan, Saudi Arabia.
Shafiul HaqueResearch and Scientific Studies Unit, College of Nursing and Health Sciences, Jazan University, Jazan, Saudi Arabia. shafiul.haque@hotmail.com.

Funding

Deputyship for Research & Innovation, Ministry of Education, Saudi Arabia ISP23-101
6 · The paper itself

Abstract

Lung cancer is a leading global cause of mortality, with non-small cell lung cancer (NSCLC) accounting for a significant portion of cases. Immune checkpoint inhibitors (ICIs) have transformed NSCLC treatment; however, many patients remain unresponsive. ICI resistance in NSCLC and its association with cellular plasticity, epithelial-mesenchymal transition (EMT), enhanced adaptability, invasiveness, and resistance is largely influenced by epigenetic changes, signaling pathways, tumor microenvironment, and associated immune cells, fibroblasts, and cytokines. Immunosuppressive cells, including M2 tumor-associated macrophages, myeloid-derived suppressor cells, and regulatory T cells, contribute to resistance by suppressing the immune response. This cellular plasticity is influenced when B cells, natural killer cells, and T cells are exhausted or inhibited by components of the tumor microenvironment. Conversely, diverse T cell, NK cell, and B cell subsets hold potential as predictive response markers particularly cytotoxic CD8

Indexed as

Carcinoma, Non-Small-Cell LungCell PlasticityDrug Resistance, NeoplasmImmunotherapyKiller Cells, NaturalLung NeoplasmsT-LymphocytesAnimalsHumansTumor MicroenvironmentB cellsEpithelial-mesenchymal transition (EMT)Natural killer cellsNon-small cell lung cancer (NSCLC)Single-cell sequencingT cellsTherapeutic resistanceTumor-associated macrophages

Identifiers

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.