Evidence map›Paper›PMID 41162997›Full record

ReviewJournal of translational medicine2025

Immunometabolic reprogramming in lung cancer: interplay between immune and stem-like cells in immune checkpoint inhibitor resistance.

Ji-Yong Sung, Eui Tae Kim

Abstract readReview
In one paragraph

Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Metabolism of tumor infiltrating T cells.Frontiers in immunology · 2025
    Review
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.

Ji-Yong SungDepartment of Neurosurgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam-si, Republic of Korea. 5rangepineapple@gmail.com.ORCID 0000-0002-8397-1691
Eui Tae KimDepartment of Microbiology and Immunology, Jeju National University College of Medicine, Jeju, 63241, Republic of Korea. tae@jejunu.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer remains the leading cause of cancer-related death worldwide. Despite the success of immune checkpoint inhibitors (ICIs), particularly those targeting PD-1/PD-L1 pathways, a significant number of patients exhibit either primary resistance or acquire resistance over time. While genomic and epigenetic mechanisms contribute to this resistance, increasing evidence points to the pivotal role of immunometabolism—the interface of cellular metabolism and immune regulation. This review focuses on how altered metabolic states in both immune cells and cancer stem-like cells (CSCs) within the lung tumor microenvironment contribute to ICI resistance. We discuss key metabolic pathways involved in immune suppression, the metabolic plasticity of CSCs, and how these factors interact to shape a metabolically hostile tumor niche for immune effector cells. Finally, we explore emerging therapeutic strategies targeting immunometabolism to enhance immunotherapy efficacy in lung cancer.

Indexed as

Drug Resistance, NeoplasmImmune Checkpoint InhibitorsLung NeoplasmsNeoplastic Stem CellsAnimalsHumansImmunotherapyMetabolic ReprogrammingTumor MicroenvironmentImmune Checkpoint InhibitorsCancer stem-like cells (CSCs)Immune checkpoint inhibitor (ICI) resistanceImmunometabolismImmunosuppressive nicheMetabolic plasticityMetabolic reprogrammingTumor microenvironment (TME)

Identifiers

PMID41162997
PMCPMC12574076

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.