ReviewFrontiers in immunology2026
Fibroblast transformation in the tumor microenvironment of lung adenocarcinoma: heterogeneity, regulation, and therapeutic targeting.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblasts (CAFs) are important stromal cells in the tumor microenvironment of lung adenocarcinoma (LUAD). This review discusses the different cellular sources of CAFs and the main signaling pathways involved in fibroblast-to-CAF transition, with attention to the biological settings that are especially relevant in LUAD. It further discusses CAF heterogeneity not only in terms of functional subtypes, but also from the perspective of dynamic cell states shaped by spatial niche, intercellular communication, and therapy-related stress. On this basis, we outline how distinct CAF states contribute to extracellular matrix remodeling, metabolic reprogramming, invasion and metastasis, angiogenesis, immunosuppression, and therapeutic resistance in LUAD. Particular attention is given to the treatment relevance of CAFs in driver-defined disease settings, where stromal programs may influence responses to targeted therapy and immunotherapy in a context-dependent manner. We also address the main obstacles to CAF-targeted strategies, particularly heterogeneity, plasticity, and functional compensation, and point to possible directions based on precise subtyping, functional modulation, and rational combination therapy. This review thus offers a LUAD-specific perspective for understanding CAF biology and for guiding more precise stromal intervention strategies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.