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PubMed2026

Leveraging single-cell and spatial omics for brain tumour insights to improve therapeutic strategies.

Single-cell and spatial omics (SPOs) technologies have advanced how healthcare physicians characterise brain tumours by enabling detailed understanding of their cellular architecture, functional states, and microenvironmental dynamics. These approaches provide high-resolution detection of tumour heterogeneity and allow precise analysis of the brain tumour microenvironment. Their application has also led to the discovery of novel biomarkers used for early brain tumour detection, prognosis, and improved tumour stratification. Furthermore, integrative multi-omic analyses have revealed new therapeutic targets, clarified mechanisms of drug resistance, and uncovered molecular pathways underpinning treatment failure. By bridging cellular-level insights with spatial context, SPOs hold significant promise for advancing personalised diagnostics, predicting therapeutic response, and guiding the development of targeted interventions for brain tumours. Despite these advances, several limitations constrain the full translational potential of SPOs, including high experimental costs, substantial computational demands, lack of standardised protocols, and challenges in data integration and reproducibility. Addressing these barriers through scalable bioinformatic pipelines, consensus experimental frameworks, and cost-effective platforms remains critical for broadening accessibility and enabling clinical adoption.

Brain Neoplasms↗
PubMed1975

Ribonucleases and neoplasia.

Biochemical data provide good evidence of a lack of acid and alkaline RNase activities in ascites tumour cells. Analyses of whole solid tumours appear of doubtful value, but fractionation studies reveal RNase deficiencies in mitochondrial fractions whereas inconsistent results are reported for microsomal fractions. Nuclei, nucleoli, and ribosomes isolated from tumours show relatively weak activities. Large variations are noted in determinations on purified lysosomes. Histochemical analyses by two different approaches demonstrate a multifocal loss of RNase activities in preneoplastic tissues, a lack of activities in cancer cells, and the presence of appreciable activities in stromal tissue and necrotic areas of tumours. These results suggest that RNase activities found in homogenates and cellular fractions of heterogeneous tumours may derive mainly from stromal cells, phagocytes, and extracellular fluids of necrotic areas. A close correlation seems to exist between activation of RNases and tumour regression. A large variety of therapeutic agents induce increases in tumour RNase activities whereas ineffective agents do not. The activation of RNases precedes obvious regression and apparently represents de novo synthesis of RNases in cancer cells. It emerges from these studies that loss of RNase activities could represent a critical event in carcinogenesis, that RNase deficiencies would persist in cancer cells, and that RNase activation would be closely associated with tumour regression. Losses of RNase activities in preneoplastic tissues are followed by changes in the properties of cytoplasmic RNA probably due to alterations in ribosomes in areas of neoplastic transformation. Deficiencies in the RNase system could be the source of abnormalities in cellular RNA or RNA-containing particles that would lead to neoplasia.

Animals↗
PubMed1977

Glial cell characteristics in bulk-prepared cell fractions from human brain tumours.

The heterogeneity of brain tumours, especially in the glioblastoma group, makes biochemical characterization of pieces of the tumours hazardous even with extensive histological controls. This study employs a technique by which separate cell populations are subsequently isolated from the tumours by means of density gradient centrifugation. Cells isolated from glial brain tumours with low density sedimentation rates show the highest levels of glial cell characteristics, i.e. S-100 content and active uptake of the neurotransmitter GABA.

Astrocytoma↗
PubMed2026

ABCB1 Polymorphisms Influence on Temozolomide Resistance and Overall Survival in Glioblastoma Patients: A Systematic Review of Clinical Evidence.

Glioblastoma (GB), defined as IDH-wildtype CNS WHO grade 4 tumour according to the 2021 WHO classification of CNS tumours, remains a uniformly lethal malignancy in which the efficacy of temozolomide (TMZ) continues to be constrained by both intrinsic tumur biology and the pharmacological barrier imposed by the blood-brain barrier (BBB). Given the central role of the ABCB1 (MDR1/P-glycoprotein) efflux transporter in regulating CNS drug disposition, germline variation in ABCB1 has been proposed as a potential determinant of interindividual variability in TMZ response. This systematic review synthesised clinical evidence from four independent studies, encompassing more than 400 GB patients, evaluating the association between ABCB1 polymorphisms and TMZ efficacy and patients' survival. Across the available literature, the influence of ABCB1 genetic variation emerged as limited and inconsistent. An early study reported a marked survival advantage for carriers of the ABCB1 C1236T C/C genotype treated with TMZ, suggesting reduced efflux and enhanced drug exposure. However, subsequent investigations, including epigenetic analyses, high-quality multivariate survival modelling and a pharmacokinetic study demonstrating genotype-dependent differences in plasma TMZ concentrations, did not replicate a corresponding survival effect. Across the remaining cohorts, common variants such as 1236C>T, 2677G>T/A, 3435C>T and 1199G>A showed no robust association with clinical outcome, indicating that transporter-mediated modulation is likely overshadowed by dominant prognostic drivers, including MGMT methylation, IDH status and tumour heterogeneity. Collectively, current evidence does not support ABCB1 polymorphisms as reliable predictive biomarkers of TMZ response in GB. Nonetheless, the pharmacokinetic signals observed, together with emerging technologies capable of selectively modulating efflux activity at the tumour-BBB interface, point to a continued role for ABCB1 in future therapeutic strategies. Integration of transporter genomics with spatial pharmacokinetics and molecular stratification will be essential to refine drug delivery and improve outcomes in GB.

Humans↗
PubMed2025

Next-generation sequencing in breast cancer: current clinical applications and future directions.

INTRODUCTION: Breast cancer is a heterogeneous disease that claims 670,000 lives by 2022. Omic technologies, particularly next generation sequencing (NGS) offers promising avenues for precision medicine. American Society of Clinical Oncology (ASCO) outlines genomic testing's utility, emphasizing prognostic and diagnostic potential. OBJECTIVES: This review succinctly explores NGS's evolution and clinical applications of NGS in breast cancer, thereby guiding future research to enhance patient care. METHODS: Comprehensive literature searches were conducted using databases such as PubMed, Google Scholar, and ResearchGate, focusing on keywords including breast cancer, HER-2 low breast cancer, circulating tumour DNA, single-cell RNA sequencing, and next-generation sequencing. Peer-reviewed, high-quality articles published in English were selected for inclusion. RESULTS: Previous studies have explored the evolution of NGS technology and its clinical applications in breast cancer, including genomic and transcriptomic characterization, treatment guidance, and resistance prediction. Molecular profiling of challenging entities such as early-onset breast cancer and HER-2 low tumours was summarized, with key findings highlighted. This review also discusses emerging technologies, including circulating DNA and single-cell sequencing, as promising avenues for discovery. CONCLUSION: NGS has revealed the genomic and transcriptomic diversity of breast cancer, identifying actionable alterations associated with chemotherapy response and resistance to therapies such as trastuzumab, TKIs, and CDK4/6 inhibitors. Circulating tumour DNA (ctDNA) shows potential for diagnosis, prediction, prognosis, and monitoring, despite tumour heterogeneity. Single-cell analysis enables exploration of individual cell transcriptomes, though high costs and low throughput remain barriers to widespread adoption. HER2-low tumours continue to pose significant research challenges.

Humans↗
PubMed1979

An approach to the problem of heterogeneity of human tumour-cell populations.

1. Successive sampling of ovarian cancers during cytostatic treatment showed several cases of notable changes in their ploidy distribution and one change in model chromosome number, indicating selection of a resistant tumour-cell population. 2. Studies of cell suspensions from human tumour specimens incubated with [3H]-TdR after exposure in vitro to various cytostatic agents have shown variation in labelling between different parts of the same tumour, as well as between the primary tumour and its metastases or ascitic tumour-cell population, which may be accounted for by variation in sensitivity of the tumour-cell population. 3. Studies of nuclear morphology in 20 endometrial cancers before and after progesterone therapy demonstrate considerable variation in the proportion of cells undergoing secretory conversion within the same tumour, indicating primary heterogeneity of the tumour-cell population in response to progesterone.

Antineoplastic Agents↗
PubMed2025

Evolutionary fingerprints of epithelial-to-mesenchymal transition.

Mesenchymal plasticity has been extensively described in advanced epithelial cancers; however, its functional role in malignant progression is controversial1-5. The function of epithelial-to-mesenchymal transition (EMT) and cell plasticity in tumour heterogeneity and clonal evolution is poorly understood. Here we clarify the contribution of EMT to malignant progression in pancreatic cancer. We used somatic mosaic genome engineering technologies to trace and ablate malignant mesenchymal lineages along the EMT continuum. The experimental evidence clarifies the essential contribution of mesenchymal lineages to pancreatic cancer evolution. Spatial genomic analysis, single-cell transcriptomic and epigenomic profiling of EMT clarifies its contribution to the emergence of genomic instability, including events of chromothripsis. Genetic ablation of mesenchymal lineages robustly abolished these mutational processes and evolutionary patterns, as confirmed by cross-species analysis of pancreatic and other human solid tumours. Mechanistically, we identified that malignant cells with mesenchymal features display increased chromatin accessibility, particularly in the pericentromeric and centromeric regions, in turn resulting in delayed mitosis and catastrophic cell division. Thus, EMT favours the emergence of genomic-unstable, highly fit tumour cells, which strongly supports the concept of cell-state-restricted patterns of evolution, whereby cancer cell speciation is propagated to progeny within restricted functional compartments. Restraining the evolutionary routes through ablation of clones capable of mesenchymal plasticity, and extinction of the derived lineages, halts the malignant potential of one of the most aggressive forms of human cancer.

Animals↗
PubMed2025

Single-cell copy number calling and event history reconstruction.

MOTIVATION: Copy number alterations are driving forces of tumour development and the emergence of intra-tumour heterogeneity. A comprehensive picture of these genomic aberrations is therefore essential for the development of personalised and precise cancer diagnostics and therapies. Single-cell sequencing offers the highest resolution for copy number profiling down to the level of individual cells. Recent high-throughput protocols allow for the processing of hundreds of cells through shallow whole-genome DNA sequencing. The resulting low read-depth data poses substantial statistical and computational challenges to the identification of copy number alterations. RESULTS: We developed SCICoNE, a statistical model and MCMC algorithm tailored to single-cell copy number profiling from shallow whole-genome DNA sequencing data. SCICoNE reconstructs the history of copy number events in the tumour and uses these evolutionary relationships to identify the copy number profiles of the individual cells. We show the accuracy of this approach in evaluations on simulated data and demonstrate its practicability in applications to two breast cancer samples from different sequencing protocols. AVAILABILITY AND IMPLEMENTATION: SCICoNE is available at https://github.com/cbg-ethz/SCICoNE.

Single-Cell Analysis↗
PubMed2026

Patient-derived models of prostate cancer: Capturing tumour complexity from initiation to metastasis.

Prostate cancer is a growing global health challenge. To identify new ways to improve patient care, researchers need a variety of preclinical models that faithfully recapitulate human tumours across the disease continuum, from initiation to metastasis. These complementary models include primary cultures of prostate epithelial cells (PrECs), co-cultures, patient-derived explants (PDEs), patient-derived organoids (PDOs) and patient-derived xenografts (PDXs). Collectively, these models enable researchers to study tumour biology and therapeutic responses in clinically relevant contexts. Yet, there is still a need to improve the fidelity of preclinical models to human tumours by integrating diverse cell types from the tumour microenvironment and mimicking biomechanical features. By improving culture methods with matrix components that resemble the tumour microenvironment and new formulations of media that imitate human plasma, in vitro models will more accurately reflect human physiology, nutrient availability, and metabolism. In time this may reduce the reliance on animal testing through organ-on-chip and related techniques. These more complex models are suited to more detailed experimental readouts, including single-cell and spatial analyses. Intravital imaging also enables dynamic visualisation of cell-cell interactions and treatment responses in vivo. Collectively, these approaches are facilitating a shift towards sophisticated models that capture patients' tumour heterogeneity, different cellular niches, and provide opportunities to carefully study tumorigenesis, metastasis, lineage plasticity, and therapy resistance. In this review, we discuss the current progress and future directions for patient-derived models of prostate cancer, highlighting how they can be generated, refined, characterised and shared to accelerate the worldwide effort in translational research.

Humans↗
PubMed2026

A system-level metastable model of cancer evolution: integrating replication stress, cell cycle deregulation and chromosomal instability.

INTRODUCTION: Cancer cell proliferation occurs within the context of persistent genomic instability. In this review, we propose the RS-CCD-CIN axis as a systems-level framework in which replication stress (RS), cell cycle deregulation (CCD) and chromosomal instability (CIN) form an interdependent triad that shapes tumour evolution. This axis represents a constrained metastable state in which genomic instability is tolerated and buffered. The objective of this review is to synthesize the current understanding of how the RS-CCD-CIN axis contributes to tumour heterogeneity, adaptability and therapy response. DISCUSSION: Evidence indicates that RS, CCD and CIN operate as a dynamic, interconnected network rather than as independent processes. Replication stress induces DNA damage and mutagenesis, while partial checkpoint disruption permits cells with unresolved lesions to proliferate. Chromosomal instability generates both structural and numerical alterations, contributing to intratumoural heterogeneity. Together, these processes facilitate adaptation to environmental and therapeutic pressures. Extrachromosomal DNA, micronuclei formation and cytosolic DNA signalling, including the cGAS-STING pathway, connect genomic instability to adaptive responses and immune modulation. Single-cell and spatial profiling reveal temporal and spatial variability in RS, CCD and CIN states, highlighting the limitations of static biomarkers. Therapeutically, targeting individual components often yields limited durability, whereas approaches that simultaneously perturb multiple aspects of the RS-CCD-CIN axis may improve clinical outcomes. CONCLUSIONS: This review highlights the RS-CCD-CIN axis as a fragile and metastable architecture that supports cancer evolution, while also being susceptible to collapse. A deeper understanding of this interconnected framework may inform the development of therapeutic strategies and enhance the management of resistance.

Humans↗
PubMed2026

Integrative analysis of single-cell sequencing identifies CD8+ TIM3+ CD101+ T cell-associated genes as prognostic biomarkers in breast cancer.

BACKGROUND: Breast cancer is a prevalent and deadly malignancy that significantly impacts women's quality of life and imposes financial burdens. Despite therapeutic advancements, tumour heterogeneity and frequent relapses remain major challenges. Accordingly, this study aimed to characterize immune features associated with CD8+ TIM3+ CD101+ T cells and develop a prognostic signature for breast cancer. METHODS: This study integrated single-cell and bulk transcriptomic datasets to characterize CD8+ TIM3+ CD101+ T cell (CCT)-related immune features and construct a prognostic signature in breast cancer. Single-cell RNA-seq data were sourced from the Gene Expression Omnibus (GEO) repository, and bulk transcriptomic data were from The Cancer Genome Atlas (TCGA) and GEO databases. Analytical methods included pseudo-time trajectory reconstruction (Monocle2), intercellular signalling analysis (CellChat), functional enrichment (ClusterProfiler), and immune profiling (ssGSEA). Prognostic modeling was conducted using least absolute shrinkage and selection operator (LASSO) Cox regression, with validation via Kaplan-Meier and time-dependent receiver operating characteristic (ROC) analyses. RESULTS: Single-cell analysis identified 17 clusters spanning seven cell types, including T cells, myeloid cells, and epithelial cells. T-cell sub-clustering revealed four subtypes. Pseudotime analysis suggested a potential state-transition relationship between CD8+ CD101- TIM3+ and CD8+ CD101+ TIM3+ T-cell states. A total of 121 differentially expressed genes were enriched in vital biological processes. An 11-gene prognostic model showed strong predictive power across cohorts. Single-cell T-cell reclustering identified a CD8+ CD101+ TIM3+ T-cell subpopulation, which was primarily characterized by the expression of markers such as CD101 and HAVCR2/TIM3. CONCLUSIONS: This study maps cellular heterogeneity and molecular networks in breast cancer, offering insights for targeted therapy and improved prognosis.

Breast invasive carcinoma↗
PubMed2026

A serpin-myeloid axis in pancreatic cancer heterogeneity and immune evasion.

Pancreatic ductal carcinoma (PDAC) is characterized by a highly immunosuppressive, extracellular matrix-rich microenvironment, yet tumours display marked heterogeneity1-4. This raises the question of whether immune resistance is a global tumour property or is organized within spatially restricted niches. Here, using Perturb-map spatial functional genomics, we determine how different genes shape the growth and cellular environments of PDAC clones across space and time. This analysis revealed early gene-driven remodelling of local immune neighbourhoods preceding late-stage spatial clonal dominance. We identify SERPINE1 (encoding plasminogen activator inhibitor 1 (PAI1)) and SERPINB2 (encoding PAI2) as dominant regulators of tumour microenvironment control and immune evasion. These serpins promote stabilization of fibrin-rich extracellular matrix niches that spatially retain and programme macrophages towards immunosuppressive states while excluding cytotoxic T cells. Loss of Serpine1 or Serpinb2, or pharmacological inhibition of PAI1 or CD18, improves tumour control in mice and synergizes with anti-PD-1. Multimodal spatial analysis of patient tumours revealed that immunosuppressive niches form around rare SERPINB2- and SERPINE1-expressing PDAC subpopulations, dominated by SPP1+/MARCO+ macrophages. These findings identify cancer-derived SERPINE1 and SERPINB2 as local spatial organizers of immune suppression, linking tumour-intrinsic heterogeneity to local microenvironmental control and immunotherapy resistance in PDAC.

Journal Article↗
PubMedDate not supplied

Metastatic potential of malignant tumours.

The term 'metastatic potential' is examined, together with some of the factors that may contribute to it. The evidence is drawn from clinical and experimental sources. Morphological factors include the site of the tumour, its size, histological appearances and pattern of local spread. The scope and limitations of each are discussed and the potential application of newer morphological techniques is noted. Certain non-morphological factors are considered: these are (1) the functional heterogeneity of tumour cell populations with resepct to the metastatic capacity; (2) the elaboration of certain tumour-associated products which may potentiate tumour spread; and (3) immunological factors in the form of local host cell infiltrates in and around primary tumours. The tumour-associated products include collagenases, prostaglandins and angiogenesis factor; their likely origin from tumour and host cells is stressed, together with their implications in physiological and pathological processes other than neoplasia. It is concluded that the metastatic potential of tumours cannot be assessed in the terms of conventional tumour pathology alone. A more functional approach is needed before the term 'metastatic potential' acquires solid conceptual or practical value.

Angiogenesis Inducing Agents↗
PubMed1977

Alterations in serum prolactin heterogeneity by provocative tests in a patient with a pituitary tumour.

The proportion of serum prolactin heterogeneity were investigated in a patient with a pituitary adenoma producing both prolactin and growth hormone. Glucose tolerance (GTT) and insulin tolerance (ITT) tests were performed alone and in combination with chlorpromazine both before and after hypophysectomy. Serum prolactin multiple forms were separated by Sephadex G-100 column chromatography at 3 degrees C. None of the provocative tests altered the already elevated serum prolactin either before (300 ng/ml) or after (100 ng/ml)hypophysectomy. Chlorpromazine or ITT did not alter the proportion of prolactin heterogeneity; GTT, whether in conjunction with chlorpromazine or alone and both before and after hypophysectomy, increased the proportions of the larger molecular species. In five tests in which the GTT was not performed the prolactin heterogeneity was as follows: 'void volume', 4.9%; 'big', 13.1%; 'little', 82.1%; in those experiments in which the GTT was performed the proportions of prolactin heterogeneity were: 'void volume', 13.5%, 'big', 19.2%; 'little', 67.3%.

Adenoma, Acidophil↗
PubMed2026

CRISPR-Engineered CAR-T Cell Therapy for Epstein-Barr Virus-Associated Nasopharyngeal Carcinoma: A Review of Emerging Therapeutic Prospects.

Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC) remains a clinically challenging malignancy, particularly in recurrent or metastatic disease where durable responses to chemoradiotherapy and immune checkpoint blockade are limited. The viral aetiology of NPC provides a strong biological rationale for immune-based treatment; however, translation of chimaeric antigen receptor (CAR) T-cell therapy into this solid tumour setting is constrained by poor tumour trafficking, antigen heterogeneity, limited surface accessibility of EBV latent antigens, T-cell exhaustion, and an immunosuppressive tumour microenvironment. This review critically evaluates the emerging therapeutic prospects of CRISPR-engineered CAR-T cell therapy for EBV-associated NPC. It synthesises evidence on EBV latency biology, NPC immune evasion, solid-tumour CAR-T limitations, and genome-engineering strategies including conventional CRISPR-Cas9, base editing, prime editing, and double-strand-break-sparing targeted integration. Particular attention is given to genotoxicity, chromosomal rearrangements, chromosome loss, bystander and off-target editing, manufacturing heterogeneity, and the regulatory and biological barriers that currently separate technical feasibility from NPC-specific clinical implementation. Available clinical evidence from checkpoint blockade, EBV-specific adoptive T-cell therapy, base-edited CAR-T cells in haematologic malignancy, and early CRISPR-edited T-cell trials supports the feasibility of immune and genetic redirection but does not establish efficacy of a clinically validated CRISPR-engineered CAR-T platform for NPC. Future development should prioritise surface-accessible antigen validation, fit-for-purpose selection of editing technology, genomic safety, scalable manufacturing, and biomarker-driven early-phase trials.

Humans↗
PubMed2026

How prevalent is fear of cancer recurrence beyond 5 years: a systematic review of validated assessments across tumour types.

PURPOSE: Fear of cancer recurrence (FCR) is an established challenge for cancer survivors. Research however has largely focussed early in treatment, with varying assessments and often single tumour sites. This systematic review set out to determine prevalence of FCR in survivors beyond 5 years across all tumour types. METHOD: We designed a search strategy to identify publications assessing FCR in survivors beyond 5 years with sample size greater than 50, using validated measures. Applying PRISMA methodology and with defined inclusion and exclusion criteria two authors independently assessed the studies for eligibility. Data extraction recorded number of participants, tumour type, study design, FCR tool, time points for assessment and reported prevalence. Risk of bias was assessed to address quality. RESULTS: Ten papers were included, reporting FCR from 5 years to beyond 20 years. Validated tools employed were FCRI-SF and FOP-Q-SF. Sample sizes ranged from 64 to 5983 participants, with a heterogeneous mix of tumour types and age. Only two studies reported longitudinal measurements. Prevalence of FCR above defined threshold ranged from 13 to 33.9% for those studies with acceptable risk of bias reporting distinct cohorts beyond 5 years. CONCLUSION: The limited evidence suggests that clinically relevant FCR persists in some survivors at 5 years. Our review demonstrates the challenge of heterogeneous patient populations in FCR research emphasising the need for improved consensus on measurements and more prospective longitudinal research representing a comprehensive variety of tumour types. We address the clinical implications of persistent FCR and the need to implement effective interventions.

Humans↗
PubMed2026

Multiomics analysis reveals that senescent CXCL16+ macrophages promote lung adenocarcinoma progression through TGF-β signalling.

BACKGROUND: Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer and remains a leading cause of cancer-related mortality worldwide. Although, immunotherapy has become a cornerstone of first-line treatment, only 20-30% of patients achieve a durable clinical benefit, largely because of the complexity and heterogeneity of the tumour immune microenvironment. Emerging evidence indicates that cellular senescence, particularly within immune cells, contributes to tumour progression by impairing antitumour immunity; however, its mechanistic role in LUAD remains incompletely understood. METHODS: We performed an integrative multiomics analysis incorporating genome-wide association studies (GWASs), bulk RNA sequencing, single-cell RNA sequencing, and spatial transcriptomics to characterize immune heterogeneity in LUAD. Cellular senescence was validated by performing staining for senescence-associated β-galactosidase and the canonical markers p16 and p21. SHAP analysis was applied to evaluate the contribution of CXCL16+ macrophages. Functional roles were assessed using coculture assays, in vitro and in vivo tumour models, orthotopic tumour implantation, and multiplex immunofluorescence staining of clinical specimens. RESULTS: A summary data-based on Mendelian randomization analysis integrating GWAS and TCGA data identified CXCL16 as a senescence-associated gene that is causally linked to the LUAD risk. Single-cell RNA sequencing revealed that CXCL16 is predominantly expressed in macrophages, and the pseudotime analysis together with β-galactosidase staining confirmed its association with macrophage senescence. Spatial transcriptomics and immunofluorescence staining showed the marked enrichment of CXCL16+ macrophages in LUAD tissues. The cell-cell communication analysis further revealed a strong association between the number of CXCL16+ macrophages and the activation of the TGF-β signalling pathway within the tumour microenvironment. Functionally, CXCL16+ macrophages promoted LUAD progression via TGF-β signalling, as validated in vitro and in subcutaneous and orthotopic tumour models. Molecular dynamics simulations additionally suggested that LUAD patients with high levels of CXCL16+ macrophage infiltration may exhibit increased sensitivity to bosutinib. CONCLUSIONS: CXCL16 promotes macrophage senescence, and senescent CXCL16+ macrophages drive LUAD progression through TGF-β signalling. These findings identify CXCL16+ macrophages as a biologically and therapeutically relevant immune cell population, highlighting a potential target for precision intervention in LUAD.

Humans↗