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Ferroptosis and Cancer Prognosis · Journal article
Korean Journal of Physiology and Pharmacology · August 12, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a hypothesis-generating retrospective signature study that uses integrated single-cell and bulk transcriptomics to propose a three-gene immune escape signature (CD9, NPC2, PSMB9) for thyroid cancer risk stratification. Patients stratified as low-risk showed an immune-hot phenotype with higher CD8+ T cells and immunotherapy sensitivity markers, while high-risk patients displayed immune-cold features and higher tumor mutation burden despite reduced immune activity. The work lacks independent external validation, prospective clinical data, or direct evidence of immunotherapy response prediction.
Retrospective cohort study with integrated single-cell and bulk RNA sequencing. Thyroid cancer patients; specific eligibility, enrollment criteria, and setting not stated.. Intervention: Three-gene immune escape signature (CD9, NPC2, PSMB9) risk stratification. Compared with: High-risk versus low-risk patient groups stratified by signature.
Three-gene signature (CD9, NPC2, PSMB9) effectively stratified patients into high- and low-risk groups with distinct survival outcomes Low-risk tumors exhibited immune-hot phenotype with increased CD8+ T cells and activated NK cells, higher checkpoint expression, and elevated immunophenoscore High-risk tumors showed immune-cold microenvironment with M2 macrophage enrichment; despite higher TMB, displayed reduced immune activity indicating impaired immune recognition
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This signature is proposed as a framework for thyroid cancer risk stratification and to predict immunotherapy responsiveness; however, the absence of independent validation, prospective immunotherapy trials, or treatment outcome data means it should not yet guide clinical decision-making. Clinicians should view this as a promising candidate marker requiring validation in independent cohorts and prospective studies.
A single-center retrospective signature development study using integrated omics with no independent validation cohort or prospective clinical trial, reporting associations with survival but not clinical outcomes or treatment guidance.
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Quoted from the source exactly as published.
This signature is proposed as a framework for thyroid cancer risk stratification and to predict immunotherapy responsiveness; however, the absence of independent validation, prospective immunotherapy trials, or treatment outcome data means it should not yet guide clinical decision-making. Clinicians should view this as a promising candidate marker requiring validation in independent cohorts and prospective studies.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Immune escape drives cancer progression and therapy resistance, yet its prognostic role and impact on the tumor immune microenvironment in thyroid cancer remain unclear. We integrated single-cell and bulk RNA sequencing data to systematically characterize immune escape and its clinical significance. scRNA-seq analysis characterized cellular heterogeneity and quantified immune escape activity via AUCell. A prognostic gene signature was constructed from differential expression analysis combined with univariate Cox and LASSO regression, and validated using Kaplan-Meier and time-dependent ROC analyses. The immune landscape was profiled using ssGSEA, CIBERSORT, and ESTIMATE, while immunophenoscore (IPS) was used to predict immunotherapy responsiveness. Functional enrichment, CellChat, SCISSOR, tumor mutation burden (TMB), and CellMiner analyses were further performed to explore underlying mechanisms and therapeutic implications. A three-gene signature (CD9, NPC2, PSMB9) effectively stratified patients into highand low-risk groups with distinct survival outcomes. Low-risk tumors exhibited an "immune-hot" phenotype with increased CD8+ T cells and activated NK cells, higher checkpoint expression, and elevated IPS, suggesting greater immunotherapy sensitivity. In contrast, high-risk tumors showed an immune-cold microenvironment with M2 macrophage enrichment. Despite higher TMB, high-risk tumors displayed reduced immune activity, indicating impaired immune recognition. Single-cell analysis further identified MIF and CCL signaling as key mediators of multicellular immune evasion. Overall, our single-cell-informed immune escape signature provides a promising framework for thyroid carcinoma risk stratification and offers insights into personalized immunotherapy.
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