Loading
Cancer Risks and Factors / Metabolism, Diabetes, and Cancer / Adipokines, Inflammation, and Metabolic Diseases · Journal article
Cancer Letters · September 5, 2026
Encouraging direction, but not yet definitive.
This integrated multi-omics and experimental study identifies obesity-associated immune-metabolic remodeling in TNBC, including elevated checkpoint expression and lipid dysregulation, and reports higher anti-PD-1 response rates in overweight/obese patients across four clinical trials. While mechanistically coherent and supported by consistent multi-level data, the observational design and retrospective trial analysis do not establish causation or provide evidence sufficient to change clinical practice without prospective validation.
Observational cohort study with experimental validation and retrospective clinical trial analysis. 465 patients with triple-negative breast cancer in multi-omics database; mice with tumour xenografts; patients from four independent anti-PD-1 immunotherapy trials. Intervention: Obesity (overweight/obese BMI category); anti-PD-1-based immunotherapy in trial population. Compared with: Normal BMI; standard anti-PD-1 treatment in observational context. n = 465.
OW/OB TNBC patients exhibited worse survival and elevated tumor microenvironment inflammation Higher expression of immune checkpoints and dysregulated lipid metabolism in OW/OB patients Obese mouse tumors displayed faster growth rates and higher proportion of PD-1+ CD8+ T cells
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Integrated multi-omics analysis in a large single-centre TNBC cohort with mechanistic mouse experiments and supportive clinical trial data, but observational design, no randomized comparator, and reliance on retrospective trial analysis limit definitive claims about causation or clinical practice change.
As stated by the source record.
Quoted from the source exactly as published.
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.
Triple-negative breast cancer (TNBC) is a highly aggressive and heterogeneous breast cancer subtype with limited therapeutic options. While the prevalence of overweight/obese (OW/OB) women continues to rise, the impact of obesity on molecular features of TNBC remains incompletely understood. We investigated clinicopathological and molecular data (including genomic, transcriptomic, proteomic and metabolomic profiling) using our largest original multi-omics database of TNBC (N = 465) for associations with patient body mass index (BMI). Multi-omics profiling revealed that OW/OB patients exhibited worse survival as well as elevated inflammation of tumor microenvironment, higher expression of immune checkpoints, and dysregulated lipid metabolism. Our in vivo experiments demonstrated that tumors in obese mice displayed faster growth rates, a higher proportion of PD-1 + CD8 + T cells and enhanced responsiveness to anti-PD-1 treatment. In addition, we analyzed data from four independent clinical trials and discovered that OW/OB patients demonstrated higher pathological complete response rates and longer progression-free survival following anti-PD-1-based immunotherapy. In conclusion, our study systematically revealed that obesity is associated with coordinated immune-metabolic remodeling in TNBC, characterized by checkpoint enrichment and lipid dysregulation, which may help explain the enhanced anti-PD-1 responsiveness and should be taken into account in the field of precision medicine.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.