Published online Mar 24, 2024. doi: 10.5306/wjco.v15.i3.391
Peer-review started: October 17, 2023
First decision: December 31, 2023
Revised: January 14, 2024
Accepted: February 3, 2024
Article in press: February 3, 2024
Published online: March 24, 2024
Processing time: 156 Days and 20 Hours
Our study identified a 4-gene model that, when combined with the tumor mutation burden (TMB) score, may have critical implications for clinical medical decisions and personalized treatment of patients with HER2-positive breast cancer.
This study aimed to identify and evaluate fresh ferroptosis-related biomarkers for HER2+ breast cancer (BC).
Identifying reliable prognostic biomarkers can direct clinical practice and help develop a more individualized clinical follow-up approach.
The prediction model was constructed using data from the TCGA and METABRIC databases. Subsequently, patients were categorized into high-risk and low-risk groups according to their median risk scores, independent predictors for overall survival (OS). We investigated immune infiltration, mutations, and drug sensitivity across risk groups. Moreover, we integrated tumor mutational burden (TMB) with risk scores to assess patient prognosis. Finally, we analyzed vital gene expression through single-cell RNA sequencing (scRNA-seq) in cancerous and normal epithelial cells.
Our model helps guide the prognosis of HER2+ breast cancer patients, and its combination with the TMB can aid in more accurate assessment of patient prognosis and provide new ideas for further diagnosis and treatment.
By analyzing the RNA expression data of HER2-positive breast cancer patients, we constructed a risk score model (PROM2, SLC7A11, FANCD2, and FH) for ferroptosis and evaluated the relationship between the high-risk score and patient prognosis. We verified that the high-risk group was associated with poorer immune infiltration and a greater tumor mutation load. By combining the risk score with the TMB, we found that patients with a high TMB-score had the worst prognosis, while patients with a low TMB-score had the best prognosis.
The prediction model was constructed using data from the TCGA and METABRIC cohorts. Patients were subsequently categorized into high-risk and low-risk groups according to their median risk score, an independent predictor of overall survival. We investigated immune infiltration, mutations, and drug sensitivity across risk groups. Moreover, we integrated the TMB with risk scores to assess patient prognosis. Finally, we analyzed vital gene expression through single-cell RNA sequencing in cancerous and normal epithelial cells.