A study on metabolic characteristics and metabolic markers of gastrointestinal tumors

Tumor cells have significant heterogeneity in metabolism and are closely related to prognosis, gene mutation, and subtype. However, this association has not been demonstrated in reports of gastrointestinal tumors. In this study, we constructed four metabolic subtypes and identified four gene signatures using the expression data and clinical information of 252 metabolism-related genes from TCGA and NCBI databases for gastric adenocarcinoma (STAD) and colorectal cancer (COAD and READ). MC1 had the worst prognosis compared to other classifications. GSig1 was mainly related to drug metabolism and was the highest in MC1 with the worst prognosis, while the other subtypes were mainly related to glucose metabolism pathways. This difference also existed in other different malignant tumors. In addition, metabolic typing was associated with chemotherapeutic drug response and tumor heterogeneity, which indicated that monitoring metabolic typing could contribute to drug efficacy and gene-targeted therapy. In conclusion, we identified differences among subtypes in clinical characteristics such as prognosis and revealed the potential function of metabolic subtype in response to chemotherapeutic agents and oncogene mutations. This work highlighted the potential clinical meaning of metabolic subtype and characteristics in drug therapy and prognosis assessment of malignant tumors.

Automated summary

This study identified significant heterogeneity in tumor cell metabolism and its association with prognosis, gene mutation, and subtype. By analyzing expression data and clinical information, four metabolic subtypes and four gene signatures were constructed. The worst prognosis was observed in MC1 subtype, which was mainly related to drug metabolism, while other subtypes were associated with glucose metabolism pathways. Additionally, metabolic typing was linked to chemotherapeutic drug response and tumor heterogeneity, highlighting its importance in drug efficacy and gene-targeted therapy.