As tumor research has deepened, the deregulation of cellular metabolism has emerged as yet another recognized hallmark of cancer. Tumor cells adapt different biochemical pathways to support their rapid growth, proliferation, and invasion, resulting in distinct anabolic and catabolic activities compared with healthy tissues. Certain metabolic shifts, such as altered glucose and glutamine utilization and increased de novo fatty acid synthesis, are critical early on, while others may become essential only during metastasis. These metabolic adaptations are closely shaped by, and in turn remodel, the tumor microenvironment, creating favorable conditions for their spread. Anticancer metabolic strategies should integrate pharmacological approaches aimed at inhibiting specific biochemical pathways with well-defined dietary interventions as adjunctive therapies, considering also the role of gut microbiota in modulating diet and treatment responses. Given the established link between the consumption of foods rich in saturated fatty acids and sugars and an increased cancer risk, the effects of diet cannot be ignored. However, current evidence from controlled and multicenter clinical trials remains insufficient to provide definitive clinical recommendations. Further research using modern omics methods, such as metabolomics, proteomics, and lipidomics, is necessary to understand the changes in the metabolic profiles of various cancers at different stages of their development and to determine the potential for modifying these profiles through pharmacological agents and dietary modifications. Therefore, clinical trials should combine standard treatments with novel approaches targeting metabolic reprogramming, such as inhibition of specific enzymes and transporters or binding proteins, alongside the implementation of dietary restrictions that limit nutrient availability for tumor growth. However, to optimize therapeutic efficacy, a precision medicine approach should be adopted that balances the destruction of cancer cells with the protection of healthy ones. This approach, among others, should be based on cell type-specific metabolic profiling, which is crucial for personalizing oncology treatment.
随着肿瘤研究的深入，细胞代谢失调已成为公认的癌症特征之一。肿瘤细胞通过调整不同的生化途径来支持其快速生长、增殖和侵袭，导致其合成代谢与分解代谢活动与健康组织存在显著差异。某些代谢转变（如葡萄糖和谷氨酰胺利用方式的改变以及脂肪酸从头合成的增加）在肿瘤早期即发挥关键作用，而其他代谢变化可能仅在转移阶段变得至关重要。这些代谢适应既受肿瘤微环境的深刻影响，又反过来重塑微环境，为肿瘤扩散创造有利条件。抗癌代谢策略应将针对特定生化途径的药物治疗与明确的饮食干预作为辅助治疗相结合，同时需考虑肠道微生物群在调节饮食和治疗反应中的作用。鉴于富含饱和脂肪酸和糖类的食物摄入与癌症风险增加之间存在明确关联，饮食的影响不容忽视。然而，目前来自对照研究和多中心临床试验的证据仍不足以提供明确的临床建议。有必要运用代谢组学、蛋白质组学和脂质组学等现代组学方法进一步研究，以理解不同癌症在发展阶段代谢谱的变化，并确定通过药物和饮食调整改变这些代谢谱的潜力。因此，临床试验应将标准治疗与靶向代谢重编程的新方法相结合，例如抑制特定酶、转运蛋白或结合蛋白，同时实施限制肿瘤生长所需营养的饮食控制。但为优化治疗效果，应采用精准医疗策略，在摧毁癌细胞的同时保护健康细胞。该策略应建立在细胞类型特异性代谢谱分析的基础上，这对肿瘤治疗的个体化至关重要。
Metabolic Adaptations in Cancer Progression: Optimization Strategies and Therapeutic Targets
肿瘤(癌症)患者之家