细胞生物量的积累与生物能量和生物合成需求的显著增加相关。代谢重编程，曾经被认为是一种表观现象，目前与疾病进展有关，也与细胞外命定性信号的响应有关。多形性胶质母细胞瘤患者经常遭受误诊、生存时间短、生活质量低和疾病管理选择差的状况。今天，肿瘤遗传学检测和组织学分析指导诊断和治疗。我们和其他人认为代谢产物在疾病描述和表型描述中补充了翻译性生物标志物和分子标记。在此，我们结合了混合方法内容分析和基于质谱的无靶代谢组学分析，对多形性胶质母细胞瘤患者的血浆样本进行研究，以揭示代谢重编程在生物可塑性和疾病严重程度中的作用。在数据处理和分析后，我们建立了一个由线粒体功能和氧化还原状态、脂类和能量底物协调的生物能量谱。我们的发现表明，表观遗传修饰剂在多形性胶质母细胞瘤细胞代谢中是关键的参与者，特别是当考虑到微小RNA时。我们提出，多形性胶质母细胞瘤中的生物可塑性是一种适应和抗药机制，这在生物能学中得到了精确的揭示。

The accumulation of cell biomass is associated with dramatically increased bioenergetic and biosynthetic demand. Metabolic reprogramming, once thought as an epiphenomenon, currently relates to disease progression, also in response to extracellular fate-decisive signals. Glioblastoma multiforme patients often suffer misdiagnosis, short survival time, low quality of life, and poor disease management options. Today, tumor genetic testing and histological analysis guide diagnosis and treatment. We and others appreciate that metabolites complement translational biomarkers and molecular signatures in disease profiling and phenotyping. Herein, we coupled a mixed-methods content analysis to a mass spectrometry-based untargeted metabolomic analysis on plasma samples from glioblastoma multiforme patients to delineate the role of metabolic remodeling in biological plasticity and, hence, disease severity. Following data processing and analysis, we established a bioenergetic profile coordinated by the mitochondrial function and redox state, lipids, and energy substrates. Our findings show that epigenetic modulators are key players in glioblastoma multiforme cell metabolism, in particular when microRNAs are considered. We propose that biological plasticity in glioblastoma multiforme is a mechanism of adaptation and resistance to treatment which is eloquently revealed by bioenergetics.