Cancer, Hypoxia, and Metabolism

The paper maps overflow metabolism to Giffen behaviour, revealing that both arise from trade-offs and complementarity in metabolic and economic systems.

This study uses FALCON to infer metabolic flux differences from TCGA data, revealing cancer-specific metabolic patterns and divergent pathways.

The paper uses metabolomics and gene expression data to identify glutamine metabolism as important in breast cancer and shows drug targeting affects cell viability.

The paper compares the time-dependent transcriptional responses of HIF target genes under chemical hypoxia and oxygen-glucose deprivation in mouse hippocampal cultures.

The paper develops a computational pipeline to analyze single-cell metabolic gene expression in human tumors, revealing higher metabolic activity and variation in malignant cells compared to bulk tumor studies.

This study shows that dLDH is dispensable for larval growth but its absence is compensated by increased G3P production, which affects redox balance and interacts with GPDH1 to influence development.

The paper models the coupling of gene regulation and metabolic pathways in cancer, showing AMPK and HIF-1 activity correlates with metabolic pathway activities in tumor samples.

This study identifies BCL2 hyperactivity's role in enhancing glutaminolytic flux and mitochondrial metabolism in lymphoma, revealing metabolic dependencies as therapeutic targets.

This study identifies SINHCAF/FAM60A as a component of the SIN3A-HDAC complex that regulates the hypoxia response and shows its inverse correlation with HIF2 mRNA levels, predicting cancer patient survival.