metabolism pathways

Metabolism

AMPK

AMP-activated protein kinase senses AMP:ATP ratio, restraining anabolic mTOR signalling and favouring catabolic programmes including fatty-acid oxidation.

Metabolism

Glycolysis

Aerobic glycolysis (Warburg metabolism) supports ATP, biomass and redox buffering even when oxygen is available. Hexokinase, PKM2 and lactate export are frequent nodes.

Metabolism

Glutaminolysis

Glutamine supplies nitrogen and anaplerotic carbon via glutaminase and glutamate dehydrogenase, supporting nucleotide synthesis and TCA replenishment in MYC-driven and other tumours.

Metabolism

Fatty-acid metabolism

De novo lipogenesis, fatty-acid oxidation and lipid uptake are rewired in a tumour-type-specific way, especially in hypoxic, obese-host, or OXPHOS-dependent subsets.

Metabolism

Mitochondrial oxidative phosphorylation

Despite Warburg metabolism, many tumours retain or upregulate OXPHOS, including residual disease, CSC-like fractions and some oncogene-driven subsets.

Metabolism

Lactate metabolism

Lactate export acidifies the extracellular space and can fuel oxidative tumour or stromal compartments (metabolic symbiosis). MCT transporters are central.

Metabolism

Oxidative stress

Reactive oxygen species are both signalling molecules and sources of damage. Tumours often upregulate antioxidant programmes to live with higher ROS set-points.

Metabolism

NRF2

NRF2/KEAP1 controls antioxidant and detoxification transcription. KEAP1 or NFE2L2 mutations in lung and other cancers stabilize NRF2 and can confer therapy resilience.

Metabolism

One-carbon / methionine metabolism

Folate-methionine cycles supply nucleotides and methylation. Some tumours show methionine dependence and PHGDH or SHMT rewiring.

Metabolism

NAD+/NADH

NAD+ pools support redox balance, PARP activity and sirtuins. NAMPT-dependent salvage is a vulnerability in some models.

This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.