tumorstoffwechsel

Tumorstoffwechsel refers to the metabolic processes that are altered within cancer cells to support their growth and proliferation. Cancerous cells often exhibit distinct metabolic characteristics compared to normal cells, enabling them to sustain rapid division and survive in challenging environments. One hallmark of tumor metabolism is increased glycolysis, even in the presence of oxygen, a phenomenon known as the Warburg effect. This metabolic shift allows cancer cells to generate the energy and biosynthetic precursors necessary for cell growth more rapidly, though it produces less ATP per glucose molecule compared to oxidative phosphorylation.

In addition to glycolysis, tumor cells also adapt their metabolic pathways by enhancing glutamine uptake and metabolism. Glutamine serves as an important nitrogen and carbon source, supporting nucleotide and amino acid biosynthesis. Other metabolic changes include altered lipid metabolism and increased reliance on alternative pathways such as the pentose phosphate pathway, which provides reducing equivalents and nucleotide precursors.

Tumor metabolism is regulated by genetic and epigenetic factors that influence key enzymes and signaling pathways, including those involving hypoxia-inducible factors (HIFs), MYC, and PI3K/Akt/mTOR pathways. These changes not only support tumor growth but also contribute to the tumor microenvironment, immune evasion, and resistance to therapy.

Understanding tumorstoffwechsel is crucial for developing targeted treatments. Therapeutic strategies aim to inhibit specific metabolic pathways critical for tumor survival, such as glycolysis or glutaminolysis, thereby selectively impairing cancer cell viability. Research continues to explore how metabolic reprogramming can be exploited for improved cancer therapies and diagnostic tools.