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The molecule that fits into a receptor and switches it on: growth factors, hormones and cytokines are all ligands. Cancers make their own ligands or mutate receptors so none is needed, and some drugs act on the ligand itself, as bevacizumab does by soaking up VEGF.
Ligand binding changes the receptor's shape and starts a signal inside the cell; the specificity of the fit is why one growth factor activates one family of receptors. Cancers exploit ligands by making their own (autocrine signalling), by persuading neighbouring cells to make them, or by mutating receptors so they no longer need the ligand at all. Several drugs act on ligands rather than receptors: bevacizumab soaks up VEGF before it can reach its receptor, and 'radioligands' are small molecules or peptides that bind a receptor such as PSMA to deliver radiation.
In plain words · The signal tumours use to grow their own blood supply. Blocking it starves tumours and, surprisingly, helps immunotherapy work.
Showing the target this term concerns: VEGF / VEGFR.
Shares PSMA, Radioligand therapy (beta emitters).
Shares Growth factor, VEGF / VEGFR, Anti-angiogenic therapy.
Shares PSMA, Radioligand therapy (beta emitters).
Shares PSMA, Radioligand therapy (beta emitters).
Shares VEGF / VEGFR, Anti-angiogenic therapy.
Shares PSMA, Radioligand therapy (beta emitters).
Shares PSMA, Radioligand therapy (beta emitters).
Shares PSMA, Radioligand therapy (beta emitters).