NGFR and neoplasm: Decreased expression of D2 dopamine receptors in tumor cells, alterations in other receptors modulating dopamine receptors [e.g. nerve growth factor receptor (NGFR)], changes in downstream cascades (e.g. in G protein subunit), increased angiogenic markers, and increased fibrosis through disruptions in the transforming growth factor (TGF)-β1 pathway have all been suggested as possible mechanisms playing a role in DA-resistance [25–29].