Gastrin releasing peptide receptor (GRPR) plays a critical role in itch, inflammation and cancer, and GRPR antagonist has obvious effect on cancer, inflammation and itch.
Recently, GRPR/NMBR are receiving considerable attention because they act as growth factor receptors often in an autocrine manner in different lung-cancers, affect tumor angiogenesis, their inhibition increases the cytotoxic potency of tyrosine-kinase inhibitors reducing lung-cancer cellular resistance/survival and their overexpression can be used for sensitive tumor localization as well as to target cytotoxic agents to the cancer.
Bombesin receptor 2 (BB<sub>2</sub>) and integrin α<sub>v</sub>β<sub>3</sub> receptor are privileged targets for molecular imaging of cancer because of their overexpression in a number of tumor tissues.
The GRPR antagonist radioligands <sup>67</sup>Ga-, <sup>111</sup>In-, and <sup>177</sup>Lu-NeoBOMB1, independent of the radiometal applied, have shown comparable behavior in prostate cancer models, in favor of future theranostic use in GRPR-positive cancer patients.
ProCA1.GRPR is expected to have important preclinical and clinical implications for the early detection of cancer and for monitoring treatment effects.
These data suggest that accumulation of mutations within the GRPR gene ultimately resulting in the production of nonfunctional receptors may represent a previously unappreciated mechanism allowing for the dedifferentiation of tumor cells within any particular colon cancer; and that poorly-differentiated tumor cells within any individual cancer may arise clonally from their better-differentiated precursors.