Potential induction of gnrhr expression by kisspeptin and/or pulsatile GnRH treatment suggests that autocrine and paracrine signaling, mediated by endogenous production of these peptide hormones by tumor cells, is sufficient to maintain adequate transcript abundance for GnRHR protein production, which could subsequently sensitize COS cells to further GnRH. This evidence concerns the gene KISS1 and neoplasm.