Dysregulation of the signaling pathways that govern lactotrope biology 
contributes to tumorigenesis of prolactin (PRL)-secreting adenomas, or 
prolactinomas, leading to a state of pathological hyperprolactinemia. 
Prolactinomas cause hypogonadism, infertility, osteoporosis, and tumor mass 
effects, and are the most common type of neuroendocrine tumor. In this review, 
we highlight signaling pathways involved in lactotrope development, homeostasis, 
and physiology of pregnancy, as well as implications for signaling pathways in 
pathophysiology of prolactinoma. We also review mutations found in human 
prolactinoma and briefly discuss animal models that are useful in studying 
pituitary adenoma, many of which emphasize the fact that alterations in 
signaling pathways are common in prolactinomas. Although individual mutations 
have been proposed as possible driving forces for prolactinoma tumorigenesis in 
humans, no single mutation has been clinically identified as a causative factor 
for the majority of prolactinomas. A better understanding of lactotrope-specific 
responses to intracellular signaling pathways is needed to explain the mechanism 
of tumorigenesis in prolactinoma.