Pituitary tumor-transforming gene (PTTG) was only recently discovered. Its overexpression occurs in a wide variety of endocrine and non-endocrine tumors, including ones of pituitary, thyroid, ovary, breast, prostate, lung, esophagus, colon, and the central nervous system. It affects tumor invasiveness and recurrence in several systems, functions as a securin during cell cycle progression, and inhibits premature sister chromatid separation. PTTG is involved in multiple cellular pathways, including proliferation, DNA repair, transformation, angiogenesis induction, invasion, and the induction of genetic instability. In thyroid carcinomas, PTTG expression is a marker of invasiveness. PTTG is overexpressed in most pituitary adenomas, where it appears to correlate with recurrence and angiogenesis. Increasing evidence also points to the role of PTTG in endocrine organ development. For example, PTTG knockout mice show defective pancreatic b-cell proliferation. Herein, we review the current knowledge regarding PTTG-mediated pathways based on evidence from in vivo and in vitro studies as well as knockout mice models. We also summarize the issue of PTTG expression and its correlation with clinicopathologic parameters in patients with neoplasms, particularly of endocrine organs. In addition, we discuss in vitro and in vivo therapeutic models targeting PTTG overexpression.

KI-67, A MARKER of cellular proliferation, has been studied extensively in pituitary neoplasia. It is of relevance to various clinicopathological parameters, including tumor subtype, size, invasiveness, and recurrence, as well as patient age and sex. Generally, pituitary tumors behaving aggressively have increased Ki-67 labeling indices. Nonetheless, there is considerable overlap in Ki-67 labeling between noninvasive and invasive adenomas as well as between adenomas and pituitary carcinomas. Not only is there no general agreement regarding the relationship of Ki-67 labeling index and tumor invasiveness, but the same is also true of the association with pituitary tumor size, growth fraction, and recurrence. Whereas a number of studies found conclusive associations of Ki-67 labeling indices with aggressive behavior, size, and/or adenoma subtype, others fail to do so. It is evident that discrepant data regarding tumor behavior in part has its basis in nonuniform study criteria. For example, different investigators use varying criteria of tumor invasion and recurrence. Herein, we review the literature relating Ki-67 expression and various other clinicopathological parameters and conclude that uniform definitions and methods, as well as new markers, are key to improved treatment of pituitary tumors.

Cadaver and MRI findings show an intimate relationship between the adductor longus; rectus abdominis; and symphyseal cartilage, disk, and capsular tissues.

Underlying adenohypophysial pathology in patients dying after TBI is acute infarction. Loss of large numbers of adenohypophysial cells causes reduced secretion of adenohypophysial hormones and may contribute to post-traumatic hypopituitarism.