Topic
Pituitary tumors
About: Pituitary tumors is a research topic. Over the lifetime, 5041 publications have been published within this topic receiving 137818 citations.
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TL;DR: Findings indicate that p27(Kip1) acts to regulate the growth of a variety of cells, and surprises us by keeping the cell cycle arrest mediated by TGFbeta, rapamycin, or contact inhibition intact in p27(-/-) cells.
1,599 citations
TL;DR: The goals of the current study were to determine the prevalence of pituitary adenomas and to explore the clinical relevance of the findings.
Abstract: BACKGROUND
Pituitary adenomas display an array of hormonal and proliferative activity. Once primarily classified according to size (microadenomas, < 1 cm; macroadenomas, ≥ 1 cm), these tumors are now further classified according to immunohistochemistry and functional status. With these additional classifications in mind, the goals of the current study were to determine the prevalence of pituitary adenomas and to explore the clinical relevance of the findings.
METHODS
The authors conducted a metaanalysis of all existing English-language articles in MEDLINE. They used the search string (pituitary adenoma or pituitary tumor) and prevalence and selected relevant autopsy and imaging evaluation studies for inclusion.
RESULTS
The authors found an overall estimated prevalence of pituitary adenomas of 16.7% (14.4% in autopsy studies and 22.5% in radiologic studies).
CONCLUSIONS
Given the high frequency of pituitary adenomas and their potential for causing clinical pathologies, the findings of the current study suggest that early diagnosis and treatment of pituitary adenomas should have far-reaching benefits. Cancer 2004. © 2004 American Cancer Society.
1,085 citations
TL;DR: Findings suggest that human tumors may harbor oncogenic mutations in various G protein alpha chain genes, referred to as gip2.
Abstract: Somatic mutations in a subset of growth hormone (GH)-secreting pituitary tumors convert the gene for the alpha polypeptide chain (alpha s) of Gs into a putative oncogene, termed gsp. These mutations, which activate alpha s by inhibiting its guanosine triphosphatase (GTPase) activity, are found in codons for either of two amino acids, each of which is completely conserved in all known G protein alpha chains. The likelihood that similar mutations would activate other G proteins prompted a survey of human tumors for mutations that replace either of these two amino acids in other G protein alpha chain genes. The first gene so far tested, which encodes the alpha chain of Gi2, showed mutations that replaced arginine-179 with either cysteine or histidine in 3 of 11 tumors of the adrenal cortex and 3 of 10 endocrine tumors of the ovary. The mutant alpha i2 gene is a putative oncogene, referred to as gip2. In addition, gsp mutations were found in 18 of 42 GH-secreting pituitary tumors and in an autonomously functioning thyroid adenoma. These findings suggest that human tumors may harbor oncogenic mutations in various G protein alpha chain genes.
989 citations
TL;DR: Experimental studies show that chronic administration of somatostatin analogs causes growth inhibition of a number of (transplantable) tumors in animals, including chondrosarcomas, pancreatic, prostatic, breast, and pituitary cancers.
Abstract: I. Introduction LONG-term therapy with somatostatin analogs has been reported to result in the control of hormonal hypersecretion, in improvement of symptomatology, and in tumor shrinkage in patients with acromegaly, endocrine pancreatic tumors, and metastatic carcinoids. One of these somatostatin analogs, octreotide, has been approved for clinical use in most countries, including the United States. It is a well-tolerated, but expensive drug. Experimental studies show that chronic administration of somatostatin analogs causes growth inhibition of a number of (transplantable) tumors in animals, including chondrosarcomas, pancreatic, prostatic, breast, and pituitary cancers. Somatostatin receptors have been demonstrated on a variety of human tumors by classical biochemical binding techniques, as well as by in vitro autoradiography. These tumors include those with amine precursor uptake and decarboxylation (APUD) characteristics (pituitary tumors, endocrine pancreatic tumors, carcinoids, paragangliomas, smal...
806 citations
TL;DR: Effective control of GH and IGF1 hypersecretion and ablation or stabilization of the pituitary tumor mass lead to improved comorbidities and lowering of mortality rates for this hormonal disorder.
Abstract: Dysregulated growth hormone (GH) hypersecretion is usually caused by a GH-secreting pituitary adenoma and leads to acromegaly - a disorder of disproportionate skeletal, tissue, and organ growth. High GH and IGF1 levels lead to comorbidities including arthritis, facial changes, prognathism, and glucose intolerance. If the condition is untreated, enhanced mortality due to cardiovascular, cerebrovascular, and pulmonary dysfunction is associated with a 30% decrease in life span. This Review discusses acromegaly pathogenesis and management options. The latter include surgery, radiation, and use of novel medications. Somatostatin receptor (SSTR) ligands inhibit GH release, control tumor growth, and attenuate peripheral GH action, while GH receptor antagonists block GH action and effectively lower IGF1 levels. Novel peptides, including SSTR ligands, exhibiting polyreceptor subtype affinities and chimeric dopaminergic-somatostatinergic properties are currently in clinical trials. Effective control of GH and IGF1 hypersecretion and ablation or stabilization of the pituitary tumor mass lead to improved comorbidities and lowering of mortality rates for this hormonal disorder.
577 citations