Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pituitary is an endocrine gland with ability to uptake diverse radiopharmaceuticals and, therefore, susceptible to be investigated by nuclear medicine diagnostic procedures. Although this topic has been scarcely scrutinized, we have data indicating that somatostatin receptor scintigraphy with111In-DTPA-D-Phe-octreotide or 99mTc-EDDA/HYNIC-TOC may be of clinical utility in the diagnosis of some pituitary adenomas (PA). Only a few studies have evaluated the diagnostic performance of 99mTc-MIBI and 99mTc (V)-DMSA scintigraphy in pituitary disease. Scintigraphy using 123I-methoxybenzamide (123I-IBZM) might be useful in macroprolactinomas expressing dopamine D2 receptors. Pituitary gland does not usually accumulate 2-deoxy-2-[18F]fluoro-d-glucose (18F-FDG) and, therefore, it is not visualized on positron emission tomography (PET) imaging studies with this radiotracer. The pituitary uptake on18F-FDG PET/CT scans performed in the follow-up of oncological patients are uncommon. However, 60% of these incidental findings are due to PA, mainly non-functioning pituitary macroadenomas, and a small percentage to metastases or other pituitary lesions. Interestingly, 18F-FDG PET/CT may identify hypophysitis induced by different immunotherapeutic agents used in cancer patients. Positive 18F-FDG uptake has been reported in a high percentage of patients with PA, mainly macroadenomas and it seems that there is correlation between tumor size and SUVmax. 68Ga-DOTA-TATE PET/CT may identify functioning and non-functioning PA, although this technique is more useful in the detection of remaining normal pituitary tissue after transsphenoidal adenomectomy, and in the confirmation of recurrence of functioning PA, such as thyrotroph-secreting PA. Furthermore, 68Ga-DOTA-TATE uptake has potential therapeutic implications on molecular-targeted therapy. Lastly, other radiopharmaceuticals that have shown to be taken up in some patients with pituitary disease include 18F-DOPA (prolactinoma), 11C-methionine (residual or recurrent PA), O-(2-18F-fluoroethyl)-l-tyrosine (metastasis), 18F-choline (silent adenoma, ectopic corticotropinoma), and 13N-ammonia (hypopituitarism).
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PMID:The pituitary in nuclear medicine imaging. 3151 79

Drivers of sporadic benign pituitary adenoma growth are largely unknown. Whole-exome sequencing of 159 prospectively resected pituitary adenomas showed that somatic copy number alteration (SCNA) rather than mutation is a hallmark of hormone-secreting adenomas and that SCNAs correlate with adenoma phenotype. Using single-gene SCNA pathway analysis, we observed that both cAMP and Fanconi anemia DNA damage repair pathways were affected by SCNAs in growth hormone-secreting (GH-secreting) somatotroph adenomas. As somatotroph differentiation and GH secretion are dependent on cAMP activation and we previously showed DNA damage, aneuploidy, and senescence in somatotroph adenomas, we studied links between cAMP signaling and DNA damage. Stimulation of cAMP in C57BL/6 mouse primary pituitary cultures using forskolin or a long-acting GH-releasing hormone (GHRH) analog increased GH production and DNA damage measured by H2AX phosphorylation and a comet assay. Octreotide, a somatostatin receptor ligand that targets somatotroph adenoma GH secretion in patients with acromegaly, inhibited cAMP and GH and reversed DNA damage induction. In vivo long-acting GHRH treatment also induced pituitary DNA damage in mice. We conclude that cAMP, which induces somatotroph proliferation and GH secretion, may concomitantly induce DNA damage, potentially linking hormone hypersecretion to SCNA and genome instability. These results elucidating somatotroph adenoma pathophysiology identify pathways for targeted treatment.
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PMID:DNA damage and growth hormone hypersecretion in pituitary somatotroph adenomas. 3267 91

A 71-year-old man complained of nausea and loss of appetite for eight months prior to admission. He was transported to a hospital with disorientation and diagnosed with primary hyperparathyroidism by laboratory examinations. However, ultrasonography, computed tomography, and technetium-99m labeled methoxyisobutyl isonitrile (99mTc-MIBI) with single-photon emission computed tomography did not yield definite results. In contrast, somatostatin receptor scintigraphy successfully identified the lesion responsible for the over-secretion of parathyroid hormone within the middle mediastinum. The tumor was successfully resected by surgery, and a histopathological analysis confirmed the parathyroid adenoma nature of the tumor.
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PMID:Mediastinal Cystic Parathyroid Adenoma Diagnosed by Somatostatin Receptor Scintigraphy. 3328 Nov 67


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