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

Ninety-three polypectomized cases from the sigmo-rectal region were examined by lectin histochemistry. On the apical surface, the UEA-1 binding sites were positive in 24/29 carcinomas and in 25/62 adenomas; while the GSA-1 binding sites were positive in 16/29 carcinomas and in 0/62 adenomas. In 2 non-neoplastic polyps, only one case was UEA-1 positive; none was GSA-1 positive. In neighbouring regions, adenomas adjacent to carcinomas were UEA-1 positive in 9/27 cases and GSA-1 positive in 3/37 cases. Thus, the GSA-1 binding sites were expressed more specifically on carcinomas. In the Golgi area, none of the polyps was UEA-1 positive while most of the cells showing GSA-1 positivity were apt to do so within the cells without showing GSA-1 positivity on the apical surface. There were no correlations between the positive rate of the lectin binding sites on the apical surface and the stage of cancer development or the histology of the adenoma on which a cancer developed. The meaning of this restricted appearance of the GSA-1 binding sites on the cancer cell surface was discussed in relation to observations previously reported in the literature.
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PMID:Appearance of Ulex europaeus agglutinin-1 and Griffonia simplicifolia agglutinin-1 binding sites on cancer cells in sigmo-rectal polyps. 147 28

A comparison of the histochemical affinities of three lectins reputedly specific to human large bowel carcinoma, namely Griffonia simplicifolia agglutinin-II (GSA-II), peanut agglutinin (PNA) and Ulex europaeus agglutinin-I (UEA-I), was done using 28 specimens in which normal mucosa, adenoma and carcinoma tissue were present and in contact with each other. In the normal mucosa, GSA-II and PNA revealed only weak affinity to the Golgi region of epithelial cells, whereas UEA-I showed binding to the apical surface of columnar cells and goblet cell mucins, especially in the right colon. Adenoma was characterized by relatively intense reactivity of the Golgi regions of epithelial cells for GSA-II and PNA as well as reactivity of the apical surface of the columnar cells for UEA-I. In carcinomas the apical surface of columnar cell-type tumor cells was stained most intensely with UEA-I, and then in descending order with GSA-II and PNA. GSA-II- and PNA-reactive carcinoma cells occurred more frequently in invasive carcinoma than in intramucosal carcinoma. Goblet cell-type tumor cells retained the properties of their normal counterparts. Staining with these lectins, especially GSA-II-horseradish peroxidase, might be helpful in the identification of carcinoma cells and for analysis of carcinoma-associated antigens.
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PMID:Histochemical comparison of specificity of three bowel carcinoma-reactive lectins, Griffonia simplicifolia agglutinin-II, peanut agglutinin and Ulex europaeus agglutinin-I. 323 92

In the pituitary gland, activating mutations of the GNAS1 (Gsalpha) gene at Gln227 have been identified in adrenocorticotrophin secreting, growth hormone secreting, and prolactin secreting adenomas. To date, mutations at the codon encoding R201, typically underlying the McCune-Albright syndrome and isolated fibrous dysplasia of bone, have been demonstrated only in growth hormone secreting pituitary adenomas. In this study, a polymerase chain reaction amplified target sequence in exon 8 of the GNAS1 gene was sequenced, identifying the first R201 mutation seen in an isolated basophilic adenoma which generated Cushing's disease in a child. This case adds Cushing's disease to the range of human diseases caused by R201 mutations of the GNAS1 gene.
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PMID:An R201H activating mutation of the GNAS1 (Gsalpha) gene in a corticotroph pituitary adenoma. 1183 49

Pituitary adenomas are common benign neoplasms, accounting for approximately 15% of intracranial tumors. In systematic autopsy, pituitary tumors are found in 25%, of the population, but only one-third of these tumors give rise to clinical manifestations. Why most of these neoplasms remain undiagnosed and pituitary carcinomas are extremely rare? The progress in the studies concerning pituitary tumorigenesis is rather slow and, due to several limitations, including the anatomic inaccessibility of human pituitary gland, the lack of functional human cell lines in culture and the discrepancies between human and animal pituitary oncogenesis (in rodents pituitary hyperplasia is a prerequisite for adenoma development). In humans, the majority of pituitary tumors are monoclonal in origin and derived from single mutated pituicyte, rarely hyperplasia is a prerequisite for adenoma formation. As in the case of other tumors, activating mutations in oncogenes (GNAS1, PTTG) and inactivating mutations in tumor suppressor genes (MEN1, CNC1) lead to pituitary tumors development. However, mutations in classic oncogenes are very rarely associated with these tumors. Moreover, the important role of some hypothalamic hormones, peripheral hormones and their receptors (e.g. GHRH, dopamine D2 receptor, PRL receptor, estrogens, thyroid hormone receptor) and growth factors (e.g. FGF, EGF, TGF) is postulated and partially proved in promotion of pituitary tumorigenesis. Further studies are required to determine which of these events are truly primary changes in pituitary tumorigenesis, what may allow development of gene therapy.
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PMID:[Molecular aspects of pituitary tumors]. 1635 Jul 28