Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of six lectins (Arachis hypogaea, B. simplicifolia I, concanavalin A, Dolichus biflorus, Triticum vulgaris, Lotus tetragonolobus) was studied in 24 adenocarcinomas, 24 adenomas, 20 metaplastic polyps, 17 specimens of mucosal prolapse (solitary ulcer syndrome) and 10 of normal mucosa, all taken from the rectum. Qualitative, quantitative and distributive differences in lectin expression were observed between adenocarcinoma and normal mucosa. These cancer-associated glycoprotein alterations were also observed, though to a lesser extent, in benign neoplastic and non-neoplastic lesions of the rectum. It appears therefore that the glycoprotein modifications associated with malignant transformation are not specific indicators of malignancy. It is suggested that the common denominator is a disturbance in the activities of enzymes, particularly the glycosyl-transferases and glycosidases, involved in the biosynthesis of glycoprotein. This disturbance can occur in situations where cells are less differentiated either through developmental immaturity, rapid cellular division or neoplastic de-differentiation. These changes are therefore more likely to reflect the state of differentiation rather than the malignant nature of the cells. It is shown that the greater the deviation of the lesion from normal the greater the glycoprotein alterations. The potential usefulness of lectin expressions as predictive indicators of biological behaviour of adenocarcinomas of the large bowel needs further studies.
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PMID:Lectin expression in neoplastic and non-neoplastic lesions of the rectum. 321 93

The Malpuech, Michels, Mingarelli, Carnevale (3MC) syndrome is a rare, autosomal recessive genetic- disorder associated with mutations in the MASP1/3, COLEC1,1 or COLEC10 genes. The number of 3MC patients with known mutations in these three genes reported so far remains very small. To date, 16 mutations in MASP-1/3, 12 mutations in COLEC11 and three in COLEC10 associated with 3MC syndrome have been identified. Their products play an essential role as factors involved in the activation of complement via the lectin or alternative (MASP-3) pathways. Recent data indicate that mannose-binding lectin-associated serine protease-1 (MASP-1), MASP-3, collectin kidney-1 (collectin-11) (CL-K1), and collectin liver-1 (collectin-10) (CL-L1) also participate in the correct migration of neural crest cells (NCC) during embryogenesis. This is supported by relationships between MASP1/3, COLEC10, and COLEC11 gene mutations and the incidence of 3MC syndrome, associated with craniofacial abnormalities such as radioulnar synostosis high-arched eyebrows, cleft lip/palate, hearing loss, and ptosis.
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PMID:Association of Polymorphisms of MASP1/3, COLEC10, and COLEC11 Genes with 3MC Syndrome. 3275 29