Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oncology of the hypertrophic prostate and histogenesis of the cancer. Histological examine of 286 hypertrophic prostates collected by suprapubic way, on histologic macrosections including the whole visceral area, with the "step section technique". N. 286 hypertrophic prostates collected through suprapubic way have been examined on histologic macrosections including the whole visceral area, with the step section technique. There have been used object holders slides measuring cm. 12 x 9 and cover objects measuring cm. 5 x 7. Colourings: hematoxylin-eosin , Goldner. Localisation of the tumours has been determined in the prostate area. The cases with the presence of tumours-microcarcinoma (MCP), with maximum axis up to 1 millimeter; small carcinoma (PCP), maximum axis from mm. 1.1 to mm. 5, and the classic carcinoma (CPcl) have been 232 (81%). CPcl appeared in 33 cases (11.53%). Histogenesis of the MCP has been ascertained (from terminal secretory micro-ducts of the prostate). Of PCP (from groups of MCP n. 56 in picture 7), and of CPcl (from PCP in progressive growth) or from grouping of MCP (in picture 14, 101 MCP of the 235 present in the area of mm2 40). CPcl has shows invading growth in ten cases; in 23 cases it consisted in infiltrating growth but limited, the border towards the prostatic tissue appears circumscribed by pseudocapsule, the cells show nucleoli of varying sizes. In seven cases it turned out to be adenocarcinoma with limited growth as said before, partly with pseudocapsules, and the cells appear seriously atypical, hypertrophic, hyperstained nuclei, thickening of the nuclear membrane, prominent nucleoli, in the absence of any invading tendency. Specific oncogenic agents are thought to transform the prostate cells into definite morphologic malignancy, while another oncogenic agent causes the invading proliferation.
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PMID:[Oncology of the hypertrophic prostate and study of the histogenesis of carcinoma. Histological analysis of 286 prostates obtained using the suprapubic route and examined using macro-sections including the entire visceral surface using the step-section technique]. 768 75

Adenocarcinomas of the nose are regarded as an occupational disease in Germany and other European countries, and workers exposed to oak or beech wood-dust in the course of their work receive compensation if they incur adenocarcinoma of the nose. This has prompted a joint research project to record the functional and morphological changes of the nasal mucosa and/or paranasal sinus of 149 exposed subjects and 33 controls in accordance with a defined occupational exposure. To ensure the quantitative and qualitative reliability of the exposure data, 1,349 measurements at the company workplace were taken and analyses of 614 wood samples performed; parallel to this, the genotoxic effects of the most important substances used in the wood-working industry were tested. Apart from this, latency periods and morbidity rates in Germany were investigated. Partial findings of this research projects have been evaluated by the International Agency for Research on Cancer (IARC). According to these evaluations and the findings presented here, the following points can be made: i) Morphological changes in the nasal mucosa after exposure to wood-dust resulted in an increase in cylindrocellular hyperplasias and, in functional terms, a tendency towards improved nasal clearance was observed. Chromium and formaldehyde, on the other hand, tended to give rise to an increase in the number of squamous metaplasias. This might explain the preference for the histological types of adenocarcinoma among subjects exposed to wood-dust. ii) In tissue samples more dysplasias were found among those exposed to oak and beech wood-dust. Subjects exposed to wood preserving agents had dysplasias only if they were simultaneously exposed to oak and beech wood-dust. The latter effect did not quite reach the level of significance (p = 0.07) on account of the low numbers of cases. iii) The investigation of genotoxic effects showed that oak and beech contain genotoxic substances that can be dissolved by means of ethanol and cyclohexane; they also showed that 3 out of 8 wood preservatives, 5 out of 16 stains, and 2 out of 11 paints from the wood-working industry are genotoxic too. Apart from this, lindane and PCP have proved to be genotoxic in the nasal cells of rats and human beings. Analysis of 614 wood samples from wood-preserving agents showed that almost 73% contained agents of this type, even in woods described by the companies as being guaranteed free of wood preservatives. iv) According to an analysis of 147 cases accepted since 1985 as a pensionable occupational illness by the Holz-Berufsgenossenschaft (an industrial compensation society for employees in the wood-working industry), the disease was much more apparent in small companies where there is multi-factorial exposure, than in large companies where the exposure factor tends to have a single component. This points to the combined effects of hardwood dusts and chemicals as being the cause. v) According to published findings, the incidence of the disease in England seems to be on the decline. In Germany, increasing latency periods also point to a decline in the number of cases, although both countries have only very recently introduced effective prevention measures against exposure to wood-dust. This also leads to the assumption that wood-dusts cannot be the only cause of this type of cancer. vi) These findings tally with the evaluation by the IARC confirming the special part that hardwood dusts play in the development of nasal cancer. The findings presented here also indicate combined effects as being the cause of this type of cancer. This hypothesis cannot be confirmed until the conclusion of long-term animal experiments, currently being conducted, to test how the effects of chemicals such as lindane, PCP, and chromate compare with use of oak wood-dust.
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PMID:The role of combination effects on the etiology of malignant nasal tumours in the wood-working industry. 972 90

WNT signals play key roles in carcinogenesis and embryogenesis through the specification of cell fate and polarity. Dishevelled proteins are implicated in the WNT - beta-catenin pathway and the WNT-PCP pathway. DAAM1/KIAA0666 is a Dishevelled-binding protein transducing WNT signals to the PCP pathway. Here, we identified and characterized DAAM2 gene by using bioinformatics. Uncharacterized FLJ34430 and KIAA0381 cDNAs were homologous to DAAM1. FLJ34430 was recombined with URB (XM_087331) in the 3'-region, and KIAA0381 was truncated in the 5'-region. Nucleotide sequence of DAAM2 cDNA was determined in silico by adding nucleotide position 1-793 of FLJ34430 onto the 5'-end of KIAA0381. DAAM2 gene consists of 27 exons, and gives rise to four splicing variants due to alternative splicing of alternative promoter type as well as of cassette exon type. DAAM2 gene was linked to the MOCS1 gene on human chromosome 6p21.3 with an interval less than 1 kb. DAAM2 mRNA was expressed in fetal heart, adult hypothalamus, eye, spinal cord, lung, prostate, kidney, and also in glioblastoma, oligodendroglioma, melanoma, mammary adenocarcinoma and chondrosarcoma. DAAM2 was a 1077-amino-acid protein with Formin-homology FH1 and FH2 domains, which showed 68.9% total-amino-acid identity with DAAM1. Among Formin-homology proteins, FDD (Formin-like, Diaphanous, Daam) domain was conserved in FMNL1/FMNL/KW-13, FMNL2/KIAA1902/FHOD2, DIAPH1, DIAPH2, DAAM1 and DAAM2, but not in Fmn1, Fmn2, FHOD1 and Grid2ip. Therefore, it was concluded that FMNL1, FMNL2, DIAPH1, DIAPH2, DAAM1 and DAAM2 proteins constitute the Formin-homology FDD subfamily.
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PMID:Identification and characterization of human DAAM2 gene in silico. 1263 87