CCL

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1.

001-es BibID:BIBFORM041668
Első szerző:Ádány Róza (megelőző orvostan és népegészségtan szakorvos)
Cím:Kvantitativ polimeráz láncreakció gének metilációs állapotának vizsgálatára / Ádány Róza, Iozzo Renato V.
Dátum:1991
Tárgyszavak:Orvostudományok Klinikai orvostudományok magyar nyelvű folyóiratközlemény hazai lapban
Megjelenés:Laboratóriumi Diagnosztika. - 18 (1991), p. 253-255. -
További szerzők:Iozzo, Renato V.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM041394
035-os BibID:PMID:1710888
Első szerző:Ádány Róza (megelőző orvostan és népegészségtan szakorvos)
Cím:Hypomethylation of the decorin proteoglycan gene in human colon cancer / Róza Ádány, Renato V. Iozzo
Dátum:1991
Megjegyzések:We have previously reported that the connective tissue stroma of human colon carcinoma contains elevated amounts of decorin, a small proteoglycan involved in the regulation of matrix formation and cell proliferation. These biochemical changes were correlated with increased mRNA levels and general hypomethylation of the decorin gene in human colon cancer DNA. In this report we use a quantitative polymerase chain reaction method coupled with digestion of the DNA template by methylation-sensitive restriction endonucleases to investigate in detail the location of hypomethylated sites in decorin gene. We demonstrate that a specific site in the 3' region of the gene, encompassing codons 360-361, is specifically hypomethylated in both colon carcinoma and benign polyp. In contrast, three HpaII sites, clustered in the 5' untranslated region, show full methylation in normal and neoplastic DNA. The lack of such changes in ulcerative colitis DNA suggests that chronic inflammation alone is not sufficient to alter cytosine methylation in the decorin gene. These results suggest the possibility that the 3' region of the decorin-coding sequence may be involved in the control of decorin gene expression.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Biochemical Journal. - 276 : Pt 2 (1991), p. 301-306. -
További szerzők:Iozzo, Renato V.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041396
035-os BibID:PMID:2222452
Első szerző:Ádány Róza (megelőző orvostan és népegészségtan szakorvos)
Cím:Altered methylation of versican proteoglycan gene in human colon carcinoma / Róza Ádány, Renato V. Iozzo
Dátum:1990
Megjegyzések:We show for the first time that DNA isolated from human colon carcinoma tissue exhibits a selective hypomethylation of versican gene, which encodes a large chondroitin sulfate proteoglycan. The degree of methylation of CpG sequences of versican gene locus, as determined by isoschizomeric endonucleases and Southern hybridization, is about three times lower than that found in either normal colon or ulcerative colitis tissues. Hypomethylation can be observed in both benign and malignant colonic neoplasms; however, there is no correlation with increased expression since versican mRNA levels do not significantly vary between normal and neoplastic tissues. We further show that versican gene locus from malignant tissue, but not from normal or ulcerative colitis tissues, contains Hind III hypersensitive sites which also comprise hypomethylated CpG sequences. Analysis of versican methylation status in colon carcinoma cells and benign mesenchymal cells derived from human colon suggests that the changes observed in vivo derive from demethylating events involving host stromal cells rather than tumor cells themselves. These findings demonstrate that changes in versican gene methylation are specific for colonic neoplasms, that these changes may precede malignant transformation, and that inflammation and tissue remodelling alone are not enough to generate these changes in proteoglycan gene methylation and nuclease hypersensitivity.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Biochemical and Biophysical Research Communications. - 171 : 3 (1990), p. 1402-1413. -
További szerzők:Iozzo, Renato V.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM041399
035-os BibID:PMID:2162845
Első szerző:Ádány Róza (megelőző orvostan és népegészségtan szakorvos)
Cím:Altered expression of chondroitin sulfate proteoglycan in the stroma of human colon carcinoma : hypomethylation of PG-40 gene correlates with increased PG-40 content and mRNA levels / Róza Ádány, Ralph Heimerg, Bruce Caterson, J. Michael Sorrell, Renato V. Iozzo
Dátum:1990
Megjegyzések:The connective tissue stroma of malignant tumors is a newly formed tissue that supports the growth and progression of neoplastic cells. Proteoglycans are intrinsic components of this complex structure and molecular changes in this class of macromolecules can significantly affect behavioral properties of transformed cells. We report that human colon carcinoma contained increased levels of a chondroitin sulfate proteoglycan that exhibited an altered glycosaminoglycan structure in which 0- and 6-sulfated units, as detected by specific monoclonal antibodies, predominated. Proteoglycans with such epitopes were localized primarily to the connective tissue stroma surrounding the tumor cells but not to the tumor cells themselves or the native, non-cancerous connective tissue. Analysis of mRNA encoding PG-40, the main chondroitin sulfate proteoglycan of colon tissue, revealed a 7-fold increase in the two transcripts encoding this gene product. This increase was evident whether the data were normalized to total RNA content or beta-actin mRNA levels. The altered steady state levels of PG-40 mRNA did not correlate with any significant gene amplification or rearrangement of PG-40 in human colon cancer. However, when genomic DNA was tested for degree of methylation, the colon carcinoma tissue showed a marked hypomethylation of PG-40 gene locus, a finding that has been associated with increased gene activation. Interestingly, PG-40 gene was also hypomethylated in cultured colon fibroblasts, which express PG-40, but not in colon carcinoma cells which do not express this gene. These results indicate that specific proteoglycan changes occur in colon carcinoma and that these alterations are the product of stromal cells that are topologically associated with and functionally respondent to the growing malignant cells. This is the first evidence that enhanced PG-40 expression in a human malignant tissue is associated with a hypomethylated gene and suggests that the control of PG-40 gene expression may represent an important factor in the progression of colon carcinoma.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:The Journal of Biological Chemistry. - 265 : 19 (1990), p. 11389-11396. -
További szerzők:Heimer, Ralph Caterson, Bruce Sorrell, J. Michael Iozzo, Renato V.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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