FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1775241352> ?p ?o ?g. }

• W1775241352 endingPage "81" @default.
• W1775241352 startingPage "7277" @default.
• W1775241352 abstract "Renal cell carcinoma (RCC), the most common adult kidney neoplasm, is histopathologically heterogeneous, with most sporadic RCCs ( approximately 80%) classified as clear cell (CC) tumors. Chromosome 3p allele loss is the most frequent genetic alteration in RCC but is associated specifically with sporadic and hereditary forms of clear cell RCC (CC-RCC) and is not a feature of non-CC-RCC, such as papillary (chromophilic) RCC. The VHL tumor suppressor gene (TSG) maps to chromosome 3p25, and somatic inactivation of the VHL gene occurs in up to 70% of CC-RCC tumors and cell lines. However, VHL inactivation is not sufficient for CC-RCC tumorigenesis, and inactivation of 3p12-p21 TSG(s) appears to be necessary in CC-RCC irrespective of VHL gene inactivation status. Recently, we demonstrated that the candidate 3p21 TSG, RASSF1A, is hypermethylated in most small cell lung cancers. We have now investigated the role of RASSF1A inactivation in primary RCC tumors. RASSF1A promoter methylation was detected in 23% (32 of 138) of primary CC-RCC tumors. In CC-RCC cell lines, RASSF1A methylation was associated with silencing of RASSF1A expression and restoration of expression after treatment with 5'-azacytidine. The frequency of RASSF1A methylation was similar in CC-RCC with and without VHL gene inactivation (24% versus 21%), and there was no association between epigenetic silencing of the RASSF1A and VHL TSGs, because 0 of 6 tumors with VHL hypermethylation had RASSF1A methylation, and VHL was not methylated in 26 CC-RCCs with RASSF1A methylation. Although 3p allele loss has been reported rarely in papillary RCC, we identified RASSF1A methylation in 44% (12 of 27) of papillary RCCs analyzed. Thus: (a) inactivation of RASSF1A is a frequent event in both CC-RCC and papillary RCC tumors; (b) there is no relationship between epigenetic silencing of RASSF1A and VHL inactivation status in CC-RCC. Fifty-four CC-RCCs analyzed for RASSF1A methylation were informative for 3p21 allele loss, and 20% (7 of 35) with 3p21 allele loss demonstrated RASSF1A methylation. All informative CC-RCCs with 3p21 allele loss and no RASSF1A methylation also demonstrated allele losses at other regions of 3p so that tumorigenesis in these cases may result from: (a) haploinsufficiency of RASSF1A; (b) inactivation of other 3p21 TSGs; or (c) inactivation of 3p TSGs from outside of 3p21. RASSF1A is the first TSG to be inactivated frequently in both papillary and CC-RCCs. The finding of frequent epigenetic inactivation of RASSF1A in papillary RCCs despite previous studies reporting infrequent 3p21 allele loss in this tumor type illustrates how the systematic identification of all major human cancer genes will require detailed analysis of the cancer genome and epigenome." @default.
• W1775241352 created "2016-06-24" @default.
• W1775241352 creator A5001823258 @default.
• W1775241352 creator A5017425394 @default.
• W1775241352 creator A5024325273 @default.
• W1775241352 creator A5028262007 @default.
• W1775241352 creator A5035346994 @default.
• W1775241352 creator A5053110552 @default.
• W1775241352 creator A5056034710 @default.
• W1775241352 creator A5056418703 @default.
• W1775241352 creator A5059540059 @default.
• W1775241352 creator A5073770568 @default.
• W1775241352 creator A5074883658 @default.
• W1775241352 creator A5076510325 @default.
• W1775241352 creator A5088627051 @default.
• W1775241352 creator A5090829869 @default.
• W1775241352 date "2001-10-01" @default.
• W1775241352 modified "2023-10-03" @default.
• W1775241352 title "Epigenetic inactivation of the RASSF1A 3p21.3 tumor suppressor gene in both clear cell and papillary renal cell carcinoma." @default.
• W1775241352 cites W1504197144 @default.
• W1775241352 cites W1514961004 @default.
• W1775241352 cites W1538717269 @default.
• W1775241352 cites W1592698345 @default.
• W1775241352 cites W1609687385 @default.
• W1775241352 cites W1739103212 @default.
• W1775241352 cites W181147267 @default.
• W1775241352 cites W1825787668 @default.
• W1775241352 cites W1828777933 @default.
• W1775241352 cites W1839547316 @default.
• W1775241352 cites W1899791338 @default.
• W1775241352 cites W1927527067 @default.
• W1775241352 cites W1950889666 @default.
• W1775241352 cites W1964382251 @default.
• W1775241352 cites W1965297768 @default.
• W1775241352 cites W1969229561 @default.
• W1775241352 cites W1981432410 @default.
• W1775241352 cites W1995684639 @default.
• W1775241352 cites W2010160635 @default.
• W1775241352 cites W2016475398 @default.
• W1775241352 cites W2019573100 @default.
• W1775241352 cites W2030116438 @default.
• W1775241352 cites W2033222240 @default.
• W1775241352 cites W2041263849 @default.
• W1775241352 cites W2052333525 @default.
• W1775241352 cites W2061445402 @default.
• W1775241352 cites W2068555261 @default.
• W1775241352 cites W2085048776 @default.
• W1775241352 cites W2087284992 @default.
• W1775241352 cites W2092641158 @default.
• W1775241352 cites W2092813484 @default.
• W1775241352 cites W2094010209 @default.
• W1775241352 cites W2094483021 @default.
• W1775241352 cites W2101628607 @default.
• W1775241352 cites W2103800652 @default.
• W1775241352 cites W2105159111 @default.
• W1775241352 cites W2109603821 @default.
• W1775241352 cites W2109619765 @default.
• W1775241352 cites W2111756139 @default.
• W1775241352 cites W2113459016 @default.
• W1775241352 cites W2121161701 @default.
• W1775241352 cites W2124105932 @default.
• W1775241352 cites W2128146359 @default.
• W1775241352 cites W2136055213 @default.
• W1775241352 cites W2141805646 @default.
• W1775241352 cites W2150162153 @default.
• W1775241352 cites W2164171045 @default.
• W1775241352 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11585766" @default.
• W1775241352 hasPublicationYear "2001" @default.
• W1775241352 type Work @default.
• W1775241352 sameAs 1775241352 @default.
• W1775241352 citedByCount "71" @default.
• W1775241352 countsByYear W17752413522012 @default.
• W1775241352 countsByYear W17752413522013 @default.
• W1775241352 countsByYear W17752413522014 @default.
• W1775241352 countsByYear W17752413522015 @default.
• W1775241352 countsByYear W17752413522016 @default.
• W1775241352 countsByYear W17752413522017 @default.
• W1775241352 countsByYear W17752413522018 @default.
• W1775241352 countsByYear W17752413522019 @default.
• W1775241352 countsByYear W17752413522020 @default.
• W1775241352 countsByYear W17752413522022 @default.
• W1775241352 crossrefType "journal-article" @default.
• W1775241352 hasAuthorship W1775241352A5001823258 @default.
• W1775241352 hasAuthorship W1775241352A5017425394 @default.
• W1775241352 hasAuthorship W1775241352A5024325273 @default.
• W1775241352 hasAuthorship W1775241352A5028262007 @default.
• W1775241352 hasAuthorship W1775241352A5035346994 @default.
• W1775241352 hasAuthorship W1775241352A5053110552 @default.
• W1775241352 hasAuthorship W1775241352A5056034710 @default.
• W1775241352 hasAuthorship W1775241352A5056418703 @default.
• W1775241352 hasAuthorship W1775241352A5059540059 @default.
• W1775241352 hasAuthorship W1775241352A5073770568 @default.
• W1775241352 hasAuthorship W1775241352A5074883658 @default.
• W1775241352 hasAuthorship W1775241352A5076510325 @default.
• W1775241352 hasAuthorship W1775241352A5088627051 @default.
• W1775241352 hasAuthorship W1775241352A5090829869 @default.
• W1775241352 hasConcept C104317684 @default.
• W1775241352 hasConcept C119056186 @default.

• next