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• W173674337 abstract "Deficiency of DNA repair has been shown to lead to cancer in multiple human disease states. We therefore hypothesized that deficiency of Nucleotide Excision Repair is involved in the etiology of breast cancer. This work was carried out using a novel in vitro culture system for both normal and cancerous breast tissue developed in the Latimer laboratory. Primary cultures of non-diseased and tumor tissue were utilized in functional studies, and cell lines generated from these primary cultures were used for expression analysis. Cell lines were generated from the Latimer primary culture system without the use of exogenously transforming agents. Using the Unscheduled DNA Synthesis Assay, we have shown that stage I and stage II breast tumors are deficient in functional NER capacity as compared to non-diseased controls. Analysis of the steady-state mRNA expression levels of 20 genes in the NER pathway using an RNase Protection kit showed that 7 genes (CSB, XPA, XPB, TFIIHp52, TFIIHp44, TFIIHp34, and Cdk7) also showed a loss of expression in early stage tumor cell lines. Microarray analyses corroborated these trends and protein expression was also lost in early stage tumor cell lines for the XPA and CSB genes. In contrast to the loss of DNA repair capacity manifested in early stage tumors, stage III tumors showed an increase in repair capacity. Gain of mRNA expression and protein expression was seen for our candidate genes in late stage tumors. Because loss of expression was reversible and occurred in multiple genes and cell lines, we hypothesized that the mechanism responsible was epigenetic regulation of gene expression. Two early stage cell lines that demonstrated loss of expression of these candidate genes were treated with the demethylating agent 5-aza-2'deoxycytidine, resulting in the re-expression of 3 genes: TFIIHp52, TFIIHp34, and Cdk7. In contrast, two of the candidate genes that were not reactivated by azacytidine treatment (CSB and XPA) showed a 7-element transcription factor framework that may begin to explain their coordinate regulation. The functional loss of NER capacity in early stage tumors is consistent with a transcriptional regulatory mechanism including both methylation and other transcription factor based functions." @default.
• W173674337 created "2016-06-24" @default.
• W173674337 creator A5079427446 @default.
• W173674337 date "2006-12-01" @default.
• W173674337 modified "2023-09-25" @default.
• W173674337 title "Molecular Mechanism of Nucleotide Excision Repair Deficiency in Novel Breast Cancer Cell Lines" @default.
• W173674337 cites W111861070 @default.
• W173674337 cites W1481421933 @default.
• W173674337 cites W1481565370 @default.
• W173674337 cites W1492640274 @default.
• W173674337 cites W1493303652 @default.
• W173674337 cites W1493767608 @default.
• W173674337 cites W1494340358 @default.
• W173674337 cites W1504303645 @default.
• W173674337 cites W1506804030 @default.
• W173674337 cites W1514995986 @default.
• W173674337 cites W1521044274 @default.
• W173674337 cites W1521601785 @default.
• W173674337 cites W1524171152 @default.
• W173674337 cites W1533555842 @default.
• W173674337 cites W1546709038 @default.
• W173674337 cites W1547406244 @default.
• W173674337 cites W1554775680 @default.
• W173674337 cites W1557475781 @default.
• W173674337 cites W1565166977 @default.
• W173674337 cites W1571666545 @default.
• W173674337 cites W1574658543 @default.
• W173674337 cites W1582007138 @default.
• W173674337 cites W1587566453 @default.
• W173674337 cites W1589876235 @default.
• W173674337 cites W1597743639 @default.
• W173674337 cites W1604381017 @default.
• W173674337 cites W1616243898 @default.
• W173674337 cites W1643390591 @default.
• W173674337 cites W165864682 @default.
• W173674337 cites W1752198036 @default.
• W173674337 cites W1772131958 @default.
• W173674337 cites W1776676565 @default.
• W173674337 cites W1782413320 @default.
• W173674337 cites W1816419917 @default.
• W173674337 cites W1839722510 @default.
• W173674337 cites W1843309205 @default.
• W173674337 cites W1848203461 @default.
• W173674337 cites W185740322 @default.
• W173674337 cites W1879187490 @default.
• W173674337 cites W1889725400 @default.
• W173674337 cites W190545792 @default.
• W173674337 cites W1906450972 @default.
• W173674337 cites W1917603270 @default.
• W173674337 cites W1920958927 @default.
• W173674337 cites W1956911580 @default.
• W173674337 cites W1963528972 @default.
• W173674337 cites W1963735070 @default.
• W173674337 cites W1964301645 @default.
• W173674337 cites W1964574639 @default.
• W173674337 cites W1965923719 @default.
• W173674337 cites W1966284016 @default.
• W173674337 cites W1966542709 @default.
• W173674337 cites W1969306277 @default.
• W173674337 cites W1969600377 @default.
• W173674337 cites W1970294374 @default.
• W173674337 cites W1971246275 @default.
• W173674337 cites W1973604371 @default.
• W173674337 cites W1974341281 @default.
• W173674337 cites W1975190094 @default.
• W173674337 cites W1976126527 @default.
• W173674337 cites W1978788828 @default.
• W173674337 cites W1979541010 @default.
• W173674337 cites W1979604597 @default.
• W173674337 cites W1980597862 @default.
• W173674337 cites W1980989598 @default.
• W173674337 cites W1981900473 @default.
• W173674337 cites W1982638636 @default.
• W173674337 cites W1983825404 @default.
• W173674337 cites W1984201646 @default.
• W173674337 cites W1984353960 @default.
• W173674337 cites W1984680322 @default.
• W173674337 cites W1984967200 @default.
• W173674337 cites W1985895020 @default.
• W173674337 cites W1989339075 @default.
• W173674337 cites W1989656134 @default.
• W173674337 cites W1990493392 @default.
• W173674337 cites W1992069029 @default.
• W173674337 cites W1992554340 @default.
• W173674337 cites W1993086521 @default.
• W173674337 cites W1994053770 @default.
• W173674337 cites W1994096230 @default.
• W173674337 cites W1996526067 @default.
• W173674337 cites W1996973786 @default.
• W173674337 cites W1997712931 @default.
• W173674337 cites W1997897613 @default.
• W173674337 cites W1998055257 @default.
• W173674337 cites W1998749998 @default.
• W173674337 cites W1999015147 @default.
• W173674337 cites W2000067413 @default.
• W173674337 cites W2002263141 @default.
• W173674337 cites W2002576748 @default.
• W173674337 cites W2002875720 @default.
• W173674337 cites W2002891103 @default.
• W173674337 cites W2004277017 @default.

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