INT89794
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Histologic findings of a renal biopsy indicated that acute tubular necrosis (ATN) had caused ARF in this patient's case. | |||||||||||||||
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-galactosidase activity [12], increase in reactive oxygen species (ROS), telomere attrition [13] and p53/p16ink4 accumulation [11]. | |||||||||||||||
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Under the impression of exercise-induced ARF, we tried to determine the relationship between the occurrence of clinical symptoms, renal dysfunction and the characteristic CT findings by observing those changes prospectively before and after anaerobic exercise. | |||||||||||||||
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Inhibition of p16 (INK4a) activation by p16-specific siRNA blocked OGF's repressive action on proliferation of SCC-1, CAL-27, and SCC-4 HNSCC cells. | |||||||||||||||
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Inhibition of p16 (INK4a) activation by p16-specific siRNA blocked OGF's repressive action on proliferation of SCC-1, CAL-27, and SCC-4 HNSCC cells. | |||||||||||||||
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Overexpression of p16 in the carcinomatous regions of MMMT (Figure 1E) with inverse expression of p21 in these regions denotes an upregulation of p16. | |||||||||||||||
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A number of studies have shown increased levels of p16INK4a with increased occurrence of senescence [32,33]. p16INK4a is thought to be involved in the activation of the retinoblastoma cell cycle inhibitory pathway, leading to permanent growth arrest and cellular senescence [34]. | |||||||||||||||
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E6 inhibits p53 function by binding with E6-AP ubiquitin ligase, and leads to p14ARF upregulation via p53 degradation by negative feedback mechanism [22, 23]. | |||||||||||||||
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For pancreatic carcinoma, this disruption is caused exclusively by inactivation of p16INK4a gene and, only rarely, the Rb gene [24,25]. | |||||||||||||||
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Inactivation of p16 gene occurs through intragenic mutation, homozygous deletion and methylation associated transcriptional silencing. | |||||||||||||||
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LOH could also be selected as the second hit for inactivating TP53 and CDKN2A. | |||||||||||||||
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Genomic DNA from flow-purified Barrett's epithelium was evaluated for CDKN2A promoter methylation in 175 flow-purified fractions from 121 participants. | |||||||||||||||
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We found that both RHC and NRHC variants were associated with statistically significantly increased melanoma risk in CDKN2A mutation carriers, whereas a recent meta-analysis of melanoma casecontrol studies reported that most MC1R variants, except the most frequent NRHC variants, V60L and V92M, were associated with statistically significantly increased melanoma risk (12). | |||||||||||||||
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This case highlights a case of selenium intoxication from selenite broth resulting in ARF and corrosive gastritis. | |||||||||||||||
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Importantly, p16 complexed with Cdk4 was increased by OGF treatment at all time points, consistent with the hypothesis that OGF mediated growth inhibition through p16. | |||||||||||||||
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Inactivating mutations, or loss, results in inactivation of the two encoding tumor suppressor genes p16 and p14. | |||||||||||||||
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Here, we demonstrate for the first time that, in cells extracted from human NP tissue, increased levels of p16INK4a were associated with increased gene expression of the degradative enzymes MMP-13 and ADAMTS 5, which is characteristic of disc degeneration [5,39]. | |||||||||||||||
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Importantly, this study has shown that degenerate discs exhibit accelerated senescence with decreased telomere length, reduced cell replication potential, and elevated levels of p16INK4a and SA-? | |||||||||||||||
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In particular, we have found that telomeric erosion increases with age together with increased levels of p16INK4a. | |||||||||||||||
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Here, we demonstrate for the first time that, in cells extracted from human NP tissue, increased levels of p16INK4a were associated with increased gene expression of the degradative enzymes MMP-13 and ADAMTS 5, which is characteristic of disc degeneration [5,39]. | |||||||||||||||
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