INT119831
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Human glioma xenografts treated with PTEN/MMAC gene transfer exhibited...[33] | |||||||||||||||
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Nevertheless, co-expression of EGFRvIII and PTEN seem to be predictive factor of response to EGFR inhibitors currently tested in glioblastomas. | |||||||||||||||
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A recent publication by Mellinghoff et al. could identify patients expressing EGFRvIII as well as the tumor suppression protein PTEN showing a greater response to the TKIs [25]. | |||||||||||||||
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Human glioma xenografts treated with PTEN/MMAC gene transfer exhibited...[33] | |||||||||||||||
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Inactivating mutations and decreased expression (either by LOH or methylation) of PTEN, a tumor suppressor that reverses the action of PI3K, are the most frequently observed aberrations. | |||||||||||||||
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PAX6 and PTEN expression levels are deemed to be two independent and powerful prognostic markers for the outcome of patients with astrocytic malignant gliomas (24). | |||||||||||||||
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We found that indomethacin and NS-398 treatment significantly upregulated expression of the tumor suppressor gene, PTEN, the MAP kinase phosphatase-3, MKP-3, and the protein tyrosine phosphatase, SHP2. | |||||||||||||||
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These results suggest that as a consequence of increased expression of phosphatases such as PTEN and the resulting dephosphorylation of kinases, NSAIDs can negatively regulate the EGF/PDGF pathways in colon cancer cells-a novel mechanism for NSAIDs' chemopreventive actions. | |||||||||||||||
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The discovery of promising specific targets for intervention in the inflammatory arthritis process have included, S1P, IL-7R, Syk, Raf/MEK/ERK 1/2, MK5/PRAK, miRNA, PI3K/PTEN/Akt, NF-? | |||||||||||||||
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The discovery of promising specific targets for intervention in the inflammatory arthritis process have included, S1P, IL-7R, Syk, Raf/MEK/ERK 1/2, MK5/PRAK, miRNA, PI3K/PTEN/Akt, NF-? | |||||||||||||||
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The prostate cancer cell line LNCaP, lacking both critical enzymes in the negative control of PKB/Akt activation, PTEN and SHIP2, was the most sensitive to these effects, as assessed by analysing the cell cycle profile and expression of cell cycle regulating proteins. | |||||||||||||||
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On the other hand, identical PTEN mutations have been detected in MSI-negative endometrial hyperplasia with coexisting MSI-positive endometrioid endometrial carcinomas. | |||||||||||||||
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Interestingly, concordance between MSI status and PTEN mutations has been found; the mutations occur in 6086% of MSI-positive endometrioid endometrial carcinoma but in only 2435% of the MSI-negative cases [79, 13, 17]. | |||||||||||||||
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However, PTEN and KRAS mutations seem to occur earlier, since they were found in simple hyperplasia, partially associated with monoclonality. | |||||||||||||||
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In atypical hyperplasia, alterations of PTEN, ? | |||||||||||||||
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Thus, some PTEN mutations may precede MSI, and coexistence of both alterations does not necessarily mean a cause-effect relationship [9]. | |||||||||||||||
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RII), BAX, insulin-like growth factor II receptor (IGFIIR), MSH3, MSH6, caspase-5, and PTEN may promote MSI-positive endometrial carcinoma [8, 9]. | |||||||||||||||
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In the patient tumor, PTEN was under-expressed (-109.7 FC in lung relative to compendium; -440.1 FC in lung relative to blood), and we note that PTEN maps to a region of heterozygous loss in the tumor genome. | |||||||||||||||
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The drugs were repackaged in look-alike capsules containing either Daflon (500 mg) + DEC (25 mg) or DEC (25 mg). | |||||||||||||||
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The drugs were repackaged in look-alike capsules containing either Daflon (500 mg) + DEC (25 mg) or DEC (25 mg). | |||||||||||||||
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