INT205081
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Co-overexpression of AXL with Gas6 has also been reported in several types of tumors including ovarian cancer [45], and may therefore have an important role in uncontrolled cell growth/proliferation. | |||||||||||||||
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AXL expression is also elevated in leukemia, melanoma, prostate, colon, endometrial, and thyroid cancers[29][32]. | |||||||||||||||
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Although, the comparison of gene expression profiles between endometriosis and normal endometrium was done for the proliferative phase, AXL, SHC1, and ACTN4 (discussed below) were also overexpressed during secretory phase in ovarian endometriosis. | |||||||||||||||
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Therefore, it is possible that overexpression of AXL and GAS6 is a main cause for the activation of the PI3K-Akt pathway in endometriosis. | |||||||||||||||
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Overexpression of both AXL and GAS6 in ovarian endometriosis has previously been demonstrated using RT-PCR analysis and IHC [44]. | |||||||||||||||
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Similar to what we observed for AXL, SHC1 was found consistently elevated in the studied endometriotic samples. | |||||||||||||||
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Therefore, it is possible that overexpression of AXL and GAS6 is a main cause for the activation of the PI3K-Akt pathway in endometriosis. | |||||||||||||||
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As overexpression of AXL and SHC1 theoretically activates both PI3K-Akt and MAPK pathways, dysregulation of these genes in human endometriosis may correspond to oncogenic activation of K-ras or biallelic losses of Pten in the mouse model of the disease. | |||||||||||||||
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In human endometriosis, the PI3K-Akt and MAPK signaling pathways may be activated via overexpression of AXL and SHC1, respectively. | |||||||||||||||
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Our analysis identified additional genes, including AXL, MFAB, and AXIN2, whose elevated expression in islet cell tumors suggests signal transduction pathways important in their development. | |||||||||||||||
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They include carbonic anyhdrase IX, which is the RCC associated antigen G250 and is induced in many cancer types, hypoxia induced gene ADORA3, potentially oncogenic AXL gene which causes transformation when overexpressed in NIH 3T3 cells, and vitamin D receptor (VDR, up-regulated), which was found to be over-expressed in pancreatic cell lines (Albrechtsson et al. 2003) and is down-regulated by resveratrol compound (Shi et al. 2004) in RCC cell lines, which acts as a chemopreventive agent for RCC and other types of cancers. | |||||||||||||||
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