Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Addition of cGMP to cytosol of human endometrium or to cells of the endometrial cancer line HEC-1 produced severalfold increases in specific estrogen binding (EB) levels. This effect was maximal with 1 microM cGMP in the presence of 0.1 mM isobutylmethylxanthine (a phosphodiesterase inhibitor) during incubations with [3H]estradiol. In contrast, cAMP decreased EB levels under similar conditions. The effects of cyclic nucleotides on EB levels were complete in less than 15 min in the presence of Mg2+, Mn2+, or Ca2+. The EB sites generated by the addition of cGMP during labeling of cytosol with 10 nM [3H]estradiol were found to sediment in the 8S and 4S regions of low-salt glycerol gradients. No changes in EB levels were observed when cyclic nucleotides were added to cytosol depleted of ATP by preincubation at 4 degrees C for 3 hr, but responsiveness was restored by addition of exogenous ATP. The ATP requirement and the pattern of dependence of cyclic nucleotide actions on divalent cation concentrations suggest that cGMP and cAMP effects may be mediated by kinases and may involve phosphorylations. Another possibility is that the cyclic nucleotides interact allosterically with the binder in the presence of ATP. Addition of sodium molybdate, ATP, and GTP to homogenates of endometrial tissue or HEC-1 cells produces increases in EB levels similar to those obtained by the addition of cGMP. However, these compounds are much less active when added to cytoplasm or cytosol. On the basis of these and other observations, it is hypothesized that molybdate, ATP, and GTP affect EB levels primarily by increasing cGMP concentrations through processes involving a plasma membrane-bound guanylate cyclase.
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PMID:Rapid changes in specific estrogen binding elicited by cGMP or cAMP in cytosol from human endometrial cells. 630 87

There is a need for research studies into the molecular mechanisms underpinning the link between polycystic ovary syndrome (PCOS) and endometrial cancer (EC) to facilitate screening and to encourage the development of novel strategies to prevent disease progression. The objective of this review was to identify proteomic biomarkers of EC risk in women with PCOS. All eligible published studies on proteomic biomarkers for EC identified through the literature were evaluated. Proteomic biomarkers for EC were then integrated with an updated previously published database of all proteomic biomarkers identified so far in PCOS women. Nine protein biomarkers were similarly either under or over expressed in women with EC and PCOS in various tissues. These include transgelin, pyruvate kinase M1/M2, gelsolin-like capping protein (macrophage capping protein), glutathione S-transferase P, leucine aminopeptidase (cytosol aminopeptidase), peptidyl-prolyl cis-transisomerase, cyclophilin A, complement component C4A and manganese-superoxide dismutase. If validated, these biomarkers may provide a useful framework on which the knowledge base in this area could be developed and will facilitate future mathematical modelling to enhance screening and prevention of EC in women with PCOS who have been shown to be at increased risk.
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PMID:Proteomic biomarkers of endometrial cancer risk in women with polycystic ovary syndrome: a systematic review and biomarker database integration. 2352 52

The depth of myometrial invasion in patients with endometrial carcinoma is recognized as an important factor that closely correlates with prognosis. Preoperative assessment of myometrial invasion is essential for planning surgery. To enhance the contrast between myometrium and endometrium including myometrial invasion with endometrial carcinoma, we optimized the sequence parameter with phase-sensitive inversion-recovery (PSIR) in gadolinium dynamic study of uterine corpus. On a 1.5-T magnetic resonance imaging (MRI), images were acquired by three-dimensional (3D) T1 -turbo field echo (TFE) with PSIR sequence and gadolinium-diethylenetriamine pentaacetic acid( Gd-DTPA) diluted phantom (0-5 mmol/L) and myometrium model (manganese chloride tetrahydrate+agar). We calculated the null point and the contrast-to-noise ratio (CNR) at multiple TFE inversion delay times, 200 ms-maximum in each combination; flip angles (FAs), 5-35 degrees; TFE factor, 20-40; and shot interval (SI), 500-1000 ms. We assumed that dynamic scanning time was 30 seconds when the sensitivity encoding factor was 2, namely, in this study, the scanning time was 1 minute with no sensitivity encoding. In addition, we compared CNR between optimized PSIR sequence ande-Thrive. We recognized a successful CNR of the 3D PSIR parameter was TFE inversion delay times, 335 ms; FA, 25 degrees; TFE factor, 20; and SI, 500 ms. In each gadolinium-DTPA diluted phantom, the average CNR of the optimized PSIR sequence was approximately 1.7 times (maximum: 3 times) higher than e-Thrive. Optimizing sequence parameter of PSIR is applicable in gadolinium dynamic study of uterine corpus.
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PMID:[An Examination for Uterine Dynamic Study with Phase-sensitive Inversion-recovery]. 2679 31