Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is believed that ovarian endometriosis may be generated by a celomic metaplastic process from existing epithelium in the ovary. However, no morphologic evidence of metaplastic process has been described. In this study, we intended to identify the earliest morphologic changes of endometriosis within the ovary to examine if evidence of metaplasia exists. Included in this study were 110 ovarian endometriosis cases and 30 benign ovaries without endometriosis but with ovarian epithelial inclusions (OEIs). Among the 110 well-established ovarian endometriosis cases, 34 cases showed areas of initial endometriosis (IE), which is defined as lesions showing direct transitions from normal-looking ovarian tissue to areas of minimal formation of endometriosis and/or to areas of full-blown endometriosis. We further divided IE into two types: type I IE was present on the ovarian surface, which was associated with ovarian surface epithelia; type II was located within the ovarian cortex, which was associated with OEIs. Sections containing IE, OEIs, and well-formed endometriosis were subject to CD10 and aromatase immunostaining. In IE lesions, the number of CD10-positive cells were significantly higher than the number of that in OEIs, but lower than that of well-formed endometriosis areas (p < 0.05). Aromatase expression was detected in both epithelial and stromal components of the IE lesions, indicating that estrogen local production may be involved in this initial process of endometriosis. Microvessel density was higher in IE lesions than in areas of OEI (p < 0.05). Based on the morphologic characteristics of IE, we believe that IE represent a spectrum of the earliest morphologic changes of endometriosis identifiable by routine microscopy. The morphologic transitions from ovarian surface epithelium or OEI to IE lesions provide direct metaplastic evidence for the pathogenesis of ovarian endometriosis. This metaplastic process may not only involve the ovarian epithelial cells, but also stromal components. Local production of estrogen, probably in high-levels, may be related to the initial process of endometriosis, although detailed mechanisms remain to be clarified.
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PMID:Initial endometriosis showing direct morphologic evidence of metaplasia in the pathogenesis of ovarian endometriosis. 1578 73

Endometriosis is an estrogen-dependent gynaecological disease associated with pain and infertility, which occurs in humans and menstruating primates. In this study, the marmoset monkey (Callithrix jacchus), which is a non-menstruating primate with high circulating estrogen levels, was used to test firstly the hypothesis that endometriosis is based on uterine shedding into the peritoneal cavity, secondly to study the pathogenesis of endometriosis due to its estrogenic situation. Female marmoset monkeys (n = 29) were exposed to two different experimental procedures (non-invasive versus invasive) for intrapelvic placement of endometrial cells by uterine flushing over an experimental period of 2-3 years. First endometriotic foci were detected by colour Doppler ultrasound at the bladder, the uterus and the ovaries at the earliest after 4 months of either treatments. However, invasive induction was more effective in terms of the time-course of induction and the number of resulting endometriotic foci. The analysis of the endometriotic foci by histology, immunohistochemistry and molecular techniques allowed a division into two distinct groups: an initial developing stage occurred, which under further treatment led to the second stage of established endometriosis. Both procedures showed a treatment-dependent increase of vascular supply to the endometriotic foci over the experimental period. The invasive method induced the final established stage of endometriosis more rapidly, with the expression of steroid receptors, aromatase, 17betaHSD1 and CD10. Altogether, 72% of the treated marmoset monkeys developed endometriosis under our endometrial reflux protocols. Our data support the theory that endometriosis can be induced artificially in a non-menstruating primate (C. jacchus) by endometrial shedding into the peritoneal cavity. Because the marmoset is a primate with very high peripheral estrogen levels, this offers an interesting model for studying the pathogenesis of this estrogen-dependent disease, as well as for therapeutic impacts on enzymes involved in steroid metabolism.
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PMID:Induction of endometriosis in the marmoset monkey (Callithrix jacchus). 1660 6

As brain testosterone plays both androgenic and estrogenic actions due to its conversion into estrogen via aromatase naturally, it is unclear that the age-related reduction of testosterone increased risk of Alzheimer's disease (AD) in men is mediated through androgen alone or both androgen and estrogen mechanisms. Our previous studies using a gene-based approach in mouse model to block the conversion of testosterone into estrogen (aromatase gene knock-out, ArKO), found a depletion of estrogen and increase in testosterone endogenously in males. Here, we use crossing the ArKO mice with APP23 transgenic mice, a mouse model of AD, to produce APP23/Ar(+/-) mice to study the estrogen-independent effect of testosterone on AD. We found a significant reduction in brain plaque formation, improved cognitive function and increase NEP activity in male APP23/Ar(+/-) mice compared with age-matched male APP23 controls. In addition, we found, for the first time, a reduction of beta-secretase (BACE1) enzyme activity, mRNA level and protein expression in the male APP23/Ar(+/-) mice, suggesting that endogenous testosterone, independent from estrogen, may protect against AD in males via two major mechanisms, downregulation of BACE1 activities at transcriptional level to reduce beta amyloid production and upregulation of NEP activities to enhance bate amyloid degradation.
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PMID:Genetic targeting aromatase in male amyloid precursor protein transgenic mice down-regulates beta-secretase (BACE1) and prevents Alzheimer-like pathology and cognitive impairment. 2050 99

Endometrial stromal sarcoma is known to be a hormone-dependent tumor. Efficacy of hormonal therapy including high-dose progestins, aromatase inhibitors or gonadotropin-releasing hormone analogs has been reported. We report a case of recurrent endometrial stromal sarcoma, the tumor cells of which were strongly positive for CD10, estrogen and progesterone receptors. Although almost all of the pelvic tumors infiltrating the rectum or pelvic side wall remained, the patient is alive with slight disease 9 years and 6 months after the initial failure. During the treatment period of 4 years and 3 months, the patient was treated exclusively with dydrogesterone at a daily dose of 10 mg and the tumor clinically disappeared. Dydrogesterone at a daily dose of 10 mg may be effective in treating low-grade endometrial stromal sarcoma.
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PMID:Successful use of dydrogesterone as maintenance therapy in recurrent endometrial stromal sarcoma: a case report. 2405