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endometrial hyperplasia/phosphatase
Линкът е запазен в клипборда
Страница 1 от 36 резултата
Loss of phosphatase and tensin homologue deleted on chromosome 10 and phosphorylation of mammalian target of rapamycin are associated with progesterone refractory endometrial hyperplasia.
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The objective of our study was to evaluate the phosphatase and tensin homologue deleted on chromosome 10 (PTEN), p27, and mammalian target of rapamycin (mTOR) expressions in women with progesterone-responsive and refractory endometrial hyperplasia (EH) samples and to determine if these markers could
Dual-specificity phosphatase 6 predicts the sensitivity of progestin therapy for atypical endometrial hyperplasia.
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OBJECTIVE
We previously found that Dual-specificity phosphatase 6 (Dusp6) over-expression enhanced the growth-promoting effect of estrogen in endometrial adenocarcinoma cells. The aim of this study was to explore the correlation of Dusp6 expression with progestin sensitivity in atypical endometrial
Study of the Association of Phosphatase and Tensin Homolog and p27 Expressions in Endometrial Hyperplasia and Carcinoma.
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Measurement of C-reactive protein and prostaglandin F2α metabolite concentrations in differentiation of canine pyometra and cystic endometrial hyperplasia/mucometra.
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Canine pyometra is a dioestrus period disease in which systemic inflammatory response syndrome (SIRS) is a common outcome due to the response of the body to the bacterial infection. The purpose of this study was i) to differentiate canine pyometra and cystic endometrial hyperplasia (CEH)/mucometra
An estrogen-induced endometrial hyperplasia mouse model recapitulating human disease progression and genetic aberrations.
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Endometrial hyperplasia (EH) is a condition originating from uterine endometrial glands undergoing disordered proliferation including the risk to progress to endometrial adenocarcinoma. In recent years, a steady increase in EH cases among younger women of reproductive age accentuates the demand of
Immunohistochemical reaction of the glandular epithelium in endometrial hyperplasia compared to endometrial carcinoma.
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The histopathological and immunohistochemical diagnosis of endometrial biopsies is used for estimating the risk of progression in endometrial hyperplastic lesions in carcinoma and for guiding the clinical management. The objective of this study was to evaluate the immunohistochemical expression of
PTEN immunohistochemistry in endometrial hyperplasia: which are the optimal criteria for the diagnosis of precancer?
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Guidelines recommend protein phosphatase and tensin homolog (PTEN) immunohistochemistry for differentiating between benign endometrial hyperplasia (BEH) and atypical endometrial hyperplasia/endometrioid intraepithelial neoplasia (AEH/EIN). However, it is unclear when PTEN expression should be
PTEN sequence analysis in endometrial hyperplasia and endometrial carcinoma in Slovak women.
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Phosphatase and tensin homolog (PTEN) is a protein that acts as a tumor suppressor by dephosphorylating the lipid second messenger phosphatidylinositol 3,4,5-trisphosphate. Loss of PTEN function has been implicated in the pathogenesis of a number of different tumors, particularly endometrial
Prediction of Relapse After Therapy Withdrawal in Women with Endometrial Hyperplasia: A Long-term Follow-up Study.
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To investigate whether risk of relapse of endometrial hyperplasia persists many years after successful primary therapy and whether clinical or biological markers observed at primary diagnosis may predict relapse.
A series of 57 women with endometrial hyperplasia received levonorgestrel-impregnated
Malignant transformation of atypical endometrial hyperplasia after progesterone therapy showing germ-cell tumor-like differentiation.
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A 31-year-old woman was treated for atypical endometrial hyperplasia (AEH) with high-dose medroxyprogesterone acetate (MPA) therapy to preserve fertility. The AEH was found by repeated cytologic and histologic examinations to have completely disappeared with the therapy, but 3 years after her last
Detection of PTEN immunoreactivity in endometrial hyperplasia and adenocarcinoma.
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OBJECTIVE
To investigate PTEN (phosphatase and tensin homolog deleted on chromosome 10) expression in endometrial hyperplasia and adenocarcinoma as analyzed by immunohistochemistry.
METHODS
PTEN protein expression was evaluated by immunohistrochemical study of 70 paraffin-embedded curettage
Expression of PAX2 and PTEN Correlates to Therapy Response in Endometrial Hyperplasia.
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OBJECTIVE
To investigate if a levonorgestrel-impregnated intrauterine system (LNG-IUS) was more efficient compared to oral progestin in the clearance of the paired box 2 gene (PAX2) - and phosphatase and tensin homolog (PTEN)-null endometrial glands and assess the significance of PAX2- and PTEN-null
Immunohistochemical localization of placental proteins and tumor-associated antigens in endometrial cancer and endometrial hyperplasia.
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As to endometrial cancer and endometrial hyperplasia, this study represents the localizations of the placental proteins and the tumor-associated antigens by both immunohistochemical light microscopy (ILM) and immunoelectron microscopy (IEM). The reagents examined include human placental lactogen
Reduced progression of endometrial hyperplasia with oral mTOR inhibition in the Pten heterozygote murine model.
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OBJECTIVE
Phosphatase and tensin homolog (PTEN) mutations are associated with human endometrial cancers, and PTEN heterozygote(+/-) mice have a high rate of endometrial neoplasia. The objective of this study was to evaluate an oral mTOR inhibitor (mTOR-I) on the reduction of endometrial hyperplasia
Alkaline phosphatase activity in relation to LDH5 (L-lactate: NAD+ - oxidoreductase, E.C.1.1.1.27) in patients with precancerous conditions of the endometrium.
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We investigated the serum activity of the fifth fraction of L-lactate: NAD-oxidoreductase (E.C.1.1.1.27) and serum alkaline phosphatase activity prior to diagnostic curettage in patients with abnormal and atypical endomertial hyperplasia. We also determined them in 75 patients with carcinoma of the
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