endometrial hyperplasia/tyrosine

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Activation of the receptor protein tyrosine kinase EphB4 in endometrial hyperplasia and endometrial carcinoma.

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BACKGROUND Members of the Eph family of tyrosine kinases have been implicated in embryonic pattern formation and vascular development; however, little is known about their role in the adult organism. We have observed estrogen-dependent EphB4 expression in the normal breast suggesting its implication

Molecular basis of endometrial cancer.

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BACKGROUND Most human cancers are thought to arise from alterations in oncogenes and tumor suppressor genes. METHODS Molecular techniques have been used to identify specific genetic alterations in endometrial cancers. RESULTS Overexpression of the HER-2/neu oncogene occurs in 10% of endometrial

Relationships between C-kit expression and mean platelet volume in benign, preneoplastic and neoplastic endometrium.

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BACKGROUND c-Kit is a proto-oncogene that encodes a tyrosine kinase receptor (CD117). Mean platelet volume (MPV) is a useful marker for demonstrating thrombocyte function. We aimed to investigate whether c-kit is expressed in benign, preneoplastic and neoplastic endometrial tissues and whether MPV

GPER and ERα expression in abnormal endometrial proliferations.

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G-protein coupled estrogen receptor 1 (GPER), a particular extranuclear estrogen receptor (ER), seems not to be significantly involved in normal female phenotype development but especially associated with severe genital malignancies. This study investigated the GPER expression in different types of

Focal adhesion kinase overexpression in endometrial neoplasia.

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Focal adhesion kinase (FAK) is a protein tyrosine kinase that is a critical mediator of signaling events between cells and their extracellular matrix. Elevations in FAK mRNA and protein overexpression have been linked to tumor cell capacity for invasion and metastasis. FAK expression has been shown

Endometrial Cancer-Associated FGF18 Expression Is Reduced by Bazedoxifene in Human Endometrial Stromal Cells In Vitro and in Murine Endometrium.

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Endometrial cancer develops during exposure to estrogen unopposed by progesterone. Traditional formulations for menopausal hormone therapy include a progestin in women with a uterus. However, progestin exposure increases breast cancer risk in postmenopausal women. Alternatives to progestin include

Autophagy in the physiological endometrium and cancer.

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Autophagy is a highly conserved catabolic process and a major cellular pathway for the degradation of long-lived proteins and cytoplasmic organelles. An increasing body of evidence has unveiled autophagy as an indispensable biological function that helps to maintain normal tissue

Overexpression of the insulin-like growth factor I receptor and activation of the AKT pathway in hyperplastic endometrium.

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OBJECTIVE Although there is considerable information on the molecular aberrations associated with endometrial cancer, very little is known of the changes in gene expression associated with endometrial hyperplasia. METHODS To address this, we have compared the level of expression of

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