alpha prostaglandin f 2/breast neoplasms

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A prostaglandin E (PGE) receptor EP4 antagonist protects natural killer cells from PGE2-mediated immunosuppression and inhibits breast cancer metastasis.

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Cyclooxygenase-2 is frequently upregulated in epithelial tumors and contributes to poor outcomes in multiple malignancies. The COX-2 product prostaglandin E2 (PGE2) promotes tumor growth and metastasis by acting on a family of four G protein-coupled receptors (EP1-4). Using a novel small molecule

Relationship of the suppression of macrophage mediated tumor cytotoxicity in conjunction with secretion of prostaglandin from the macrophages of breast cancer patients.

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Peripheral blood monocyte derived macrophages obtained from breast cancer patients are non-cytotoxic towards human tumor cells. However, when indomethacin, a prostaglandin synthetase inhibitor, was added to the macrophage tumor cell incubation mixture, the breast cancer patient's macrophages became

Can cyclo-oxygenase-2 be a useful prognostic and risk stratification marker in breast cancer?

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Cyclo-oxygenase-2 (COX-2) is a prostaglandin synthease that catalyses the synthesis of prostaglandin G2 (PGG2) and PGH2 from arachidonic acid. COX-2 plays an important role in tumourigenesis of different carcinoma types and it is thought to take part in breast carcinoma. In this study, the aim was

The role of cytokines in regulating estrogen synthesis: implications for the etiology of breast cancer.

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Cytokines, such as IL-6 and tumor necrosis factor (TNF)-alpha, have an important role in regulating estrogen synthesis in peripheral tissues, including normal and malignant breast tissues. The activities of the aromatase, estradiol 17beta-hydroxysteroid dehydrogenase and estrone sulfatase are all

Dormancy and growth of metastatic breast cancer cells in a bone-like microenvironment.

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Breast cancer can reoccur, often as bone metastasis, many years if not decades after the primary tumor has been treated. The factors that stimulate dormant metastases to grow are not known, but bone metastases are often associated with skeletal trauma. We used a dormancy model of MDA-MB-231BRMS1, a

Type 5 17beta-hydroxysteroid dehydrogenase/prostaglandin F synthase (AKR1C3): role in breast cancer and inhibition by non-steroidal anti-inflammatory drug analogs.

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Aldo-keto reductase (AKR) 1C3 catalyzes the NADPH-dependent reduction of Delta(4)-androstene-3,17-dione to yield testosterone, reduction of estrone to yield 17beta-estradiol and reduction of progesterone to yield 20alpha-hydroxyprogesterone. In addition, it functions as a prostaglandin (PG) F

MPGES-1-derived PGE2 suppresses CD80 expression on tumor-associated phagocytes to inhibit anti-tumor immune responses in breast cancer.

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Prostaglandin E2 (PGE2) favors multiple aspects of tumor development and immune evasion. Therefore, microsomal prostaglandin E synthase (mPGES-1/-2), is a potential target for cancer therapy. We explored whether inhibiting mPGES-1 in human and mouse models of breast cancer affects tumor-associated

COX2 regulation of breast cancer bone metastasis.

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High expression levels of cyclooxygenase 2 expression and infiltration by regulatory T cells (Tregs) are often associated with tumor progression. We have recently reported a prostaglandin E2 (PGE2)-dependent recruitment of Tregs to the tumor, suggesting that targeting specific PGE2 receptors may

Functional heterogeneity of breast fibroblasts is defined by a prostaglandin secretory phenotype that promotes expansion of cancer-stem like cells.

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Fibroblasts are important in orchestrating various functions necessary for maintaining normal tissue homeostasis as well as promoting malignant tumor growth. Significant evidence indicates that fibroblasts are functionally heterogeneous with respect to their ability to promote tumor growth, but

Sphingosine-1-phosphate regulates the expression of the liver receptor homologue-1.

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In this study, we examined the role of sphingosine-1-phosphate (S1P) in regulating the transcription of the liver receptor homologue-1 (LRH-1) in breast cancer cells. We show that S1P induces LRH-1 mRNA expression in MCF-7 cells in a prostaglandin E2 (PGE2)-dependent manner. Both S1P and PGE2

[Mifepristone (RU 486): present status, prospectives].

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Mifepristone (RU 486) has many therapeutic possibilities, which largely exceed simple interruption of pregnancy. They are due to its unique properties of progesterone--and glucocorticosteroid--receptor blockage. In early interruption of pregnancy, the association with a prostaglandin analogue

Mifepristone. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential.

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Mifepristone is a potent oral antiprogestogen which acts at the level of the receptor, having a high affinity for the progesterone receptor. Most of the clinical trials have studied its efficacy in the termination of early pregnancy when used in conjunction with a low dosage of a prostaglandin

Steroid hormone transforming aldo-keto reductases and cancer.

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Prostate and breast cancer are hormone-dependent malignancies of the aging male and female and require the local production of androgens and estrogens to stimulate cell proliferation. Aldo-keto reductases (AKR) play key roles in this process. In the prostate, AKR1C3 (type 5 17beta-HSD) reduces

Characterization of a 15-lipoxygenase in human breast carcinoma BT-20 cells: stimulation of 13-HODE formation by TGF alpha/EGF.

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Epidemiological and experimental data suggest a role for polyunsaturated fatty acids in the etiology of breast cancer. In this report we have studied arachidonic acid and linoleic acid metabolism in the human breast carcinoma cell line BT-20 which overexpresses both EGF receptor and the homologous

Aldo-Keto Reductase (AKR) 1C3 inhibitors: a patent review.

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BACKGROUND AKR1C3 is a drug target in hormonal and hormonal independent malignancies and acts as a major peripheral 17β-hydroxysteroid dehydrogenase to yield the potent androgens testosterone and dihydrotestosterone, and as a prostaglandin (PG) F synthase to produce proliferative ligands for the PG

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