antiandrogens/hypoxia

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The impact of antiandrogen flutamide on the hypoxia inducible factor 1α and vascular endothelial growth factor A gene and protein expression in the pig placenta during late pregnancy.

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BACKGROUND In contrast to estradiol action, little is known about androgen signaling in placental development. The purpose of this study was to evaluate the impact of diminished androgen action on hypoxia inducible factor 1a (HIF-1a) and vascular endothelial growth factor A (VEGFA) protein

Effect of hypoxia on the uptake of [methyl-3H]choline, [1-14C] acetate and [18F]FDG in cultured prostate cancer cells.

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BACKGROUND Choline, acetate and glucose ([2-(18)F]fluoro-2-deoxyglucose, [(18)F]FDG) analogs are under investigation as positron emission tomography (PET) tracers for the imaging of prostate cancer; however, their response to tumor hypoxia has not been clarified. METHODS The uptake of

Androgen deprivation results in time-dependent hypoxia in LNCaP prostate tumours: informed scheduling of the bioreductive drug AQ4N improves treatment response.

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Androgen withdrawal induces hypoxia in androgen-sensitive tissue; this is important as in the tumour microenvironment, hypoxia is known to drive malignant progression. Our study examined the time-dependent effect of androgen deprivation therapy (ADT) on tumour oxygenation and investigated the role

Comparison of the effect of the antiandrogen apalutamide (ARN-509) versus bicalutamide on the androgen receptor pathway in prostate cancer cell lines.

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Apalutamide (ARN-509) is an antiandrogen that binds selectively to androgen receptors (AR) and does not show antagonist-to-agonist switch like bicalutamide. We compared the activity of ARN versus bicalutamide on prostate cancer cell lines. The 22Rv1, PC3, and DU145 cell lines were used to study the

Hypoxia modifies the response to flutamide and linuron in male three-spined stickleback (Gasterosteus aculeatus).

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Hypoxia is a major stressor in aquatic environments and it is frequently linked with excess nutrients resulting from sewage effluent discharges and agricultural runoff, which often also contain complex mixtures of chemicals. Despite this, interactions between hypoxia and chemical toxicity are poorly

Androgen withdrawal in patients reduces prostate cancer hypoxia: implications for disease progression and radiation response.

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Hypoxia is a feature of many human malignancies, and leads to aggressive clinical behavior and recurrence after treatment. Here, we show for the first time that androgen withdrawal reduces prostate cancer hypoxia in patients. Oxygen measurements were done in 248 patients with clinically localized

Androgens stimulate hypoxia-inducible factor 1 activation via autocrine loop of tyrosine kinase receptor/phosphatidylinositol 3'-kinase/protein kinase B in prostate cancer cells.

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OBJECTIVE Androgen deprivation is implicated in reducing neoangiogenesis in prostate cancer (PCA). Androgens regulate the expression of the vascular endothelial growth factor (VEGF); hypoxia stimulates VEGF expression through the activation of the transcriptional factor, hypoxia-inducible factor 1

Mitochondrial respiratory function induces endogenous hypoxia.

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Hypoxia influences many key biological functions. In cancer, it is generally believed that hypoxic condition is generated deep inside the tumor because of the lack of oxygen supply. However, consumption of oxygen by cancer should be one of the key means of regulating oxygen concentration to induce

Androgen blockade does not affect sleep-disordered breathing or chemosensitivity in men with obstructive sleep apnea.

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As sleep apnea is more prevalent in men and testosterone has known effects on sleep apnea and chemosensitivity, reduction of androgen activity may influence sleep-disordered breathing and respiratory control. We studied the effect of 1 wk of treatment with flutamide, a nonsteroidal antiandrogen, on

Vascular endothelial growth factors are differentially regulated by steroid hormones and antiestrogens in breast cancer cells.

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Vascular endothelial growth factor (VEGF) is a major inducer of tumor angiogenesis and an important prognostic factor in breast cancer. Hypoxia is an important inducer of VEGF expression but less is known of the role of hormones in VEGF regulation. We have studied the regulation of VEGF, VEGF-B,

Changes of protein expression in prostate cancer having lost its androgen sensitivity.

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OBJECTIVE The majority of prostate cancers require androgen hormones for growth, and androgen ablation is an important part of the systemic treatment of advanced prostate cancer. Nevertheless, most of these cancers eventually relapse as they become less sensitive to androgen ablation and

Nilutamide pneumonitis: a report on eight patients.

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BACKGROUND Nilutamide is a new, specific synthetic antiandrogen, released in several countries for the treatment of metastatic carcinoma of the prostate. Eight patients at the University Medical Centre at Dijon and affiliated referring hospitals developed reversible pulmonary opacities and

New players for advanced prostate cancer and the rationalisation of insulin-sensitising medication.

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Obesity and type 2 diabetes are recognised risk factors for the development of some cancers and, increasingly, predict more aggressive disease, treatment failure, and cancer-specific mortality. Many factors may contribute to this clinical observation. Hyperinsulinaemia, dyslipidaemia, hypoxia, ER

The MAO inhibitors phenelzine and clorgyline revert enzalutamide resistance in castration resistant prostate cancer

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The antiandrogen enzalutamide (Enz) has improved survival in castration resistant prostate cancer (CRPC) patients. However, most patients eventually develop Enz resistance that may involve inducing the androgen receptor (AR) splicing variant 7 (ARv7). Here we report that high expression of monoamine

A phase II trial of gallium nitrate in patients with androgen-metastatic prostate cancer.

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BACKGROUND Due to in vitro data suggesting antitumor activity with gallium nitrate, we sought to evaluate the safety and activity in patients with androgen-independent prostate cancer. METHODS Patients were eligible for this study if they had an ECOG performance status of < or = 2, stage D2

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