Surgical Stress Delays Prostate Involution in Mice

Hassan, Sazzad; Karpova, Yelena; Flores, Anabel; D’Agostino, Ralph B.; Kulik, George

doi:10.1371/journal.pone.0078175

Cited by 12 publications

(11 citation statements)

References 17 publications

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“…In normal prostate physiology, the sympathetic nervous system regulates prostate differentiation and secretory activity of luminal cells, predominantly through ADRB2 ( 34 , 35 , 40 , 41 ). We know from in vitro and in vivo prostate cancer models that chronic elevation of ADRB activity by exposing mice to repeated stress or by adding ADRB agonists promotes neuroendocrine differentiation ( 70 , 84 – 86 ), metastasis ( 58 , 103 ), angiogenesis ( 78 , 81 , 112 , 115 ), and apoptosis-resistance ( 116 , 120 ); together indicating that adrenergic signaling promotes prostate cancer progression (Figure 2 ).…”

Section: Controversies Clinical Implications and Conclusionmentioning

confidence: 99%

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Î²-Adrenergic Receptor Signaling in Prostate Cancer

et al. 2015

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Enhanced sympathetic signaling, often associated with obesity and chronic stress, is increasingly acknowledged as a contributor to cancer aggressiveness. In prostate cancer, intact sympathetic nerves are critical for tumor formation, and sympathectomy induces apoptosis and blocks tumor growth. Perineural invasion, involving enrichment of intra-prostatic nerves, is frequently observed in prostate cancer and is associated with poor prognosis. β2-adrenergic receptor (ADRB2), the most abundant receptor for sympathetic signals in prostate luminal cells, has been shown to regulate trans-differentiation of cancer cells to neuroendocrine-like cells and to affect apoptosis, angiogenesis, epithelial–mesenchymal transition, migration, and metastasis. Epidemiologic studies have shown that use of β-blockers, inhibiting β-adrenergic receptor activity, is associated with reduced prostate cancer-specific mortality. In this review, we aim to present an overview on how β-adrenergic receptor and its downstream signaling cascade influence the development of aggressive prostate cancer, primarily through regulating neuroendocrine differentiation.

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Section: Controversies Clinical Implications and Conclusionmentioning

confidence: 99%

“…Stress has been reported to reduce apoptotic activity ( 116 , 120 ), whereas sympathectomy increases apoptosis in mouse prostate cancer models ( 42 ). Thus, prolonged elevation of catecholamines may promote prostate cancer progression by inducing resistance to apoptosis.…”

Section: Adrenergic Regulation Of Apoptosismentioning

confidence: 99%

Î²-Adrenergic Receptor Signaling in Prostate Cancer

et al. 2015

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“…According to the study of Hassan et al (19), surgical stress prevented prostatic apoptosis and delayed prostatic involution in rats administered with androgen ablation. One of the important points is the effect of testosterone replacement treatment (TRT) on PSA levels.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Surgical Stress on Serum Prostate Specific Antigen Level

Karabakan¹,

Aktaş²,

Bulut³

et al. 2015

JAREM

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Objective: Invasive surgical interventions creating acute stress may give rise to immunological and hormonal disturbances in patients undergoing surgery. Previous studies reported elevations in serum prostate-specific antigen (PSA) level following coronary bypass and myocardial infarction. The current study aims to investigate the effect of surgical stress on serum PSA level.Methods: Thirty-three patients who underwent open renal stone surgery, without any known infectious prostatic disorder or prostate cancer that may elevate serum PSA level, were included in the study. In all patients, serum levels of total and free PSA (tPSA and fPSA), follicle-stimulating hormone (FSH), luteinizing hormone (LH), total and free testosterone, C-reactive protein (CRP), fibrinogen, albumin, and ferritin and erythrocyte sedimentation rate (ESR) were measured both at baseline and post-operative day 3. Wilcoxon signed-rank test was used for the statistical analysis.Results: The mean age of patients was 53.9±8 (40-66). The mean baseline and post-operative levels of the measured serum parameters are given in Table 1. All of them differed significantly between baseline and post-operative day 3, except for LH, tPSA, and fPSA. CRP, fibrinogen, ferritin, and ESR are known as acute phase reactants of the post-operative endocrine response. However, serum total and free testosterone levels, albumin, and FSH decreased on the contrary acute phase reactants in the present study.Conclusion: According to our results, serum PSA level was not affected by acute surgical stress. (JAREM 2015; 5: 22-4)

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“…Western blot analyses were determined as described by us previously [32] , [33] . OE 19 xenograft tissue samples were homogenized in a cold lysis buffer (20 mM HEPES, 150 mM NaCl, 1 mM EDTA, 0.5% Na+deoxycholate, 1% Nonidet P-40,and 1 mM DTT, pH 7.4) containing protease and phosphatase inhibitor cocktails (both from Sigma-Aldrich, St. Louis, MO) using a glass dounce tissue homogenizer.…”

Section: Methodsmentioning

confidence: 99%

Superior Therapeutic Efficacy of Nanoparticle Albumin Bound Paclitaxel Over Cremophor-Bound Paclitaxel in Experimental Esophageal Adenocarcinoma

Hassan

Awasthi

et al. 2018

Translational Oncology

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Esophageal adenocarcinoma (EAC) is the fastest growing cancer in the western world and the overall 5 year survival rate of EAC is below 20%. Most patients with EAC present with locally advanced or widespread metastatic disease, where current treatment is largely ineffective. Therefore, new therapeutic approaches are urgently needed. Nanoparticle albumin-bound paclitaxel (nab-paclitaxel) is a novel albumin-stabilized, cremophor-free and water soluble nanoparticle formulation of paclitaxel, and the potential role of nab-paclitaxel has not been tested yet in experimental EAC. Here we tested the antiproliferative and antitumor efficacy with survival advantage of nab-paclitaxel as monotherapy and in combinations in in-vitro, and in murine subcutaneous xenograft and peritoneal metastatic survival models of human EAC. Nab-paclitaxel significantly inhibited in-vitro cell proliferation with higher in-vivo antitumour efficacy and survival benefit compared to paclitaxel or carboplatin treatments both in mono- and combination therapies. Nab-paclitaxel treatment increased expression of mitotic-spindle associated phospho-stathmin, decreased expression of proliferative markers and enhanced apoptosis. This study demonstrates that nab-paclitaxel had stronger antiproliferative and antitumor activity in experimental EAC than the current standard chemotherapeutic agents which supports the rationale for its clinical use in EAC.

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Surgical Stress Delays Prostate Involution in Mice

Cited by 12 publications

References 17 publications

Î²-Adrenergic Receptor Signaling in Prostate Cancer

Î²-Adrenergic Receptor Signaling in Prostate Cancer

The Effect of Surgical Stress on Serum Prostate Specific Antigen Level

Superior Therapeutic Efficacy of Nanoparticle Albumin Bound Paclitaxel Over Cremophor-Bound Paclitaxel in Experimental Esophageal Adenocarcinoma

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