Salvage Radiotherapy for Recurrent Prostate Cancer

Anscher, Mitchell S.

doi:10.1001/jama.291.11.1380

Cited by 25 publications

(22 citation statements)

References 48 publications

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“…Frequently, the PSA begins to increase long before recurrent disease can be localized clinically or by imaging (8). There is, therefore, continuing controversy regarding when treatment should be initiated and which treatment modality is most appropriate (21). Attempts have been made to predict the probability for PSA relapse, to determine the likelihood for local recurrence versus systemic relapse (e.g., in lymph nodes or bones; refs.…”

Section: Discussionmentioning

confidence: 99%

2-[18F]Fluoro-2-Deoxyglucose Positron Emission Tomography for the Detection of Disease in Patients with Prostate-Specific Antigen Relapse after Radical Prostatectomy

Schöder¹,

Herrmann²,

Gönen³

et al. 2005

Clinical Cancer Research

190

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Experimental Design: Retrospective cohort study in 91patients with prostate-specific antigen (PSA) relapse following prostatectomy, imaged with 2-[18 F]fluoro-2-deoxyglucose positron emission tomography (FDG-PET) in a tertiary care cancer center between February 1997 and March 2003. Comparison was made with magnetic resonance imaging (n = 64), bone scan (n = 56), and computed tomography (n = 37). The standard of reference included biopsy or clinical and imaging follow-up. We calculated sensitivity and specificity of PET and correlated PET findings with PSA values, other clinical parameters, and conventional imaging, when available. Results: PET was true positive in 28 of 91 (31%) patients, showing isolated disease in the prostate bed (n = 3) or metastatic disease with (n = 2) or without (n = 23) simultaneous disease in the prostate bed. In detail, PET identified lesions in the prostate bed (n = 5, all true positives), bones (n = 22; 20 true positives, 2 false positives), lymph nodes (n = 7; 6 true positives, 1likely false positive), and one liver metastasis. Mean PSA was higher in PET-positive than in PETnegative patients (9.5 F 2.2 versus 2.1 F 3.3 ng/mL). PSA of 2.4 ng/mL and PSA velocity of 1.3 ng/mL/y provided the best tradeoff between sensitivity (80%; 71%) and specificity (73%; 77%) of PET in a receiver operating curve analysis. Combination with other clinical parameters in a multivariate analysis did not improve disease prediction. There were only two patients in whom other imaging studies showed isolated local recurrence or metastatic disease. Conclusions: FDG-PETdetected local or systemic disease in 31% of patients with PSA relapse referred for this test. There is a link to tumor burden and tumor biology in that the probability for disease detection increased with PSA levels.

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Section: Discussionmentioning

confidence: 99%

2-[18F]Fluoro-2-Deoxyglucose Positron Emission Tomography for the Detection of Disease in Patients with Prostate-Specific Antigen Relapse after Radical Prostatectomy

Schöder¹,

Herrmann²,

Gönen³

et al. 2005

Clinical Cancer Research

190

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“…When a biochemical recurrence occurred, further investigations are needed to distinguish local recurrence in the prostatic bed from distant metastases [3]. In patients who did not receive adjuvant radiation therapy, salvage radiotherapy to the prostatic bed is often prescribed with good results [4].…”

Section: Introductionmentioning

confidence: 99%

CyberKnife stereotactic radiotherapy for isolated recurrence in the prostatic bed

et al. 2015

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“…Prostate cancer, the most common noncutaneous malignant transformation in American men (1), starts as an androgen-dependent lesion in the prostate gland that can be successfully treated with surgical removal of the tumor or local radiation (2). Locally advanced and metastatic diseases are treated with endocrine therapies aimed to (i) decrease circulating androgen levels via chemical or physical castration, (ii) block androgen receptor (AR) 1 activation with anti-androgens, or (iii) achieve both (3).…”

mentioning

confidence: 99%

“…Human prostate cancer biopsies show elevated expression of the GPCRs for endothelin (13), bradykinin (14), and lysophosphatidic acid, 2 compared with benign specimens. The cancerous prostate also expresses elevated levels of GPCR ligands, including endothelin-1, follicle-stimulating hormone, and several neuropeptides (11,13,15).…”

mentioning

confidence: 99%

Androgen Receptor Activation by Gs Signaling in Prostate Cancer Cells

Kasbohm

Guo

Yowell

et al. 2005

Journal of Biological Chemistry

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The androgen receptor (AR) is activated in prostate cancer patients undergoing androgen ablative therapy and mediates growth of androgen-insensitive prostate cancer cells, suggesting it is activated by nonandrogenic factors. We demonstrate that activated ␣ subunit of heterotrimeric guanine nucleotide-binding G s protein activates the AR in prostate cancer cells and also synergizes with low concentration of androgen to more fully activate the AR. The G␣ s activates protein kinase A, which is required for the nuclear partition and activation of AR. These data suggest a role for G␣ s and PKA in the transactivation of AR in prostate cancer cells under the environment of reduced androgen levels.Prostate cancer, the most common noncutaneous malignant transformation in American men (1), starts as an androgen-dependent lesion in the prostate gland that can be successfully treated with surgical removal of the tumor or local radiation (2). Locally advanced and metastatic diseases are treated with endocrine therapies aimed to (i) decrease circulating androgen levels via chemical or physical castration, (ii) block androgen receptor (AR) 1 activation with anti-androgens, or (iii) achieve both (3). The hormonal therapies cause only a temporary shrinkage in tumor mass, and the cancer invariably reappears in the form of androgen-insensitive (AI) disease. Despite decades of intense basic and clinical research, to date there is no cure for AI prostate cancer.Accumulating evidence suggests that the AR itself is involved in the transition of prostate cancer from androgen-dependent to AI (4). AI prostate tumors express AR-regulated genes, including human kallikrein 2 and 3 (5), also known as prostate-specific antigen (PSA), suggesting that the AR is activated in these tumors despite the continued presence of the hormonal therapies. In vitro, the AR can be activated by factors other than androgens (6, 7), and in animal models increased AR expression was reported to be the only change associated with progression to hormone refractory disease (8). In humans, the AR is overexpressed in up to one-third of AI prostate carcinomas, suggesting that it could respond to low serum levels of androgens (9). Also, AI lesions exhibit frequent mutations in the AR that may allow it to be activated by other androgens or even anti-androgens (10). Hence, AR is a focal point in progression of the prostate cancer to advanced stage. However, the mechanisms regulating AR activation in the presence of low androgen concentrations and their significance to the progression to AI disease remain unclear.Transition of the prostate cancer to the AI stage is associated with increased expression of plasma membrane-localized G protein-coupled receptors (GPCRs) (11), which mediate cellular responses to a diverse array of extracellular molecules, including lipid and peptide growth factors (12). Human prostate cancer biopsies show elevated expression of the GPCRs for endothelin (13), bradykinin (14), and lysophosphatidic acid, 2 compared with benign specimens. The cancer...

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Salvage Radiotherapy for Recurrent Prostate Cancer

Cited by 25 publications

References 48 publications

2-[18F]Fluoro-2-Deoxyglucose Positron Emission Tomography for the Detection of Disease in Patients with Prostate-Specific Antigen Relapse after Radical Prostatectomy

2-[18F]Fluoro-2-Deoxyglucose Positron Emission Tomography for the Detection of Disease in Patients with Prostate-Specific Antigen Relapse after Radical Prostatectomy

CyberKnife stereotactic radiotherapy for isolated recurrence in the prostatic bed

Androgen Receptor Activation by Gs Signaling in Prostate Cancer Cells

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