scholarly journals High B7‐H3 expression is linked to increased risk of prostate cancer progression

2020 ◽  
Vol 70 (10) ◽  
pp. 733-742 ◽  
Author(s):  
Sarah Bonk ◽  
Pinar Tasdelen ◽  
Martina Kluth ◽  
Claudia Hube‐Magg ◽  
Georgia Makrypidi‐Fraune ◽  
...  
2015 ◽  
Vol 4 (4) ◽  
pp. R68-R80 ◽  
Author(s):  
Renea A Taylor ◽  
Jennifer Lo ◽  
Natasha Ascui ◽  
Matthew J Watt

The global epidemic of obesity is closely linked to the development of serious co-morbidities, including many forms of cancer. Epidemiological evidence consistently shows that obesity is associated with a similar or mildly increased incidence of prostate cancer but, more prominently, an increased risk for aggressive prostate cancer and prostate cancer-specific mortality. Studies in mice demonstrate that obesity induced by high-fat feeding increases prostate cancer progression; however, the mechanisms underpinning this relationship remain incompletely understood. Adipose tissue expansion in obesity leads to local tissue dysfunction and is associated with low-grade inflammation, alterations in endocrine function and changes in lipolysis that result in increased delivery of fatty acids to tissues of the body. The human prostate gland is covered anteriorly by the prominent peri-prostatic adipose tissue and laterally by smaller adipose tissue depots that lie directly adjacent to the prostatic surface. We discuss how the close association between dysfunctional adipose tissue and prostate epithelial cells might result in bi-directional communication to cause increased prostate cancer aggressiveness and progression. However, the literature indicates that several ‘mainstream’ hypotheses regarding obesity-related drivers of prostate cancer progression are not yet supported by a solid evidence base and, in particular, are not supported by experiments using human tissue. Understanding the links between obesity and prostate cancer will have major implications for the health policy for men with prostate cancer and the development of new therapeutic or preventative strategies.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
David P. Labbé ◽  
Giorgia Zadra ◽  
Meng Yang ◽  
Jaime M. Reyes ◽  
Charles Y. Lin ◽  
...  

Abstract Systemic metabolic alterations associated with increased consumption of saturated fat and obesity are linked with increased risk of prostate cancer progression and mortality, but the molecular underpinnings of this association are poorly understood. Here, we demonstrate in a murine prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through metabolic alterations that favour histone H4K20 hypomethylation at the promoter regions of MYC regulated genes, leading to increased cellular proliferation and tumour burden. Saturated fat intake (SFI) is also associated with an enhanced MYC transcriptional signature in prostate cancer patients. The SFI-induced MYC signature independently predicts prostate cancer progression and death. Finally, switching from a high-fat to a low-fat diet, attenuates the MYC transcriptional program in mice. Our findings suggest that in primary prostate cancer, dietary SFI contributes to tumour progression by mimicking MYC over expression, setting the stage for therapeutic approaches involving changes to the diet.


2009 ◽  
Vol 27 (19) ◽  
pp. 3161-3168 ◽  
Author(s):  
Lorenzo Richiardi ◽  
Valentina Fiano ◽  
Loredana Vizzini ◽  
Laura De Marco ◽  
Luisa Delsedime ◽  
...  

Purpose There is a need to better understand prostate cancer progression and identify new prognostic markers for this tumor. We investigated the association between promoter methylation in a priori selected genes and survival in two independent large series of prostate cancer patients. Methods We followed up with two cohorts of patients (216 patients diagnosed in 1982 to 1988 and 243 patients diagnosed in 1993 to 1996) diagnosed at one hospital pathology ward in Turin, Italy. DNA was obtained from paraffin-embedded tumor tissues and evaluated for promoter methylation status in glutathione S-transferase (GSTP1), adenomatous polyposis coli (APC), and runt-related transcription factor 3 (RUNX3). Results The two cohorts had different prevalences of methylation in APC (P = .047), GSTP1 (P = .002), and RUNX3 (P < .001). Methylation in APC was associated with an increased risk of prostate cancer–specific mortality (hazard ratio [HR] = 1.42; 95% CI, 0.98 to 2.07 in the 1980s cohort; HR = 1.57; 95% CI, 0.95 to 2.62 in the 1990s cohort; HR = 1.49; 95% CI, 1.11 to 2.00 in the two cohorts combined). In subgroup analyses, the HRs were higher among patients with a Gleason score less than 8 (HR = 1.52; 95% CI, 0.85 to 2.73 in the 1980s cohort; HR = 2.09; 95% CI, 1.02 to 4.28 in the 1990s cohort). Methylation in RUNX3 was associated with prostate cancer mortality only in the 1990s cohort, and methylation in GSTP1 did not predict mortality in either cohort. Conclusion The pattern of hypermethylation may have changed after the introduction of prostate-specific antigen testing in the beginning of the 1990s. Promoter methylation in APC was identified as a marker for prostate cancer progression.


Author(s):  
T.A. Kireeva ◽  
◽  
Yu.V. Gumenetskaya ◽  
V.A. Biryukov ◽  
A.A. Obukhov ◽  
...  

One way to enhance the effectiveness of treatment for high-risk prostate cancer is to use com-bined hormonal/radiation therapy. The effectiveness of this approach has already been demon-strated and confirmed. The study results show that application of the hormonal therapy potenti-ates the total radiation effect and makes 5-year local control is more effective compared with the control achieved after application of EBRT modality. At the same time, if high dose radiation ther-apy is applied or large volume to be exposed to radiation, in both cases there is increased risk of radiation-induced side effects development. The radiation-related complications affect patients’ quality of life significantly. A natural question arises in such a case, whether inclusion of lesion free pelvic lymph nodes (N0) in patients with high risk of prostate cancer progression in the area of radiation exposure is necessary, if no data on their lesion (N0) are available and thus to in-crease the irradiated volume significantly. The considered published studies devoted to the prob-lem were considered, the most part of the studies a retrospective, results of some studies contra-dicted conclusions. This does not allow us to find definitive answer to the “natural” question. Until now, it is also unknown what criteria are to be used for deciding whether radiotherapy to the area of regional metastasis zones is necessary. In this connection, it would be reasonable to conduct a prospective randomized study, its results will possibly allow us to assess the need for prophylac-tic irradiation of the pelvic lymph nodes during combined modality radiotherapy for high risk pros-tate cancer patients.


2005 ◽  
Vol 173 (4S) ◽  
pp. 126-127
Author(s):  
Yingming Li ◽  
Melissa Thompson ◽  
Zhu Chen ◽  
Bahaa S. Malaeb ◽  
David Corey ◽  
...  

2006 ◽  
Vol 175 (4S) ◽  
pp. 155-156
Author(s):  
Matthias D. Hofer ◽  
Sven Perner ◽  
Haojie Li ◽  
Rainer Kuefer ◽  
Richard E. Hautmann ◽  
...  

2016 ◽  
Author(s):  
Foteini Kalofonou ◽  
Claire Fletcher ◽  
Jonathan Waxman ◽  
Charlotte Bevan

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