scholarly journals Epidemiological trends of hormone-related cancers in Slovenia

2016 ◽  
Vol 67 (2) ◽  
pp. 83-92 ◽  
Author(s):  
Vesna Zadnik ◽  
Mateja Krajc
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Heavy Metals ◽  
Endocrine Disrupting Chemicals ◽  
Hormone Balance ◽  
Endocrine Disrupting ◽  
Cancer Types ◽  
Breast And Prostate Cancer ◽  
Epidemiological Trends ◽  
Developed World

AbstractThe incidence of hormone-related cancers tends to be higher in the developed world than in other countries. In Slovenia, six hormone-related cancers (breast, ovarian, endometrial, prostate, testicular, and thyroid) account for a quarter of all cancers. Their incidence goes up each year, breast and prostate cancer in particular. The age at diagnosis is not decreasing for any of the analysed cancer types. The risk of breast cancer is higher in the western part of the country, but no differences in geographical distribution have been observed for other hormone-related cancers. Furthermore, areas polluted with endocrine-disrupting chemicals that affect hormone balance such as PCBs, dioxins, heavy metals, and pesticides, do not seem to involve a greater cancer risk. We know little about how many cancers can be associated with endocrine disruptors, as there are too few reliable exposure studies to support an association.

Breast and Prostate Cancer: Sources and Pathways of Endocrine-disrupting Chemicals

2003 ◽  
Author(s):  
Jane A. Plant ◽  
Devra L. Davis
Keyword(s):  
Prostate Cancer ◽  
Generation X ◽  
Endocrine Disrupting Chemicals ◽  
Cancer Registries ◽  
Dietary Factors ◽  
Endocrine Disrupting ◽  
Breast And Prostate Cancer ◽  
Environment Agency ◽  
The 1960S ◽  
Europe Today

Cancers of the breast and prostate, which together with those of the ovaries, endometrium and testes are hormone-dependent, are among the most common forms of cancers affecting women and men respectively throughout the developed world (IARC VII 1997, Miller and Sharp 1998). The incidence of breast, prostate, and testicular cancers has risen dramatically in most European and North American countries and in Japan and Australasia since cancer registries were first compiled in the 1960s (WHO/IARC Web site). For instance, women and men born in Generation X in the U.S. and Europe today have twice the risk of developing breast and prostate cancer than their grandparents faced (Dinse et al. 1999). Several lines of evidence indicate that environmental factors, broadly conceived, may account for some of the recent changes in patterns of hormonally dependent cancers. Although rates are about 4 times lower in Asian countries than in European ones, they are increasing most rapidly in the former (Hoel et al. 1992). People who migrate tend to develop the cancer rate of their new countries. Studies of highly exposed workers consistently find that those working with certain plastics, organic solvents, pesticides, and other toxic chemicals tend to have higher risks of several hormonally dependent cancers (Davis and Muir 1995). Dietary factors can be involved in these patterns in two ways. Food constituents, such as dairy and animal protein products, can affect hormonal metabolism directly. In addition, foods can contain contaminants such as growth stimulating substances, pesticides, and packaging materials that can function as endocrine disrupting chemicals (EDCs). In the past decade, a number of major national and international reports have noted the possible role of EDCs for hormone-related illnesses including breast and prostate cancer, including the Weybridge report of the European Environment Agency of 1996 (EUR 17549 1997) and the Royal Society Report on Endocrine Disrupting Chemicals (Royal Soc. 2000). This chapter presents some recent information on the sources of EDCs in the environment, outlines mechanisms by which these materials can increase the risk of hormonally dependent cancers, and discusses insights from geochemistry that may be pertinent to this work.

The antihormonal preventive therapy of breast cancer and prostate cancer

2011 ◽  
Vol 5 (2) ◽  
Author(s):  
Hans-Jörg Senn ◽  
Rudolf Morant ◽  
Florian Otto
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Cancer Prevention ◽  
Preventive Therapy ◽  
Primary Cancer ◽  
Populations At Risk ◽  
The Usa ◽  
Cancer Types ◽  
Breast And Prostate Cancer ◽  
Clinical Prevention

AbstractWith the continuing increase of median life expectancy of important segments of the world's population, cancer incidence, as well as cancer related morbidity and mortality, are constantly increasing, especially for developing countries and for breast and prostate cancer, the predominant gender-associated cancer types. In addition to continuing, with more and more expensive efforts to develop new and more effective cancer treatments, it is health-politically and medico-professionally important to realise that only successful approaches to primary cancer prevention of major and frequent cancer types will be able to change this socially and economically unfavourably outlook. It is therefore encouraging to see that primary (or pharmacologic, interventional) cancer prevention programs have been successfully developed over the past decade for individuals at elevated risk for breast and prostate cancer on the basis of several scientifically well-conducted, prospective chemoprevention trials, mainly with synthetic anti-hormones (anti-estrogens and anti-androgens) in the USA, in Europe and Australia. This paper summarises the presently published results and design of several completed and some currently running primary cancer prevention trials in breast cancer and prostate cancer, and also points to the important obstacles for their conduct and translation into general practice in the broader populations at risk outside of clinical prevention research.

scholarly journals CBP/p300: Critical Co-Activators for Nuclear Steroid Hormone Receptors and Emerging Therapeutic Targets in Prostate and Breast Cancers

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2872
Author(s):  
Aaron R. Waddell ◽  
Haojie Huang ◽  
Daiqing Liao
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Tumor Growth ◽  
Signaling Pathways ◽  
Cell Cycle Progression ◽  
Hormone Receptors ◽  
Steroid Hormone Receptors ◽  
Breast Cancers ◽  
Creb Binding Protein ◽  
Breast And Prostate Cancer

The CREB-binding protein (CBP) and p300 are two paralogous lysine acetyltransferases (KATs) that were discovered in the 1980s–1990s. Since their discovery, CBP/p300 have emerged as important regulatory proteins due to their ability to acetylate histone and non-histone proteins to modulate transcription. Work in the last 20 years has firmly established CBP/p300 as critical regulators for nuclear hormone signaling pathways, which drive tumor growth in several cancer types. Indeed, CBP/p300 are critical co-activators for the androgen receptor (AR) and estrogen receptor (ER) signaling in prostate and breast cancer, respectively. The AR and ER are stimulated by sex hormones and function as transcription factors to regulate genes involved in cell cycle progression, metabolism, and other cellular functions that contribute to oncogenesis. Recent structural studies of the AR/p300 and ER/p300 complexes have provided critical insights into the mechanism by which p300 interacts with and activates AR- and ER-mediated transcription. Breast and prostate cancer rank the first and forth respectively in cancer diagnoses worldwide and effective treatments are urgently needed. Recent efforts have identified specific and potent CBP/p300 inhibitors that target the acetyltransferase activity and the acetytllysine-binding bromodomain (BD) of CBP/p300. These compounds inhibit AR signaling and tumor growth in prostate cancer. CBP/p300 inhibitors may also be applicable for treating breast and other hormone-dependent cancers. Here we provide an in-depth account of the critical roles of CBP/p300 in regulating the AR and ER signaling pathways and discuss the potential of CBP/p300 inhibitors for treating prostate and breast cancer.

scholarly journals Regulation of mRNA Translation by Hormone Receptors in Breast and Prostate Cancer

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3254
Author(s):  
Jianling Xie ◽  
Eric P. Kusnadi ◽  
Luc Furic ◽  
Luke A. Selth
Keyword(s):  
Prostate Cancer ◽  
Protein Synthesis ◽  
Causes Of Death ◽  
Hormone Receptors ◽  
Mrna Translation ◽  
Estrogen Receptor Α ◽  
Growth And Survival ◽  
Cancer Types ◽  
Breast And Prostate Cancer ◽  
Hormone Signalling

Breast and prostate cancer are the second and third leading causes of death amongst all cancer types, respectively. Pathogenesis of these malignancies is characterised by dysregulation of sex hormone signalling pathways, mediated by the estrogen receptor-α (ER) in breast cancer and androgen receptor (AR) in prostate cancer. ER and AR are transcription factors whose aberrant function drives oncogenic transcriptional programs to promote cancer growth and progression. While ER/AR are known to stimulate cell growth and survival by modulating gene transcription, emerging findings indicate that their effects in neoplasia are also mediated by dysregulation of protein synthesis (i.e., mRNA translation). This suggests that ER/AR can coordinately perturb both transcriptional and translational programs, resulting in the establishment of proteomes that promote malignancy. In this review, we will discuss relatively understudied aspects of ER and AR activity in regulating protein synthesis as well as the potential of targeting mRNA translation in breast and prostate cancer.

scholarly journals Symbiotic Gene Activation is Interrupted by Endocrine Disrupting Chemicals

2001 ◽  
Vol 1 ◽  
pp. 653-655 ◽  
Author(s):  
Jennifer E. Fox ◽  
Matthew E. Burow ◽  
John A. McLachlan
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Estrogen Receptors ◽  
Mammalian Cell Culture ◽  
Endocrine Disrupting Chemicals ◽  
Gene Activation ◽  
Symbiotic Gene ◽  
Endocrine Disrupting ◽  
Plant Chemicals ◽  
By Products

Endocrine disrupting chemicals (EDCs) include organochlorine pesticides, plastics manufacturing by-products, and certain herbicides[1]. These chemicals have been shown to disrupt hormonal signaling in exposed wildlife, lab animals, and mammalian cell culture by binding to estrogen receptors (ER-α and ER-β) and affecting the expression of estrogen responsive genes[2,3]. Additionally, certain plant chemicals, termed phytoestrogens, are also able to bind to estrogen receptors and modulate gene expression, and as such also may be considered EDCs[4]. One example of phytoestrogen action is genistein, a phytochemical produced by soybeans, binding estrogen receptors, and changing expression of estrogen responsive genes which certain studies have linked to a lower incidence of hormonally related cancers in Japanese populations[5]. Why would plants make compounds that are able to act as estrogens in the human body? Obviously, soybeans do not intentionally produce phytoestrogens to prevent breast cancer in Japanese women.

scholarly journals Lack of Association between Common Polymorphisms in Selenoprotein P Gene and Susceptibility to Colorectal Cancer, Breast Cancer, and Prostate Cancer: A Meta-Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Hanjiang Xu ◽  
Fan Mo ◽  
Jun Zhou ◽  
Zongyao Hao ◽  
Xianguo Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Colorectal Cancer ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Selenoprotein P ◽  
Tumor Type ◽  
Cancer Breast ◽  
P Gene ◽  
Breast And Prostate Cancer

Background and Objective. Selenoprotein P (SEPP1) is the major selenoprotein in plasma. Previous studies have demonstrated that SEPP1 expression was reduced in human prostate and colon tumors. Nowadays, studies concerning SEPP1 gene polymorphisms and cancer susceptibility have been extensively investigated, whereas results from these studies remain debatable rather than conclusive. Thus, we performed the present meta-analysis to comprehensively assess the association between two common polymorphisms (rs3877899 and rs7579) in SEPP1 and cancer susceptibility. Method. We search the PubMed, Embase, Google Scholar, and Wanfang (China) databases (up to December 1, 2020) to identify all eligible publications. The pooled odds ratio (OR) correspondence with 95% confidence interval (CI) was calculated to evaluate the associations. Results. Finally, nine eligible studies with 7,157 cases and 6,440 controls and five studies with 2,278 cases and 2,821 controls were enrolled in rs3877899 and rs7579 polymorphisms, individually. However, a null significant association was detected between the two polymorphisms in SEPP1 and susceptibility to colorectal, breast, and prostate cancer in all comparison models. Subsequently, subgroup analysis based on tumor type, no significant association was identified for prostate, breast, and colorectal cancer. In addition, when the stratification analyses were conducted by the source of control, HWE status, and ethnicity, yet no significant association was found. Conclusions. The current meta-analysis shows that SEPP1 rs3877899 and rs7579 polymorphisms may not be associated with susceptibility to colon cancer, breast cancer, and prostate cancer, and further well-designed studies with a larger sample size are warranted to validate our findings.

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