Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prevention and therapeutic intervention by phytochemicals are newer dimensions in the arena of cancer management. In this regard, the cancer chemopreventive role of silymarin (Silybum marianum) has been extensively studied and has shown anticancer efficacy against various cancer sites, especially skin and prostate. In skin cancer, silymarin treatment inhibits ultraviolet B radiation or chemically initiated or promoted carcinogenesis. These effects of silymarin against skin carcinogenesis have been attributed to its strong antioxidant and anti-inflammatory action as well as its inhibitory effect on mitogenic signaling. Similarly, silymarin treatment inhibits 3, 2-dimethyl-4-aminobiphenyl-induced prostate carcinogenesis and retards the growth of advanced prostate tumor xenograft in athymic nude mice. In prostate cancer, silymarin treatment down-regulates androgen receptor-, epidermal growth factor receptor-, and nuclear factor-kappaB- mediated signaling and induces cell cycle arrest. Extensive preclinical findings have supported the anticancer potential of silymarin, and now its efficacy is being evaluated in cancer patients.
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PMID:Chemopreventive efficacy of silymarin in skin and prostate cancer. 1754 92

Prostate cancer is a major public health problem of the male population in all the developed countries. This non-skin cancer is the foremost one facing man today. Prostate cancer has become the second leading cause of cancer death2. In this study we investigated changes in the prostate carcinoma incidence and manifestation during a thirty-three years period. The study included 1226 cases of prostate cancer diagnosed from 1972 to 2005 in the Primorsko-Goranska County, Croatia. The age-adjusted incidence of prostate cancer increased from 1.69 per 100,000 men annually in 1972 to 137.58 per 100,000 men annually in 2005, which is an 81.4-fold increase. The percentage ofpatients with bone metastases on the first medical examination decreased from 1972 (75%) to 2005 (15%). The most of the patients with bone metastases at the first medical examination were between 30 and 50 years old. Early detection measures, such as prostate specific antigen testing and transrectal ultrasound guided prostate biopsy combined with the raised public awareness of the disease, most probably resulted in an increase of incidence.
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PMID:Epidemiology of prostate cancer in the mediterranean population of Croatia--a thirty-three year retrospective study. 1759 7

Preventive and screening interventions have been met with great enthusiasm. This is due to a widespread misunderstanding of what prevention can do and what it cannot do. Initiatives for prevention or early diagnosis of disease are almost always considered beneficial. Meanwhile, however, there are many impressive examples of detrimental failures of such initiatives documented by large high-quality randomised controlled trials (RCTs). These include treatment with vitamin pills to prevent cancer or cardiovascular disease or treatment of healthy women with sexual hormones which has finally turned out to be one of the biggest scandals in medicine. Systematic self-examination of the breast to detect breast cancer early does more harm than good. Most dogmas of the modern so-called healthy diet are not supported by several recently published high-quality RCTs. On the other hand, many of the promoted prevention initiatives lack evidence from high-quality RCTs such as health checks, rectal examination, screening for renal disease or diabetes, screening for colorectal cancer by coloscopy, for prostate cancer or skin cancer. Even if effective, most screening programmes will benefit only a few but harm many more, though. Harm is due to overdiagnosis and overtreatment as well as to side effects related to the investigation itself. This includes psychological and other distress related to work-up of false test results. All prevention programmes have to undergo sound scientific evaluation before they can be recommended or implemented. Ethical guidelines ask for complete, objective, unbiased, evidence-based and understandable information for potential participants of prevention programmes. Rarely is such information provided or even available. Non-participation is an explicit option for most preventive programmes and must not be penalised.
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PMID:[Is prevention better than healing?]. 1771 Dec 54

Adenocarcinoma of the prostate is the second most common cancer in men in the United States (following only skin cancer) and accounts for 33% of all newly diagnosed male cancers. It is estimated that in 2007, 218,890 men will be diagnosed with prostate cancer and 27,050 will die from this disease. While most currently diagnosed prostate cancers are localized, radical prostatectomy remains a gold standard treatment. Since its original description, radical retropubic prostatectomy has evolved over the last three decades to a precise, sophisticated procedure with minimal mortality, and excellent surgical outcomes. However, despite its efficacy, open surgical treatment is inherently associated with blood loss and significant pain. Due to these reasons, many men have sought other, less invasive forms of treatment. With its development in the late 1990s, minimally invasive surgery has significantly and irrevocably changed the surgical treatment of prostate cancer. Robotic-assisted technology has further propelled the utilization of the laparoscopic approach for radical prostatectomy, particularly for non-laparoscopic trained surgeons. The implementation of robotic technology has been rapid. Presently, 7 years after its approval by the FDA, many hospitals have established for robotic-assisted radical prostatectomy programs. This trend will undoubtedly continue to grow as more surgeons become familiar with the procedure, more robotic systems become available, and increasingly mature data is published. Robotic-assisted laparoscopic radical prostatectomy allows patients the benefits of minimally invasive surgery with functional and oncological results comparable to those from open and standard laparoscopic procedures, we believe that this surgical approach will shortly evolve into the standard surgical approach for localized prostate cancer.
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PMID:Evolution of robotic surgery in the treatment of localized prostate cancer. 1772 45

Prostate cancer is the commonest non-skin cancer in men. Incidence and mortality rates of this tumor vary strikingly throughout the world. Although several factors have been implicated to explain this remarkable variation, lifestyle and dietary factors may play a dominant role, with sex hormones behaving as intermediaries between exogenous factors and molecular targets in development and progression of prostate cancer. Human prostate cancer is generally considered a paradigm of androgen-dependent tumor; however, estrogen role in both normal and malignant prostate appears to be equally important. The association between plasma androgens and prostate cancer remains contradictory and mostly not compatible with the androgen hypothesis. Similar evidence apply to estrogens, although the ratio of androgen to estrogen in plasma declines with age. Apart from methodological problems, a major issue is to what extent circulating hormones can be considered representative of their intraprostatic levels. Both nontumoral and malignant human prostate tissues and cells are endowed with key enzymes of steroid metabolism, including 17betahydroxysteroid dehydrogenase (17betaHSD), 5beta-reductase, 3alpha/3betaHSD, and aromatase. A divergent expression and/or activity of these enzymes may eventually lead to a differential prostate accumulation of steroid derivatives having distinct biological activities, as it occurs for hydroxylated estrogens in the human breast. Locally produced or metabolically transformed estrogens may differently affect proliferative activity of prostate cancer cells. Aberrant aromatase expression and activity has been reported in prostate tumor tissues and cells, implying that androgen aromatization to estrogens may play a role in prostate carcinogenesis or tumor progression. Interestingly, many genes encoding for steroid enzymes are polymorphic, although only a few studies have supported their relation with risk of prostate cancer. In animal model systems estrogens, combined with androgens, appear to be required for the malignant transformation of prostate epithelial cells. Although the mechanisms underlying the hormonal induction of prostate cancer in experimental animals remain uncertain, there is however evidence to support the assumption that long term administration of androgens and estrogens results in an estrogenic milieu in rat prostates and in the ensuing development of dysplasia and cancer. Both androgen and estrogen have been reported to stimulate proliferation of cultured prostate cancer cells, primarily through receptor-mediated effects. As for estrogens, the two major receptor types, ERalpha and ERbeta, are expressed in both normal and diseased human prostate, though with a different cellular localization. Since these two receptors are different in terms of ligand binding, heterodimerization, transactivation, and estrogen response element activity, it is likely that an imbalance of their expression may be critical to determine the ultimate estrogen effects on prostate cancer cells. In prostate cancer, ERbeta activation appears to limit cell proliferation directly or through ERalpha inhibition, and loss of ERbeta has been consistently associated with tumor progression. Several splicing variants of both ERalpha and ERbeta exist. Little is known about their expression and function in the human prostate, although reciprocal regulation and interaction with gene promoter both warrant further investigation. In summary, although multiple consistent evidence suggests that estrogens are critical players in human prostate cancer, their role has been only recently reconsidered, being eclipsed for years by an androgen-dominated interest.
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PMID:Estrogen and prostate cancer: an eclipsed truth in an androgen-dominated scenario. 1778 30

Prostate cancer is the most commonly diagnosed non-skin cancer in men in the United States. Among environmental factors, diet may play a particularly important role in its incidence, progression, and clinical outcome. This article reviews the findings of eight observational studies and 17 intervention or laboratory trials on the effect of plant-based diets and plant nutrients on both the progression and clinical outcome of prostate cancer as well as additional studies examining mechanisms that may explain dietary effects. While additional long-term therapeutic clinical trials are needed to further elucidate the role of diet, these early investigations suggest that a recommendation for individual patients to shift their diets toward plant foods may serve as an important component of the tertiary treatment of prostate cancer.
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PMID:Diet and survival after prostate cancer diagnosis. 1866 19

Genetically engineered mice (GEM) have been extensively used to model human cancer. Mouse models mimic the morphology, histopathology, phenotype, and genotype of the corresponding cancer in humans. GEM mice are created by random integration of a transgene into the genome, which results in gene overexpression (transgenic mice); gene deletion (knock-out mice); or targeted insertion of the transgene in a selected locus (knock-in mice). Knock-out may be constitutive, i.e. total inactivation of the gene of interest in any cell, or conditional, i.e. tissue-specific inactivation of the gene. Gene knock-down (RNAi) and humanization of the mouse are more sophisticated models of GEM mice. RNA interference (RNAi) is a mechanism in which double-stranded RNAs inhibits the respective gene expression by inducing degradation of its mRNA. Humanization is based on replacing a mouse gene by its human counterpart. The alterations in genes in GEM have to be heritable. The opportunities provided by employing GEM cancer models are: analysis of the role of specific cancer genes and modifier genes, evaluation of conventional cancer therapies and new drugs, identification of cancer markers of tumor growth, analysis of the influence of the tumor's microenvironment on tumor formation, and the definition of the pre-clinical, discrete steps of tumorigenesis. The validation of mouse models of human cancer is the task of the MMHCC (Mouse Models of Human Cancer Consortium). The GEM models of breast, pancreatic, intestinal and colon, and prostate cancer are the most actively explored. In contrast, the models of brain tumors and ovary, cervical, and skin cancer are in the early stage of investigation.
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PMID:[Genetically engineered mice: mouse models for cancer research]. 1797 65

Prostate cancer is the most frequently diagnosed non-skin cancer and the third leading cause of cancer mortality in men. In the initial stages, prostate cancer is dependent on androgens for growth, which is the basis for androgen ablation therapy. However, in most cases, prostate cancer progresses to a hormone refractory phenotype for which there is no effective therapy available at present. The androgen receptor (AR) is required for prostate cancer growth in all stages, including the relapsed, "androgen-independent" tumors in the presence of very low levels of androgens. This review focuses on AR function and AR-target genes and summarizes the major signaling pathways implicated in prostate cancer progression, their crosstalk with each other and with AR signaling. This complex network of interactions is providing a deeper insight into prostate carcinogenesis and may form the basis for novel diagnostic and therapeutic strategies.
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PMID:Androgen signaling and its interactions with other signaling pathways in prostate cancer. 1800 77

Vitamin D, a fat-soluble prohormone is synthesized in response to sunlight. Experimental evidence suggests that vitamin D may reduce the risk of cancer through regulation of cellular proliferation and differentiation as well as inhibition of angiogenesis. These anticancer properties have been attributed primarily to 1,25-dihydroxyvitamin D [1,25(OH) 2 D] (calcitriol), the hormonal form of vitamin D. Extensive research has shown that cells, including cancer cells, express specific receptors (VDR) for 1,25-dihydroxyvitamin D. When bound to the VDR, 1,25-dihydroxyvitamin D regulates> 60 genes that exert prodifferentiating, antiproliferative and antimetastatic effects on cells, including effects on cell cycle. The amount of exposure to the sun has been found to correlate inversely with cancer mortality and survival in numerous epidemiological studies. An inverse relationship between solar ultraviolet-B (UV-B) exposure and non-skin cancer mortality has long been reported. Several ecological studies suggest that sunlight may protect against prostate, colon, rectal, female breast and ovarian cancer, all diseases that contribute to a substantially higher proportion of cancer mortality in the western industrialized world. Some analytical studies also suggest a protective association between circulating vitamin D in blood, which is largely derived from sunlight, or dietary vitamin D. Paricalcitol (calcitriol analogue) is as effective as 1,25-dihydroxyvitamin D in transactivating the prostatic VDR and in inhibiting the growth of prostate cancer cell lines and primary cultures of prostate cancer cells in vitro. Promising preclinical evaluations of calcitriol and analogues have appeared in prostate cancer animal models.
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PMID:Vitamin D and cancer. 1827 Mar 98

Prostate cancer is currently the most common type of neoplasm found in American men, other than skin cancer, and is the second leading cause of cancer death in males. Because cell cycle checkpoint proteins stabilize the genome, the relationship of one such protein, Rad9, to prostate cancer was investigated. We found that four prostate cancer cell lines (CWR22, DU145, LNCaP, and PC-3), relative to PrEC normal prostate cells, have aberrantly high levels of Rad9 protein. The 3'-end region of intron 2 of Rad9 in DU145 cells is hypermethylated at CpG islands, and treatment with 5'-aza-2'-deoxycytidine restores near-normal levels of methylation and reduces Rad9 protein abundance. Southern blot analyses indicate that PC-3 cells contain an amplified Rad9 copy number. Therefore, we provide evidence that Rad9 levels are high in prostate cancer cells due at least in part to aberrant methylation or gene amplification. The effectiveness of small interfering RNA to lower Rad9 protein levels in CWR22, DU145, and PC-3 cells correlated with reduction of tumorigenicity in nude mice, indicating that Rad9 actively contributes to the disease. Rad9 protein levels were high in 153 of 339 human prostate tumor biopsy samples examined and detectable in only 2 of 52 noncancerous prostate tissues. There was a strong correlation between Rad9 protein abundance and cancer stage. Rad9 protein level can thus provide a biomarker for advanced prostate cancer and is causally related to the disease, suggesting the potential for developing novel diagnostic, prognostic, and therapeutic tools based on detection or manipulation of Rad9 protein abundance.
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PMID:Rad9 has a functional role in human prostate carcinogenesis. 1831 88


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