Does altering diet affect progression of prostate cancer? The MEAL study.
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Zinc is a group IIB heavy metal. It is an important regulator of major cell signaling pathways in most mammalian cells, functions as an antioxidant and plays a role in maintaining genomic stability. Zinc deficiency leads to severe diseases in the brain, pancreas, liver, kidneys and reproductive organs. Zinc loss occurs during tumor development in a variety of cancers. The prostate normally contains abundant intracellular zinc and zinc loss is a hallmark of the development of prostate cancer development. The underlying mechanism of this loss is not clearly understood. The knowledge that excess zinc prevents the growth of prostate cancers suggests that zinc-mediated therapeutics could be an effective approach for cancer prevention and treatment, although challenges remain. This review summarizes the specific roles of zinc in several cancer types focusing on prostate cancer. The relationship between prostate cancer and the dysregulation of zinc homeostasis is examined in detail in an effort to understand the role of zinc in prostate cancer.
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Using the SEER Program of the NCI, and the U.S. total mortality rates, we calculated the probability at birth of being diagnosed with prostate cancer within one's lifetime to be 8.8%, and we subtracted the microscopic stage A cancers too small to ever be of clinical significance which gave a final probability of 8%. Prostates were examined in 139 consecutive, unselected cystoprostatectomies from patients with bladder cancers who were unknown to have prostate cancer. Prostate cancer was found in 55 patients (40%); the volume of the largest cancer in each of these 55 prostates was determined by histologic morphometry. We identified the 8% of these 139 cystoprostatectomies with the largest volume of prostate cancer. The largest 11 of the 55 cancers represented 7.9% of the 139 cystoprostatectomies. These cancers ranged in volume from 0.5 cc to 6.1 cc, representing only 20% of all patients with prostate cancer. Thus, if one accepts the strong evidence that cancer progression is proportional to cancer volume, we conclude that prostate cancers larger than 0.5 cc appear to correspond to the 8% of men who will be diagnosed with a clinically significant carcinoma, as derived from SEER data. Conversely, those 80% of prostate cancers under 0.5 cc are probably not destined to reach clinically significant size in view of the very long doubling time of this cancer.
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Prostate cancer is a common cancer disease within older male populations and its incidence rate increased year by year. The abnormal exception of connexon is one of its pathogenesis. Researches show that Cx43 expression in prostate cancer was effectively lower compared with prostate epi- thelial, what's more, there existed a gap junctional intercellular communication defects in pros- tate cancer. So, Cx43 expression defects may significantly affect the prostate cancer process. Re- searches also show that tea polyphenols substances, selenium substances, hormone-like sub- stances, vitamins, alkaloids, and other chemical substances are also have different levels of effects on the expression of Cx43 in prostate tumor cells. Therefore, they also influenced the development of prostate cancer. So, the following article will mainly state the effecting of variety chemical fac- tors on Cx43 in prostate cancer cells and therapeutic implications.
Pathogenesis
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Prostate cancer is the most common malignant neoplasm in men and the second most frequent cause of cancer death for males in the United States. Recently, emerging evidence suggests that prostate cancer stem cells (CSCs) may play a critical role in the development and progression of prostate cancer. Therefore, targeting prostate CSCs for the prevention of tumor progression and treatment of prostate cancer could become a novel strategy for better treatment of patients diagnosed with prostate cancer. In this review article, we will summarize the most recent advances in the prostate CSCs field, with particular emphasis on targeting prostate CSCs to treat prostate cancer.
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textabstractAt first glance, deciding whether to get the PSA screening
test for prostate cancer seems to be pretty straightforward and attractive. It’s a simple
blood test that can pick up the prostate cancer long before your symptoms appear. After
all, your prostate cancer is earlier treated resulting in cure and better outcome. Therefore
prostate cancer screening seems to be suitable for public commercials. However, many
of the cancers that will be detected by screening are so slow-growing that might never
cause problems during mens life. Moreover, their diagnosis by biopsy, and treatment,
might be worse than the disease itself. Therefore, prostate cancer screening looks favourable;
however, watch out for the prostate cancer bomb.
Prostate cancer screening
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To evaluate the spatial distribution of prostate cancer detected at a single positive biopsy (PBx) and a repeat PBx (rPBx).We evaluated 533 consecutive men diagnosed with prostate cancer who underwent radical prostatectomy using a clinical map document based on XML (cMDX©)-based map model of the prostate. We determined the number of cancer foci, relative tumour volume, Gleason score, zone of origin, localisation, and pathological stage after stratification according to the number of PBx sessions (PBx vs rPBx). The distribution of 3966 prostate cancer foci was analysed and visualised on heat maps. The colour gradient of the heat map was reduced to six colours representing the frequency classification of prostate cancer using an image posterisation effect. Additionally, the spatial distribution of organ-confined prostate cancer between PBx and rPBx was evaluated.Prostate cancer diagnosed on PBx was mostly localised to the apical portion and the peripheral zone of the prostate. Prostate cancer diagnosed on rPBx was more frequently found in the anterior portion and the base of the prostate. Organ-confined prostate cancer foci were mostly localised in the dorsolateral zone of the prostate in men at PBx, whereas men at rPBx had more prostate cancer foci in the anterior portion.The spatial distribution of prostate cancer with rPBx differs significantly from the spatial distribution of prostate cancer with PBx. The whole anterior portion of the prostate should be considered by rPBx.
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Prostate cancer, the most frequent non-cutaneous malignancy in men from industrialized countries, is a growing medical problem, representing the second leading cause of male cancer deaths. In the last decade, converging evidence from epidemiological and biological studies suggests that the Insulin-like Growth Factor (IGF) axis is involved in the tumorigenesis and neoplastic growth of prostate cancer. Epidemiological observations indicated that circulating IGF-I levels are positively associated with the increased risk of prostate cancer. The activation of type I IGF receptor (IGF-IR) by IGFI and/or IGF-II, has mitogenic and antiapoptotic effects on normal and malignant prostate cells. Altered expression of IGF axis components has also been reported in vitro and in animal models of prostate cancer, as well as in human prostate cancer tissue samples. In this review we address and analyze epidemiological studies, in vitro and in vivo cancer models, and human ex vivo prostate cancer researches performed to date supporting the role of IGF axis in prostate cancer.
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