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Objectives. To examine the temporal trends in radical prostatectomy (RP), brachytherapy (BT), and external beam radiotherapy (EBRT) rates among men aged 65 years or older for the period 1984 to 1997.Methods. We used the retrospective population-based analysis of treatments for prostate cancer among Medicare beneficiaries. The rates of RP were obtained from Part A (hospital) Medicare data for 20% of the national sample for 1984 to 1997. The BT and EBRT rates for the period 1993 to 1997 were obtained from a 5% national sample of Physician/Supplier Part B data. The rates of treatment, 30-day mortality, and readmissions were included.Results. The rate of RP peaked in 1992. From 1993 to 1997, its use decreased by 6% among men aged 65 to 69 years, 34% among men aged 70 to 74 years, and 50% for men aged 75 years or older. However, by 1997, the RP + BT treatment rate again approached the 1992 levels of RP alone; BT was used twice as often as RP in men aged 75 years or older. By 1997, the RP + BT + EBRT rate exceeded the 1993 rate for men aged 65 to 69 years and was again approaching the 1993 rate for men aged 70 to 74 years. From 1984 to 1997, the presence of comorbid conditions gradually declined for RP and accounted for more than 60% of the decrease in the short term mortality during this period. Variations in RP use by geographic region have also decreased.Conclusions. RP is now more selectively targeted for treatment of prostate cancer in men older than 70 years than in the past. However, since BT has been substituted for radical surgery in many of these older men, the total population-based treatment rates have changed very little over time. 相似文献
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《International journal of urology》2018,25(4):318-326
Prostate cancer is a widespread problem among men, with >160 000 new cases in 2017 alone. Androgen deprivation therapy is commonly used in prostate cancer treatment to block androgens required for cancer growth, but disease relapse after androgen deprivation therapy is both common and severe. Changes in androgen receptor signaling from androgen deprivation therapy have been linked to therapeutic resistance and tumor progression. Resistant cells can become reprogrammed to undergo epithelial–mesenchymal transition, a phenotypic switch from benign, epithelial cells to a mobile cell with mesenchymal traits. In these cells, attachment to their epithelial cell layer is no longer required for survival. Anoikis is a form of cell death that occurs when detachment from other cells and the basement membrane occurs. Epithelial cells have been shown to undergo epithelial–mesenchymal transition, avoid anoikis induction and progress to a metastatic phenotype. In prostate cancer progression to advanced disease, epithelial–mesenchymal transition induction (characterized by loss of epithelial cellular attachment protein E‐cadherin) correlates with a higher Gleason score, tumor progression, increased metastasis and higher biochemical recurrence. The concept of interfacing epithelial–mesenchymal transition with anoikis in the tumor microenvironment landscape will be discussed here, with focus on the significance of the functional exchange between the two processes in therapeutic targeting of advanced disease. The current evidence on the impact of loss of cell–cell contact, acquisition of chemoresistance, immune escape and metastatic spread in advanced tumors in response to transforming growth factor‐β on prostate cancer metastasis will be also discussed. The signaling cross‐talk between transforming growth factor‐β and androgen receptor signaling will be interrogated as a new therapeutic platform for the development of combination strategies to impair prostate cancer metastasis. 相似文献
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Association between male accesory gland infections and prostate cancer in Turkish men: A case–control study
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It is well known that chronic inflammation contributes to several forms of human cancer. Although several studies have investigated the association between prostatitis and prostate cancer, there is a lack of specifically designed study about male accessory gland infections (MAGI) and prostate cancer co‐occurrence. We aimed to investigate this association with a case–control study in Turkish men. A total of 155 patients were enrolled to the study. After the pathological examination of the transrectal ultrasound‐guided prostate biopsy specimens, patients were divided the two groups as control and prostate cancer and the presence of MAGI was determined. Of 155 patients, 145 met inclusion criteria. In the prostate cancer group, MAGI diagnose was determined in 18 of 31 patients (58.06%), while it was determined in 25 of 114 (21.93%) patients in the control group (p = .001). A significant correlation between MAGI and pathological Gleason score also revealed (p = .0001). We demonstrated that men with MAGI have increased risk for the development of prostate cancer. Moreover, in this population, most of the prostate cancers tend to be clinically significant or high grade. 相似文献
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Study Type – Prevalence (retrospective cohort)Level of Evidence 2b What’s known on the subject? and What does the study add? Benign prostatic hyperplasia is very common. It does not itself cause death, but its complications, and therapy, may. Prostatic cancer has recently overtaken lung cancer as the most commonly diagnosed cancer in men in England. Mortality rates for deaths attributed to benign prostatic hypertrophy have fallen dramatically over the past three decades. This is likely to be a consequence of improvements in quality of care of men with the condition. Over a similar period, mortality for prostate cancer initially increased, peaked in the 1990s, and since then has shown a decline. OBJECTIVE To determine mortality trends for benign prostatic hyperplasia (BPH) and prostate cancer in English populations, between1979 and 2006. SUBJECTS AND METHODS Analysis of datasets that include both the underlying cause and all other mentioned causes on death certificates (together, termed ‘mentions’): the Oxford Record Linkage Study, 1979–2006, and English national data, 1995–2006. RESULTS In the Oxford region, underlying‐cause mortality from BPH fell from 45 deaths per million in 1979 to 2.4 in 2006. For mentions, the respective rates were 93 and 7.1. In England, underlying‐cause mortality reduced from 9.2 deaths per million in 1995 to 4.5 deaths per million in 2006. For mentions, the rates were 20 and 9.9 deaths per million. When BPH was certified on death certificates, it was selected as the underlying cause of death on fewer than half. Underlying‐cause mortality for prostate cancer in Oxford increased from 213 deaths per million in 1979 to 335 by 1991, and thereafter declined to 253 deaths per million in 2006. Mentions‐mortality in Oxford followed a similar pattern. In later years, when there were comparable data for Oxford and England, the pattern of decline in England was similar to that in Oxford. Where mentioned, prostate cancer was coded as the underlying cause of death on three‐quarters of death certificates. CONCLUSIONS The fall in BPH mortality, evident in statistics on underlying cause, was confirmed by statistics on all certified causes of death. The fall is dramatic in scale, likely to be attributable to clinical care, and could be regarded as an indicator of improving standards of care. Mortality for prostate cancer increased, peaking in the 1990s, then decreased in recent years in rates as measured both by underlying cause and by mentions. 相似文献
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Transrectal ultrasonography has been considered useful for the diagnosis of prostate cancer. There have been few reports on localized cancer in the prostate diagnosed by echogram. In this paper, we discuss echograms of the prostate in cases of localized cancer, advanced cancer and well-controlled cancer. Hypoechoic lesions seem to suggest prostate cancer. 相似文献
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Review: prostate cancer epidemiology 总被引:6,自引:0,他引:6
W D Flanders 《The Prostate》1984,5(6):621-629
Prostate cancer is common among men in the United States. Factors of possible importance in the etiology of prostate cancer include diet, primarily implicated by ecologic studies of national, regional, and ethnic variation in rates; endocrine function, implicated by the importance of endocrine function in normal prostatic growth and in the treatment of prostate cancer; genetic susceptibility, supported by familial aggregation; some aspect of sexual behavior, suggested by case-control differences in sexual behavior; and occupational exposure, particularly cadmium exposure. Despite the public health importance of prostate cancer, it has received only moderate epidemiologic study; thus the etiologic importance of these and other possible determinants of prostate cancer risk is uncertain [55]. 相似文献