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Query: UMLS:C0376358 (prostate cancer)
59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The primary objective underlying hormone treatment of prostatic adenocarcinoma is to induce an effective androgen deprivation, and high dose estrogen therapy is as effective as surgical castration in abolishing the growth-promoting effects of androgens on prostatic tissue. An estradiol-chemical delivery system (E2-CDS), with sustained release of E2 in the brain, may be potentially useful in the treatment of prostatic cancer by virtue of the need for lower or less frequent doses of the estrogen. In this study we evaluated the dose- and time-dependent effects of the E2-CDS vs. 17 beta-E2 on serum testosterone (T) and weights of androgen-dependent tissues in male rats. Rats received a single iv injection of E2-CDS (0.1, 0.5, or 1.0 mg/kg), equimolar doses of 17 beta-E2, or the drug's vehicle. Sera and tissues were collected 1, 7, 14, or 21 days later for determination of hormone levels and tissue weights. The E2-CDS exhibited a dose- and time-dependent suppression of serum T and weights of the ventral prostate and seminal vesicles. In contrast, 17 beta-E2 had no significant effect on serum T or growth of these androgen-dependent tissues. Serum T levels were significantly reduced by 98%, 82%, and 59% at 1, 7, and 14 days, respectively, with the 1.0 mg/kg dose of E2-CDS. The E2-CDS significantly reduced prostate weight by 45% and 50% (1.0- and 0.5-mg/kg doses, respectively) 7 days and by 27% (0.5 mg/kg dose) 14 days after treatment. Similarly, seminal vesicle weights were reduced by 14-20% on day 1, maximally reduced by 39-48% on day 7, and still reduced by 24-36% on day 14 compared with the control levels. Weights of these tissues returned to control levels by day 21. Serum E2 was elevated through 7 days by E2-CDS or on day 1 only by 17 beta-E2. PRL secretion was stimulated for 1 week by both forms of estrogen. Anterior pituitary weights were increased by the E2-CDS through 14 days, while 17 beta-E2 had no significant effect. These data indicate that the E2-CDS causes chronic suppression of serum T, which subsequently results in regression of androgen-dependent tissue weight.
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PMID:The effects of a brain-enhanced estradiol delivery system on testosterone and androgen-dependent tissues. I. Dose-response and time-course evaluation. 185 69

Enhanced delivery and sustained release of estradiol (E2) in the brain could have potential clinical applications in the effective treatment of vasomotor "hot flushes" and prostatic cancer. We have, therefore, evaluated a brain-enhanced E2-chemical delivery system (E2-CDS), which is based upon the interconvertible dihydropyridine in equilibrium with pyridinium salt redox reaction. In this study, we evaluated the tissue distributions of E2-Q+ and E2--the inactive and active metabolites of the E2-CDS. Both E2-Q+ and E2 were detected in all tissues analyzed. In peripheral tissues, E2-Q+ and E2 were rapidly cleared, but in brain, concentrations of both compounds exhibited a slow decline with a t1/2 = 8 days. 14 Days after the E2-CDS administration, brain levels of E2-Q+ exceeded plasma levels by 170-fold, fat levels by 20-fold, and liver levels by 8-fold. Similarly, brain-E2 levels exceeded plasma levels by 38-fold, fat levels by 11-fold, and liver levels by 7-fold. Furthermore, levels of E2-Q+ In anterior pituitary, kidney, heart, and lung were initially 2- to 6-fold higher than brain levels, but 14 days after the E2-CDS administration, brain levels of E2-Q+ exceeded E2-Q+ levels in these peripheral tissues by 1.5- to 3-fold. The increased brain/peripheral tissues ratios of E2-Q+ and E2 in rats treated with the E2-CDS support brain-enhanced delivery and sustained release of E2 from this delivery system.
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PMID:Tissue distribution of a brain-enhanced chemical delivery system for estradiol. 207 86

Men diagnosed with early stage prostate cancer face multiple treatment options, each with distinctive side effects that have significant implications for post-treatment quality of life. Healing Choices for Men with Prostate Cancer is a multimedia educational and decision aid program. This nation-wide randomized controlled trial evaluated the impact of Healing Choices on reducing decisional conflict and distress. Eligible prostate cancer patients who called the National Cancer Institute's Cancer Information Service (CIS) were invited to participate. After a baseline interview, participants were randomized to usual personalized consultation with a CIS specialist (comparison condition) or CIS personalized consultation plus the Healing Choices program (intervention condition). The Decision Conflict Scale and Impact of Event Scale assessed decisional conflict about prostate cancer treatment and cancer-related distress, respectively. Analyses evaluated group differences at 2 months postenrollment. Hypothesized moderation of intervention effects by demographic and clinical characteristics were evaluated. The final sample consisted of N = 349 participants (intervention: n = 181; comparison n = 168). Men were on average 64 years old, primarily White, and well educated. The difference in total decisional conflict was not significant (DCS total score; F[1,311] = .99, p = .32). The difference in cancer-related distress at 2 months between the intervention and the comparison groups was not significant (F[1,337] = .01, p = .93). Evaluation of specific decision processes indicated a significant effect on levels of perceived decisional support (intervention, M = 34.8, SD = 15.7; comparison, M = 38.3, SD = 16.1; F[1,337] = 3.74, p = .05). The intervention effect was greatest for nonwhite minority participants (b = -9.65, SE = 4.67) and those with lower educational attainment (b = 3.87, SE = 2.21). This interactive, comprehensive education and decision aid program may be most effective for a subset of prostate cancer patients in need of educational and decisional support.
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PMID:Examining the impact of a multimedia intervention on treatment decision-making among newly diagnosed prostate cancer patients: results from a nationwide RCT. 2998 47