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

A study was undertaken to assess the ability of transrectal ultrasound (TR/US), digital rectal examination (DRE), and Prostate Specific Antigen (PSA), to diagnose persistent prostate cancer following an I125 seed implant (SI). Twenty-six patients formed the study group. The median follow-up time was 38 months, and the range was 20 to 60 months. Eighty-eight percent (23/26) had suspicious lesions on TR/US, followed by ultrasound-guided biopsies. Biopsies were performed only on those patients having suspicious lesions on TR/US. Histologically proven adenocarcinoma was found in 81% (21/26) of the patients. Statistical evaluation was done using tissue obtained at biopsy as the "gold standard." The sensitivities for the DRE and PSA were 33% and 76%, respectively. The specificities for DRE and PSA were 50% and 0%, respectively. The positive predictive values for cancer were 91% by TR/US, 100% by DRE, and 89% by PSA. The negative predictive values were 13% for DRE and 0% for PSA. Overall detection rates (N = 26) were 81% for TR/US, 27% for DRE, and 62% for PSA. We conclude that ultrasound criteria for the presence of cancer are the same for both the post-irradiated prostate and the untreated prostate, and that TR/US is the most sensitive test for the diagnosis of persistent local cancer following I125 seed implantation.
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PMID:Transrectal ultrasound in the diagnosis and staging of local disease after I125 seed implantation for prostate cancer. 246 21

The natural history of clinically localized prostate cancer is controversial. However, the data that is available suggests outcomes are good for men with well and moderately differentiated disease, but relatively poor for men with poorly differentiated cancer. For example, in one synthesis of individual-patient level data from six series, ten-year prostate cancer-specific mortality for men with well, moderate, and poorly differentiated disease was estimated at 13%, 13%, and 66%, respectively. Tumor grade is the dominant predictor of prognosis. Few studies report on risks of morbidity due to local cancer progression; the data available suggest this risk is relatively low. Cancer-specific mortality figures overestimate the impact of disease among older men with competing causes of mortality. Given the available data on prognosis of men with localized prostate cancer not treated for cure, clinical trials designed to measure the effectiveness of aggressive therapy will need to be large.
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PMID:Natural history of clinically localized prostate cancer. 775 75

To determine the changes in histologic features during the course of prostate cancer under long-term endocrine therapy, histologic grade and argyrophilic nucleolar organizer regions (AgNORs) were examined in specimens before treatment, at relapse, and at cancer death. A total of 29 patients who had received therapy and died of prostate cancer were evaluated. Among the 29 cases, biopsy tissues before treatment (25 cases) and during progression from endocrine therapy (10 cases) were compared with autopsy specimens. Histologic grade was determined by the method of Gleason, and the number of AgNORs in cancer cells was counted. Survival of the patients was compared with the histologic features. There was a tendency for a higher grade of cancer during the clinical course. Moreover, a statistically significant increase in the number of AgNORs was observed from pretreatment biopsy to autopsy. Upon comparison of metastatic sites with local cancer at autopsy, no significant difference was noticed in terms of histologic grade or AgNOR count. Although there was no correlation between the number of AgNORs and survival after initial treatment, an inverse relationship was demonstrated between the number of AgNORs and survival in patients with systemic progression after endocrine therapy. In conclusion, prostate cancer shows an increase of malignant potential, as assessed by histologic grade and the number of AgNORs. Patients with cancer of high proliferative ability showing high grade and greater numbers of AgNORs have poorer prognosis from progression.
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PMID:Changes in histologic grade and argyrophilic nucleolar organizer regions during progression of prostate cancer. 860 99

Surgery, radiation, or hormone deprivation alone does not adequately affect local control of clinical or pathologic stage T3 prostate cancer. Lack of local cancer control ultimately leads to a higher incidence of morbidity, distant metastasis, and decreased survival, with patients having disease-specific mortality exceeding 75%. Other novel therapies against this devastating and common disease are needed for the achievement of long-term local cancer control. For this purpose, therapeutic interventions should target prostate-cancer cells at the molecular and cellular level in ways not possible by current modalities of cancer treatment. Any strategy that can modify the biologic behavior of these cells may potentially have the most significant clinical impact. As prostate cancer represents an accumulation of genetic mutations that causes a prostate cell to lose the ability to control its growth, one new approach against prostate cancer may be gene therapy. Identification of key missing or mutated tumor-suppressor genes that, when replaced, may inhibit or destroy prostate-cancer cells may have the best chance of clinical success. One such gene appears to be tumor-suppressor gene p16 (also known as MTS1, INK4A, and CDKN2). Tumor-suppressor gene p16 is an important negative cell-cycle regulator whose functional loss may significantly contribute to malignant transformation and progression. Alterations in the p16 gene and its protein expression often occur in prostate cancer. An adenoviral vector containing wild-type p16 (Adp16) had a high transduction efficiency in prostate-cancer cells both in vitro and in vivo. Moreover, prostate tumors injected with Adp16 expressed p16 and the adenoviral vector expressed the transgene for up to 14 days. Wild-type p16 inhibited prostate-cancer proliferation in vitro and markedly suppressed tumors in vivo. Pathologic evaluation of the Adp16-treated tumors showed dose-dependent necrosis and fibrosis. Although the mechanism of p16 inhibition in cancer remains to be elucidated, senescence and apoptosis may both be important; however, the data suggest that p16-induced growth inhibition can function independently of the retinoblastoma gene product.
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PMID:Adenovirus p16 gene therapy for prostate cancer. 1085 45

To compare diagnostic value of transrectal prostatic biopsy in obtaining samples of tissue from different sites in patients with various levels of prostate-specific antigen (PSA) and prostate size, we made primary transrectal biopsy of the prostate in 486 patients. The patients were divided into 7 groups by the number of punctures at biopsy (from 6 to 18). Among the patients with PSA under 20 ng/ml in the number of tissue biopsy samples 18, a rise in prostatic cancer detection rate (PCDR) was 16.6%. In PSA above 20 ng/ml, a statistically significant maximal rise in PCDR occurred in the increase of biopsy number from 6 to 12 (by 9.3%). The number of local cancer forms in patients with PSA < 20 ng/ml among all the detected cases rose from 70% (biopsy from 6 sites) to 92.3% (biopsy from 18 sites). Among the patients with PSA < 20 ng/ml and the size of the prostate > 50 sm3, a significant rise of PCDR increased from 20 to 33.3% in an increase of the puncture number from 6 to 12. In the group of patients with the same PSA level and prostate > 50 cm3 PCDR improves in biopsy from 14, 16 and 18 sites (from 12.1 to 27.7%, 28.5 to 33.3%, respectively). Standard biopsy is insufficient for adequate PCDR, it is necessary to obtain samples of tissue from a large number of sites with puncture of peripheral zone of the prostate. Transrectal biopsy of the prostate according to the extended method improves PCDR, primarily, in local cancer.
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PMID:[An expanded technique of transrectal prostatic biopsy]. 1511 49

Following the studies of Huggins and colleagues in 1941, the hormonal treatment of prostatic cancer has been aimed at neutralizing the influence of testicular androgens through surgical castration or the administration of high dose estrogen. Labrie et al introduced combined use of a LHRH agonist and an androgen antagonist for prostatic cancer. Various reports demonstrated a beneficial effect for combined androgen blockade using nonsteroidal antiandrogens for advanced prostatic cancer through meta-analysis of published randomized control trials. In Japanese status, a combined androgen blockade is popular for advanced prostatic cancer as well as local cancer by J-Cap survey. There is a lot of controversy about adjuvant hormonal therapy for prostatic cancer including intermittent hormonal therapy, but the results are not gotten yet.
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PMID:[Hormonal therapy for prostatic cancer--state of the art]. 1571 83

Despite improvements in treatment of localized prostate cancer, local recurrence remains a significant problem. A total of 46 patients with proven local cancer recurrence following external beam radiotherapy entered a prospective clinical trial using ultrasound-guided cryosurgery to ablate the residual prostate gland. Persistent complications included one urethra-rectal fistula, incontinence (2), retention (3), and treatment induced erectile dysfunction (7). Using the PSA definitions for biochemical failure as PSA>or=0.3 ng/ml, the Kaplan-Meier plots showed the incidence of patients to be free of biochemical recurrence at 51 and 44% at 1 and 2 y, respectively. For a PSA>or=1.0, the values at 1 and 2 y were 72 and 58%.
Prostate Cancer Prostatic Dis 2005
PMID:Role of transrectal ultrasound guided salvage cryosurgery for recurrent prostate carcinoma after radiotherapy. 1598 27

The involvement of alpha(v)beta3 and alpha(v)beta5 integrins in angiogenesis and the use of integrin antagonists as effective antiangiogenic agents are documented. Radiotherapy is an important therapy option for cancer. It has been shown that ionizing radiation exerts primarily antiangiogenic effects in tumors but has also proangiogenic effects as the reaction of the tumor to protect its own vasculature from radiation damage. Here, we show that combined treatment with S247, an Arg-Gly-Glu peptidomimetic antagonist of alpha(v)beta3 integrin, and external beam radiotherapy are beneficial in local tumor therapy. We found that radiation up-regulates alpha(v)beta3 expression in endothelial cells and consecutively phosphorylates Akt, which may provide a tumor escape mechanism from radiation injury mediated by integrin survival signaling. In the presence of S247, the radiation-induced Akt phosphorylation is strongly inhibited. Our studies on endothelial cell proliferation, migration, tube formation, apoptosis, and clonogenic survival show that the radiosensitivity of endothelial cells is enhanced by the concurrent administration of the integrin antagonist. The in vitro data are successfully translated into human glioma (U87), epidermoid (A431), and prostate cancer (PC3) xenograft models growing s.c. on BALB/c-nu/nu mice. In vivo, the combination of S247 treatment and fractionated radiotherapy (5 x 2.5 Gy) leads to enhanced antiangiogenic and antitumor effects compared with either monotherapies. These results underline the importance of alpha(v)beta3 integrin when tumors protect their microvasculature from radiation-induced damage. The data also indicate that the combination of integrin antagonists and radiotherapy represents a rational approach in local cancer therapy.
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PMID:Inhibition of alpha(v)beta3 integrin survival signaling enhances antiangiogenic and antitumor effects of radiotherapy. 1614 31

Cocoa contains many different types of physiologically active components. It was shown that cocoa beans are rich in specific antioxidants such as flavonoids, catechins, epicatechins and proanthocyanidins. Additionally, beta-sitosterol, the most common phytosterol, may play a protective role in the development of cancer. The aim of this in-vitro study was to evaluate the inhibitory effect of different cocoa polyphenols extracts, alone or combined with beta-sitosterol, on two human prostate cancer cell lines (nonmetastatic 22Rv1 cells and metastatic DU145 cells) and a normal human prostate cell line (RWEP-1). A synergy between beta-sitosterol and cocoa polyphenols extract was also researched. Cells were treated independently with five products from 1 to 72 h: (1/) synthetic beta-sitosterol, (2/) a cocoa polyphenols extract supplemented with beta-sitosterol, (3/) three different cocoa polyphenols extracts naturally containing beta-sitosterol. In the experiment, beta-sitosterol was tested from 10(-6) to 10(-3)%; cocoa polyphenols extract supplementation was with 0.72% beta-sitosterol; finally cocoa polyphenols extracts were added to the cells at very low concentrations ranging from 0.001 to 0.2%. The growth and viability of cells were measured using colorimetric assay at 1, 3, 6, 24, 48 and 72 h of treatment. IC50 and IC100 corresponding to the concentration leading to a decrease of 50% and 100% of cell growth were determined. At the highest tested concentration, cocoa polyphenols extracts induced a complete inhibition of growth of metastatic and nonmetastatic cancer cell lines. In addition, cocoa polyphenols extracts were more active against local cancer cells than against metastatic cells. Moreover, at the highest tested concentration, cocoa polyphenols extracts are not effective on a normal prostate cell lines. Beta-sitosterol induced low growth inhibition of both cancer cell line. Cocoa polyphenols extracts, however, were significantly more active and showed a strong and fast inhibition of cell growth than beta-sitosterol alone. No synergy or addition was observed when beta-sitosterol was tested together with the cocoa polyphenols extract. Our results show that cocoa polyphenols extracts have an antiproliferative effect on prostate cancer cell growth but not on normal cells, at the highest tested concentration.
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PMID:In-vitro effects of polyphenols from cocoa and beta-sitosterol on the growth of human prostate cancer and normal cells. 1683 6

Up-to-date statistics on cancer occurrence and outcome are essential for the planning and evaluation of programmes for cancer control. Since the relevant information for 2008 is not generally available as yet, we used statistical models to estimate incidence and mortality data for 25 cancers in 40 European countries (grouped and individually) in 2008. The calculations are based on published data. If not collected, national rates were estimated from national mortality data and incidence and mortality data provided by local cancer registries of the same or neighbouring country. The estimated 2008 rates were applied to the corresponding country population estimates for 2008 to obtain an estimate of the numbers of cancer cases and deaths in Europe in 2008. There were an estimated 3.2 million new cases of cancer and 1.7 million deaths from cancer in 2008. The most common cancers were colorectal cancers (436,000 cases, 13.6% of the total), breast cancer (421,000, 13.1%), lung cancer (391,000, 12.2%) and prostate cancer (382,000, 11.9%). The most common causes of death from cancer were lung cancer (342,000 deaths, 19.9% of the total), colorectal cancer (212,000 deaths, 12.3%), breast cancer (129,000, 7.5%) and stomach cancer (117,000, 6.8%).
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PMID:Estimates of cancer incidence and mortality in Europe in 2008. 2011 97


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