PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Prostate Cancer”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources
PubMed1987

Aromatization of androstenedione to estrogen by benign prostatic hyperplasia, prostate cancer and expressed prostatic secretions.

Human prostatic tissue and expressed prostatic secretions (EPS) from patients with benign prostatic hyperplasia (BPH) and prostate cancer were incubated with (1 beta 3H) androstenedione. The extent of aromatization was determined by measuring the transfer of 3H from the 1 beta position into water. The amount of 3H2O recovered corresponds to the estrogens formed. Tissue from 5 patients with BPH yielded 2.13 (+/- 1.05) pmol/mg protein/h while the EPS from the same patients yielded 727 fmol/mg protein/h. In patients with prostate cancer the mean formation of estrogens was 388 fmol/mg protein/h (+/- 75). 4-hydroxy-androstenedione, an aromatase inhibitor, successfully inhibited aromatization in BPH and prostate cancer 53-98%.

Androstenedione↗
PubMed1985

[Reactivation of prostatic cancer and chemotherapy in reactivated prostatic cancer].

From January, 1960 to March, 1984, we studied 65 cases of prostatic cancer resistant to endocrine therapy. Treatment with ifosfamide or combination chemotherapy with vincristine, ifosfamide and peplomycin was performed in some of the 65 cases above mentioned. More cases were systemic reactivation than local reactivation. Poorly differentiated cancer accounted for the majority of the reactivated cancer. Concerning adjacent effects, treatment with ifosfamide was superior to combination chemotherapy. There was no difference between the distant effects of both chemotherapies. The patients with no effects showed predominance of pathologically low differentiated cell type. The 6-month survival rate of patients with chemotherapy was significantly higher than that of patients with other therapies. Toxicities of chemotherapies were leucopenia, digestive disturbances and falling out of hair. Hematuria and pulmonary fibrosis occurred in some cases.

Aged↗
PubMed2004

[GSTP1 CpG island hypermethylation as a molecular marker of prostate cancer].

BACKGROUND: Prostate cancer is the most commonly diagnosed cancer in men in Europe and North America. Despite its high prevalence, the molecular mechanism of its underlying development and progression is poorly understood. Many studies have revealed multiple molecular alterations during prostate cancer carcinogenesis. GSTP1 CpG island hypermethylation is one of the molecular changes that occur during carcinogenesis. METHODS: We evaluated the role of GSTP1 CpG island hypermethylation in prostatic cancers and discussed its possible role as a molecular biomarker of prostate cancer. RESULTS: Studies haven shown that GSTP1 CpG island hypermethylation is present in about 90% of prostatic carcinomas. The DNA alteration was also detectable in body fluids such as blood, urine, ejaculate, or prostatic secretions. One study showed hypermethylation in histologically unsuspicious lymph nodes in surgical specimens in patients with biochemical PSA (prostate-specific antigen) recurrence. Additionally, it is possible to distinguish between normal prostatic tissue, benign prostatic hyperplasia, and prostate cancer. CONCLUSIONS: The detection of GSTP1 CpG island hypermethylation serves as a molecular marker in prostate cancer screening, detection, and diagnosis. It may even provide information on prostate cancer prognosis. However, prospective trials to evaluate its predictive value are necessary.

Acyltransferases↗
PubMed2006

Bisphosphonates for advanced prostate cancer.

BACKGROUND: Prostate cancer is the most common cancer in men in many western countries. It is characterized by its propensity for bone metastases which occur in more than 80% of patients with advanced disease. Patients are at risk of complications including pain, hypercalcaemia, bone fracture and spinal cord compression. Hormonal treatment is the mainstay of treatment for these patients but most of them will then become hormone refractory. Bisphosphonates act by inhibiting osteoclast activities and are a potential therapeutic option for metastatic prostate cancer. In addition, they have been shown to reduce pain in patients with bone metastases as a consequence of multiple myeloma. Early uncontrolled studies of bisphosphonates in metastatic prostate cancer patients have shown encouraging results. OBJECTIVES: The objective of this review was to determine the effectiveness of bisphosphonates in relieving pain in patients with bone metastases from prostate cancer. SEARCH STRATEGY: Studies were identified by electronic search of bibliographic databases including MEDLINE, EMBASE, CancerLit and the Cochrane Controlled Trials Register. Handsearching included Proceedings of American Society of Clinical Oncology and reference lists of all eligible trials identified. SELECTION CRITERIA: Randomised controlled studies comparing the effectiveness of bisphosphonates with placebo or open control for pain relief in patients with bone metastases from prostate cancer. DATA COLLECTION AND ANALYSIS: Data were extracted from eligible studies and included study design, participants, interventions and outcomes. Comparable data were pooled together for meta-analysis with intention-to-treat principle. Outcomes included pain response, analgesic consumption, skeletal events (including pathological fractures, spinal cord compression, bone radiotherapy, bone surgery), prostate cancer death, disease progression, radiological response, PSA response, adverse events, performance status, quality of life and comparisons between different routes, doses and types of bisphosphonates. MAIN RESULTS: One thousand nine hundred and fifty-five patients from ten studies were included in this review. The pain response rates were 27.9% and 21.1% for the treatment group and the control group, respectively, with an absolute risk difference of 6.8%. The OR for pain response was 1.54 (95% CI 0.97 to 2.44, P = 0.07), showing a trend of improved pain relief in the bisphosphonate group, although this was not statistically significant. The rates for skeletal events were 37.8% and 43.0% for the treatment group and the control group, respectively, with an absolute risk difference of 5.2%. The OR for skeletal events was 0.79 (95% CI 0.62 to 1.00, P = 0.05). A significant increase in nausea was observed in patients who received bisphosphonates compared to placebo. No increase in other adverse events was observed. There was no statistically significant difference between the bisphosphonate group and the control group in terms of prostate cancer death, disease progression, radiological response and PSA response. There are insufficient data to guide the choice of bisphosphonates or the dose and the route of administration . AUTHORS' CONCLUSIONS: Bisphosphonates should be considered for patients with metastatic prostate cancer for the treatment of refractory bone pain and prevention of skeletal events. More research is needed to guide the choice of bisphosphonates, optimal treatment schedule as well as cost-benefit comparisons. Combining results from different studies is difficult because different tools were used to assess pain, and also, bisphosphonates vary considerably in potency. This review highlights the need for standardisation and co-ordination among researchers in cancer pain studies.

Bone Density Conservation Agents↗
PubMed1994

The nature of prostate cancer detected through prostate specific antigen based screening.

Prostate specific antigen (PSA) based screening nearly doubles the detection rate of early prostate cancer. However, it is unknown whether the additional tumors detected are medically important. Traditional clinical and pathological features associated with medically important cancer include a palpable tumor, multifocal or diffuse involvement and moderately or poorly differentiated histology. In contrast, microfocal, well differentiated tumors are considered to be possibly medically unimportant. We sought to examine the clinical and pathological tumor stage and tumor grade in 1,169 consecutive men whose prostate cancer was detected during serial PSA based screening protocols involving 24,346 men screened at 6-month intervals. Of the patients 97% had clinically localized (clinical stage T1 or T2) tumors, of which 39% were not palpable (stage T1). Of the men whose cancer was detected through initial screening who underwent surgical staging 69% had pathologically organ confined (pathological stage whose cancer was detected through initial screening pT1 or pT2) disease compared to 74% whose cancer was detected through serial screening (after an initially negative screening). Impalpable, clinically focal, well differentiated minimal tumors were noted in 16% of the men. However, only 3% of the men who underwent surgical staging had impalpable, pathologically microfocal, well differentiated minimal tumors. We conclude that the majority of tumors detected through PSA based screening have the clinical and pathological features associated with medically important prostate cancer.

Aged↗
PubMed1999

Overcoming bcl-2- and p53-mediated resistance in prostate cancer.

Most prostate cancers eventually develop resistance to hormonal therapy and chemotherapies. Many mechanisms for resistance to chemotherapy have been identified. Mutations or inactivation of the p53 suppressor gene and overexpression of bcl-2 are among such mechanisms. Mutations in the p53 gene can lead to resistance to certain chemotherapy agents, and such mutations are seen more often in metastatic than in primary prostate cancers. Thus, agents that are active in the setting of mutated p53 may have some advantage in prostate cancer. Overexpression of bcl-2 occurs frequently in prostate cancer and is associated with both hormonal therapy and chemotherapy resistance. In experimental systems, bcl-2 overexpression occurs after androgen deprivation and transfection of bcl-2 into sensitive cell lines makes them resistant to chemotherapy and hormonal therapies. Bcl-2 can be inactivated by phosphorylation as occurs with taxanes. The retinoids, as a class, can inhibit the growth of resistant cell lines that overexpress bcl-2, and the combination of interferon (IFN) and cis-retinoic acid (CRA) demonstrated increased antitumor activity. In our cell line model the combination of IFN and CRA greatly enhanced the cytotoxicity of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ). Based on these observations, we conducted a phase I/II trial of CRA and IFN-alpha in patients with biochemical recurrence of prostate cancer. Twenty-six percent achieved a decrease of prostate-specific antigen (PSA), which was correlated to elevated serum transforming growth factor-beta. We then conducted a phase I trial of 13-CRA, IFN-alpha, and escalating doses of paclitaxel. Eighteen patients were treated with 1 mg/kg CRA and 1x10(6) unit IFN on days 1 to 4 and paclitaxel at doses from 100 to 175 mg/m2. Eleven patients received the 175 mg/m2 paclitaxel dose. Two patients in the phase I study achieved partial responses (one cervix and one prostate cancer). We subsequently initiated a phase II study of 13-CRA, IFN-alpha, and paclitaxel in hormone refractory prostate cancer. For entry patients must show progressive disease after androgen ablation. To test the mechanism of action, we are assaying peripheral blood monocytes and, when possible, tumor tissue for bcl-2 expression. As our understanding of the mechanisms of tumor resistance to chemotherapy improves, we will be able to design better approaches in treatment targeted to overcome the mechanisms of resistance.

Antineoplastic Agents↗
PubMedDate not supplied

Prostate-specific antigen in prostate cancer.

Prostate-specific antigen (PA) has been evaluated clinically as a tumor marker of prostate cancer with the use of enzyme immunoassay (EIA). For serodetection of prostate cancer, PA was assayed in a total of 1,109 sera. From mean +/- 3 S.D. of normal controls, upper cut-off values in males were decided as 2.5 and 1.2 ng/ml in Americans and Japanese, respectively. Serum PA values in prostate cancer patients were positive in 78% of Americans and 62% of Japanese. However, in benign prostatic hypertrophy (BPH) cases, a high false positive rate of 41% was observed in Americans. Simultaneous assays of serum PA and PAP showed high sensitivity and specificity in the detection of prostate cancer. This antigen could be used, as well as PAP, for monitoring prostate cancer patients. Furthermore, serum PA levels prior to treatment may express to some degree the malignant potential of the cancer. These results suggest that PA may be useful as a tumor marker of prostate cancer.

Acid Phosphatase↗
PubMed2002

Inherited genotype and prostate cancer outcomes.

Prostate cancer is the most commonly diagnosed noncutaneous tumor in North American men and confers significant morbidity and mortality to the general population. The use of screening tools to detect prostate cancer at an early stage may have beneficial effects on an individual's prognosis. However, the intense use of these screening modalities also detects tumors that may have a relatively benign course and for which intensive treatment is not necessary. There is a large body of research that evaluated biochemical, physiological, or somatic genetic measures in relation to prostate cancer progression or prognosis. Environmental exposures may also affect these outcomes. In contrast, inherited markers of genetic susceptibility to prostate cancer have largely been used to predict occurrence of disease rather than disease outcome. The use of inherited genetic markers to evaluate prostate cancer outcome could enhance our ability to identify those men who are more likely to develop clinically significant prostate cancer and to intervene in these men to reduce morbidity and mortality resulting from prostate cancer.

Genetic Markers↗
PubMedDate not supplied

Associations between polymorphisms in the steroid 5-alpha reductase type II (SRD5A2) gene and benign prostatic hyperplasia and prostate cancer.

The prostate gland is an androgen-dependent, and polymorphisms in androgen synthesis gene steroid 5-alpha reductase type II (SRD5A2) may be associated with benign prostatic hyperplasia (BPH) and prostate cancer. We evaluated the association between 3 polymorphisms in the SRD5A2 gene (2 single nucleotide polymorphism: alanine-49 to threonine [A49T] and valine-89 to leucine [V89L], and a (TA)n dinucleotide repeat in the 3' untranslated region), and BPH and prostate cancer within a multiethnic population. Men between 60 and 86 years of age were recruited from annual prostate cancer screening programs and from a large urology clinic. Unconditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (95% CI). We genotyped 606 men (412 Hispanic, 98 Caucasian, 73 African-American, and 23 Asian), of whom 100 had prostate cancer, 393 had BPH (280 symptomatic and 113 asymptomatic), and 113 had normal prostates. Overall, the V89L variant was associated with prostate cancer; the OR for men with the leucine-leucine (LL) genotype compared to men with the valine-valine (VV) genotype was 4.47 (95% CI, 1.24-16.18). This association was stronger in Hispanics (OR=7.26; 95% CI: 1.49-35.47). Although V89L was nonsignificantly associated with BPH in overall population, BPH risk increased significantly with the number of L alleles in Hispanics (P for trend=0.03). Prostate cancer and BPH were not associated with the alanine-49 to threonine single nucleotide polymorphism and the (TA)n repeat. These results suggest that the SRD5A2 gene may play an important role in both BPH and prostate cancer.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1999

Correlation between androgen receptor expression and FGF8 mRNA levels in patients with prostate cancer and benign prostatic hypertrophy.

AIM: To investigate the correlation between androgen receptor expression and fibroblast growth factor 8 (FGF8) mRNA levels. METHODS: 39 human prostate cancers and 14 benign prostatic hypertrophy specimens were examined immunohistochemically for androgen receptor expression and by in situ hybridisation and reverse transcription polymerase chain reaction for FGF8 expression. RESULTS: In 39 tumours there was a statistically significant negative correlation between tumour grade and FGF8 expression and a positive correlation between FGF8 and androgen receptor expression. All 14 benign hypertrophy specimens expressed moderate to high levels of FGF8 and androgen receptor. CONCLUSIONS: Loss of FGF8 may be a factor involved in the development of prostatic cancer.

Fibroblast Growth Factor 8↗
PubMed1994

Prostate-specific antigen in screening of prostate cancer.

Prostate-specific antigen (PSA) is a well-characterized human prostate-specific glycoprotein. PSA has been shown to be the most effective immunohistologic marker for prostate cancer, as well as the most useful serologic test in staging and monitoring prostate cancer and in early detection of recurrent disease. The greatest clinical value of PSA is an aid for early detection of prostate cancer. Recent studies have indicated that PSA-based screening of the older population for organ-confined early-stage prostate cancer is an acceptable, practical, and reliable modality. The accuracy of PSA screening is within the same range as the mammogram. The cost-effectiveness of PSA is comparable to other cancer screening tests. Although the increase in the patient's survival due to PSA-based detection of early prostate cancer remains to be documented, it is generally agreed that the PSA test along with digital rectal examination (DRE) should be included in the annual physical examination for men 50 years of age or older. High-risk men are urged to commence at age 40. Asymptomatic men who have both a negative DRE and normal PSA blood test need only to continue an annual DRE and PSA check-up. Men who have a negative DRE and elevated PSA, and all those who have a suspicious DRE regardless of PSA results, should undergo further diagnostic workup, such as transrectal ultrasonography with biopsy of visible lesions. The cure rate is high with timely treatment, when prostate cancer is detected while still confined to the prostate.

Cost-Benefit Analysis↗
PubMed1993

Formestane. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the management of breast cancer and prostatic cancer.

Formestane (4-hydroxyandrostenedione) is an effective and competitive inhibitor of aromatase, the enzyme responsible for the conversion of androgens to estrone and estradiol. Significant reductions in plasma estradiol levels are observed following intramuscular administration of formestane to postmenopausal women with advanced metastatic breast cancer. Overall response rates to intramuscular formestane in these patients are approximately 25 to 30% and a further 20 to 30% of patients experience disease stabilisation during treatment. Response rates are improved in patients with hormone responsive tumours and in those who have responded to previous endocrine therapy. Soft tissue metastases generally show the best response to formestane treatment while visceral metastases (in particular liver) show a poor response. The median duration of response is usually between 7 months and 1 year. Formestane has been generally well tolerated in the relatively small clinical trials conducted to date with adverse effects reported in approximately 13% of patients following intramuscular administration. The most frequent adverse effects are local reactions at the injection site and systemic effects mainly related to the effect of the drug on the hormonal milieu. Thus, formestane is effective as a second-line endocrine treatment for advanced metastatic breast cancer in women with natural or artificially induced menopause, with apparent tolerability advantages over older agents such as aminoglutethimide; with wider study and experience it may yet challenge tamoxifen as a first-line endocrine therapy in metastatic breast cancer.

Androstenedione↗