Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostatic cancer (PC) is second only to lung cancer as a cause of cancer mortality in men word-wide. In Israel it is the most common cause of cancer mortality in men, after lung cancer and colo-rectal cancer. We screened, for the first time in Israel, for prostatic cancer using serum levels of PSA and a digital rectal examination (DRE). The purpose was not only to diagnose PC but also to increase public awareness of the condition. 300 men in the Haifa area who met statistical criteria for early diagnosis of PC participated. They filled a questionnaire regarding risk factors for PC (age, family history (FH) of prostatic and breast cancer, cigarette smoking, alcohol consumption, previous PSA sampling) and were examined. Those who had out-of-range, age-related PSA values, or a pathologic DRE underwent trans-rectal ultrasound (TRUS) examination and guided biopsy of the prostate. Those with a positive biopsy for PC underwent radical prostatectomy or radiation therapy. 41 (14.3%) had out-of-range, age-related PSA levels and 10 (3.5%) had a pathologic DRE. 39 (13.3%) underwent TRUS and biopsy and 6 (2.04%) had clinically significant PC, all early stages (Gleason 4-6). Correlation between age and PSA has been proven statistically significant (p < 0.05). Symptoms of urinary tract obstruction and nocturia were related to a high PSA (p = 0.035 and 0.002, respectively). Those with PC had at least 1 symptom of urinary tract obstruction; 6 (15.3%) who underwent TRUS and biopsy and a FH of prostate cancer. However, no subject with a FH of PC had biopsy-proven cancer. Those with PC had PSA values from 4.9 to 31.8 ng/ml (9.6 median). Age-related PSA had a positive predictive value of 17.1%. Results of our annual screening for early detection of PC using age-related PSA, and DRE are encouraging: cases detected were clinically significant and treatable. It would appear that screening for PC will result in decreasing the incidence of metastatic cancer and therefore mortality.
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PMID:[Screening for early detection of prostate cancer (first experience in Israel)]. 1124 98

Symptomatic brain metastases of carcinomas in patients without a previously diagnosed malignancy are frequent in neurosurgical series. Such tumors often lack distinctive morphological characteristics so that the routine histological examination can be unsuccessful in identifying the site of origin. Objectives of the present study were to evaluate the frequency of brain metastases as the only manifestation of an unknown primary cancer by the retrospective analysis of a series of consecutively operated single cerebral metastases; to verify the efficacy of clinical investigations in detecting the site of origin; to investigate whether the primary site can be identified by the immunohistochemical study of the neurosurgical specimens. Antibodies to the following antigens were used: carcinoembryonic antigen (CEA), carbohydrate antigen (CA) 19.9, CA 125, BCA-225, cytokeratin 20, PSA, HMB-45. Out of 181 patients operated for single cerebral metastasis of carcinoma, 99 (54.7%) were in patients without any previously diagnosed systemic neoplasm. In 26.7% the primary remained undiagnosed after clinical investigations, in 9 cases even at autopsy. PSA and HMB45 antibodies specifically identified metastases from prostate carcinomas and skin melanomas, respectively. No other specific immunophenotype was identified; the immunoreactivity of the single cases was more or less suggestive for a primary site. Precocious metastases of lung carcinomas expressed CEA more frequently than late metastases. It has been hypothesized that CEA plays some role as a contact mediating device. CEA expression can have some link with the tendency to metastasize precociously to the brain. No major difference of p53 and k-ras expression has been found in precocious versus late brain metastases.
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PMID:Cerebral metastases as first symptom of cancer: a clinico-pathologic study. 1126 7

A 81-year-old man was admitted to our department with the chief complaints of pollakisuria and difficulty in voiding. He presented with increased serum PSA level (over 100 ng/ml). We performed biopsy of the prostate and found a moderately differentiated adenocarcinoma. Various urological examinations showed metastases to paraaortic lymph nodes and systemic bones. He was started-on hormonal therapy. Nine months from the start of hormonal therapy, this therapy was effective and the serum PSA level was decreased to 14 ng/ml. Thereafter, the serum PSA level and the tumor volume were increased and he died 29 months from the start of treatment. The autopsy revealed small cell carcinoma with adenocarcinoma of the prostate.
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PMID:[Small cell carcinoma of the prostate: a case report]. 1128 Aug 83

The management of prostate cancer is based on several clinicopathological criteria. The ability to determine the tumor's biological potential is one goal of tumor markers in order to identify patients who may require more intensive treatment strategies. The purpose of our study was to determine if p21/(WAF1/CIP1) expression can predict biochemical failure in patients with locally advanced prostate cancer treated by radical retropubic prostatectomy (RRP). We used immunohistochemistry to analyze patterns of p21 expression in a population of 296 patients with locally advanced (pT3) prostate cancer treated by RRP. Results were correlated with clinicopathological parameters and time to PSA failure. For the entire cohort of 296 patients, after adjustment for prognostic factors, p21 expression was associated with an increased risk of PSA failure (relative risk [RR] = 1.48) of statistical significance at a median follow-up of 54.5 months. Other parameters that independently predicted the risk of PSA failure included lymph node metastasis and seminal vesicle involvement. Because neoadjuvant hormonal therapy (NHT) is known to lead to involutional changes in prostatic carcinoma, we performed multivariate analyses after stratifying for NHT prior to surgery. Among the 172 patients treated by RRP alone, p21 expression was an independent predictor of PSA failure (RR = 2.30), as were lymph node metastases (RR = 3.19) and pathological grade 5-7 and 8-10 (RR = 2.87 and 3.50, respectively). p21 over-expression is an independent predictor of PSA failure in pT3 patients treated by radical prostatectomy, especially if they did not receive NHT. This tumor marker may help clinicians identify patients who may require adjuvant treatment strategies following radical prostatectomy.
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PMID:Expression of p21 predicts PSA failure in locally advanced prostate cancer treated by prostatectomy. 1130 44

PSA is an oncodevelopmental antigen usually expressed in human tumors with high metastatic potential. Here we set up a metastatic model in nude mice by using TE671 cells, which strongly express PSA-NCAM. We observed the formation of lung metastases when TE671 cells were injected intravenously, intramuscularly, and intraperitoneally, but not subcutaneously. Intraperitoneal injections also induced peritoneal carcinosis, ascites, and liver metastases. To evaluate the putative role of PSA in the metastatic process we used a specific cleavage of PSA on NCAM by endoneuraminidase-N on intraperitoneal primary tumors. Mice with primary intramuscular tumors were taken as control. Repeated injections of endoneuraminidase-N led to a decrease in PSA expression in primary intraperitoneal nodules and ascites but not in intramuscular primary tumors. Endoneuraminidase-N also increased the delay in ascitic formation and decreased the number of lung or liver metastases in the case of intraperitoneal tumors but not in the case of intramuscular tumors. When metastases occurred in endoneuraminidase-N injected animals, they strongly expressed PSA-NCAM. Therefore, we established a relationship between PSA expression on the surface of primary tumor cells and the metastatic process.
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PMID:A nude mice model of human rhabdomyosarcoma lung metastases for evaluating the role of polysialic acids in the metastatic process. 1131 35

Within a few weeks, if therapy of the hormone sensitive, advanced prostate cancer (PCa) is sufficient, there will be a PSA-decrease to testify to the regression of the PCa. Free-PSA (f-PSA) is used for the differential diagnosis of the PCa. Values under 25% f-PSA in proportion to complete-PSA show the possibility of the existence of a Pca. The aim of the work was to study the behavior of f-PSA under hormonal ablation. Initial PSA and f-PSA was examined (RIA) in 76 patients (average age = 72.8 yrs. old) with advanced PCa. (metastases) proven by bone scintigraphy and/or computed tomography. During hormonal therapy (LHRH-agonists) monthly PSA and f-PSA abundance were examined. The percent amount of f-PSA was calculated and documented for at least 6 months. The initial PSA-values were 43.6 +/- 17.3, the f-PSA were 13.4% +/- 8.9. Under antihormonal therapy PSA decreased (while f-PSA increased) and after a period of 1 month the values were 27.4 +/- 14.9 (17.4% +/- 12.3), after 3 months 18.1 +/- 11.3 (24.5% +/- 9.9), after 6 months 7.9 +/- 6.8 (26.1 +/- 10.6). During the 6 months of hormonal ablation PSA-values continuously declined, while, after the first 3 months, f-PSA-values showed a behavior similar to benign hyperplasia of prostate. The therapeutic efficiency of the antihormonal therapy is clearly shown through f-PSA and PSA. There are no timely advantages between the two markers. Further investigations will show whether hormone insensitive PCa can be recognized quicker through f-PSA than from an increase in PSA.
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PMID:The behavior of prostate specific antigen (PSA) and free-PSA (f-PSA) under antihormonal therapy. 1132 55

Eighty-nine patients with progressive prostate cancer despite suppression of testosterone and withdrawal of anti-androgens were studied. This was a relatively advanced population, with 63 of 89 having either osseous metastases (mets) beyond the axial skeleton or visceral mets. Patients were randomly assigned to receive either ketoconazole alone, or ketoconazole with weekly doxorubicin. All patients received replacement hydrocortisone. The primary endpoints were response and survival. Based on PSA reduction criteria (>/= 80% maintained for at least 8 weeks), 14 of 45 patients (31%) in the single-agent ketoconazole arm responded. Sixteen of 44 patients (36%) in the combination ketoconazole/doxorubicin arm responded. There were no important differences between the two treatments in any outcome measure. The median overall survival for all patients was 12.5 months; median time to progression was 3.3 months. Toxicity was significant with both regimens, and more severe in the doxorubicin arm. Fully 20% of patients in each arm discontinued therapy due to intolerable side effects.Each of these regimens is toxic, and produced responses in fewer than half of treated patients. Although the observed median survival does compare favorably with reports from similar cohorts treated in the community, the potential benefit is only modest. In our view, neither of these regimens is sufficiently promising to justify phase 3 evaluation.
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PMID:Randomized phase 2 trial of ketoconazole and ketoconazole/doxorubicin in androgen independent prostate cancer. 1134 1

Circulating Chromogranin A (CgA), total PSA (TPSA) and F-PSA concentrations were measured in 211 patients (pt) with newly diagnosed prostate cancer (PC) and in 25 controls with benign prostatic hypertrophy (BPH). TPSA values ranging 3.5-5.5 ng/ml were found in 14 PC pt (6.6%), 5.5-9.9 ng/ml in 29 pt (13.7%), 10-19.9 ng/ml in 75 pt (35.6%), 20-50 ng/ml in 64 pt (30.3%) and > 50 ng/ml in 29 pt (13.7%). In those groups of PC pt false negative % F-PSA level > 18 was respectively measured in 0 out of 14, 2 out of 29 (6.9%) 6 out of 75 (8.0%), 61 out of 4 (9.4%) and 6 out of 29 (20.7%) pt, or totally in 20 out of 211 (9.5%) pt. Among 20 PC pt with false negative %F-PSA data elevated CgA level (> 80 ng/ml) was found in 18 subjects (18 out of 20 90%) or respectively in 0, 1/2 (50%), 516 (83%), 6 out of 6 (100%) and 6 out of 6 (100%) patients. Bone scintigraphy was performed in all pt with TPSA concentration > 10 ng/ml at the time of diagnosis. Bone lesions were respectively found in 4 out of 75 (5.3%) pt with TPSA 10-20 ng/ml, 12 out of 64 (14%) pt with TPSA level from 20-50 mg/ml and in 25k9 (75.9%) pt with. TPSA above 50 ng/ml. Overall osseous metastases were recorded in 41 out of 211 pt (19.4%) with newly diagnosed PC and in 18 of these Stage D2 pt (43.9%) elevated CgA concentration were measured Among them elevated CgA level and tumor dissemination matched with false negative %F-PSA parameter (> 18%) in 4 out of 18 (22.2%) pt as well as in 37 out of 191 (19.4%) pt with %F-PSA < 18% (p > > 0.05). In parallel, a positive CgA level in newly presented PC pt was closely associated with %F-PSA false negativity (18 out of 20, 90%). A negative correlation between TPSA elevation and the magnitude of CgA serotest level indicate differences in their biological origin and activities. According to the data reported herein we advocate the assessment of serum Chromogranin A concentration in first presented patients with clinically proven PC, elevated T-PSA level and %F-PSA parameter > 18%. Neuroendocrine structures are resistant toward hormonal treatment and hence CgA measurement is strongly suggested in all candidates for a systemic hormone therapy.
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PMID:Cross-correlation of serum chromogranin A, %-F-PSA and bone scans in prostate cancer diagnosis. 1139 14

Prostate cancer has a high propensity to metastasize to bone, which often resists hormone, radiation, and chemotherapies. Because of the reciprocal nature of the prostate cancer and bone stroma interaction, we designed a cotargeting strategy using a conditional replication-competent adenovirus to target the growth of tumor cells and their associated osteoblasts. The recombinant Ad-OC-E1a was constructed using a noncollagenous bone matrix protein osteocalcin (OC) promoter to drive the viral early E1a gene with restricted replication in cells that express OC transcriptional activity. Unlike Ad-PSE-E1a, Ad-OC-E1a was highly efficient in inhibiting the growth of PSA-producing (LNCaP, C4-2, and ARCaP) and nonproducing (PC-3 and DU145) human prostate cancer cell lines. This virus was also found to effectively inhibit the growth of human osteoblasts and human prostate stromal cells in vitro. Athymic mice bearing s.c. androgen receptor-negative and PSA-negative PC-3 xenografts responded to a single intratumoral administration of 2 x 10(9) plaque-forming unit(s) of Ad-OC-E1a. In SCID/bg mice, intraosseous growth of androgen receptor-positive and PSA-producing C4-2 xenografts responded markedly to i.v. administrations of a single dose of Ad-OC-E1a. One hundred percent of the treated mice responded to this systemic Ad-OC-E1a therapy with a decline of serum PSA to an undetectable level, and 80% of the mice with PSA rebound responded to the second dose of systemic Ad-OC-E1a. Forty percent of the mice were found to be cured by systemic Ad-OC-E1a without subsequent PSA rebound or tumor cells found in the skeleton. This cotargeting strategy shows a broader spectrum and appears to be more effective than systemic Ad-PSE-E1a in preclinical models of human prostate cancer skeletal metastasis.
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PMID:A conditional replication-competent adenoviral vector, Ad-OC-E1a, to cotarget prostate cancer and bone stroma in an experimental model of androgen-independent prostate cancer bone metastasis. 1150 44

A 72-year-old man had undergone surgical castration for metastatic prostate cancer (stage D2, the PSA value was 4,300 ng/ml) in September, 1997. He was well clinically for 16 months with undetected level of PSA. However, he presented with general malaise and gross hematuria in May, 1999. After admission to our hospital his condition rapidly deteriorated and he died one week later with respiratory failure. Autopsy revealed extensive involvement of the prostate and bladder by solid tumor with multiple metastases in lungs, liver, spleen, kidneys and bone. Histological examination revealed pure small cell carcinoma of the prostate.
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PMID:[Progression from adenocarcinoma to small cell carcinoma of the prostate during endocrinotherapy: a case report]. 1157 3


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