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)

Acid and alkaline phosphatase were determined in 107 breast cancer patients to study their potential value in case of bone metastases. The patients were divided into 4 groups: A, patients without metastases (n = 34); B, metastatic patients without bone lesions (n = 37); C, patients with metastases in and outside of bones (n = 24), D, patients with bone-only metastases (n = 12). Tartrate resistant acid phosphatase (TR-ACP), and bone alkaline phosphatase (bone-ALP) were significantly higher in patients with metastases than in patients without. However, no difference in TR-ACP was observed between subgroups of metastatic patients.
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PMID:Plasma acid and alkaline phosphatase in patients with breast cancer. 206 38

Serum activities of bone alkaline phosphatase (b-ALP) and of tartrate resistant acid phosphatase (tr-ACP) were evaluated in 271 cancer patients; 120 of them had bone metastases (BM) and 151 had none. Correlation coefficients, specificities, sensitivities, negative and positive predicting values were computed. They showed the important contribution that these isoenzymes can bring to the diagnosis of BM in 80 patients with prostate cancer, and to the followup of 191 patients with breast cancer. The assay results were analysed in parallel with bone scan and radiography. They were also compared to those of serum antigens: PSA and PAP for prostate cancer, and CEA and CA15.3 for breast cancer. These results clearly indicate that both isoenzymes are better correlated with BM than antigens, these antigens being markers of the whole tumor burden--primary tumor, metastases, recurrence--whereas b-ALP and tr-ACP are specific markers of bone metabolism.
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PMID:[Evaluation of two serum isoenzyme phosphatases as bone metastasis markers]. 208 Dec 81

Carcinomas of the rat prostate induced by a single injection of N-methyl-N-nitrosourea, 7,12-dimethylbenz(a)anthracene, and 3,2'-dimethyl-4-aminobiphenyl, after sequential treatment with cyproterone acetate and testosterone propionate, were evaluated as potential animal models for prostatic cancer. All ten carcinomas examined were located in the dorsolateral prostate region and did not involve the distal parts of the seminal vesicles and coagulating glands. The incidence of urinary obstruction leading to the animals' death was 6 of 10 rats, and metastases in the lung, abdominal lymph nodes, and/or liver also occurred in 6 of 10 rats. The tumors were invasive adenocarcinomas, showing frequent perineural invasion and a variable degree of differentiation. There were ultrastructural similarities with human prostatic carcinomas, such as intracellular lumina. Plasma acid phosphatase was increased. Enzyme histochemical analysis revealed similarities with the Dunning R3327H and -HI prostatic carcinomas but was not helpful in determining the site of origin of the tumors. The gross and microscopic appearance of the tumors and the observation of preneoplastic lesions exclusively located in the dorsolateral prostate suggest this lobe as site of origin of the carcinomas. Preneoplastic lesions (n = 9) included atypical hyperplasias (n = 5) and lesions with all histological characteristics of carcinoma except for local invasion and metastases, which were classified as carcinoma in situ (n = 4). Although androgen sensitivity could not be assessed, the observed characteristics of the tumors [their long latency time (46-80 weeks), the presence of preneoplastic lesions, and the short duration of the treatment, leaving the animals intact] all indicate that the present approach is a valid animal model for the study of prostatic carcinogenesis.
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PMID:Characterization of adenocarcinomas of the dorsolateral prostate induced in Wistar rats by N-methyl-N-nitrosourea, 7,12-dimethylbenz(a)anthracene, and 3,2'-dimethyl-4-aminobiphenyl, following sequential treatment with cyproterone acetate and testosterone propionate. 210 61

Twenty-nine patients with metastatic prostate cancer progressing after hormonal therapy (orchiectomy 19, diethylstilbestrol 10) and who had never received cytotoxic therapy were treated with carboplatin. Patients had good clinical performance status (66% PS 0,1) and adequate renal (creatinine less than 2.0 mg/dL) and bone marrow function. The standard dose of carboplatin administered was 400 mg/sq m. Seventeen patients received this dose and 12 either 320 mg/sq m or 250 mg/sq m based on reduced renal function or prior radiation. Five patients had bidimensionally measurable disease: one experienced a partial regression of cervical lymph node metastases of 97 days duration. Twenty-four patients had metastatic disease evaluable by clinical status, bone scan and acid phosphatase. In one patient greater than 50% reduction in number of abnormal areas of bone scan uptake occurred; 3 patients experienced improvement in clinical status; in no patient did an elevated prostate acid phosphatase return to normal. All patients entered on study have progressed and died: median time to progression was 94 days (6 to 625 days); median survival was 297 days (6-1152 days). The primary toxicity of carboplatin was myelosuppression. The median WBC and platelet nadirs after cycle one were 3150/cu mm and 93,000/cu mm, respectively. Dose escalations to grade 2 or greater myelosuppression were mandated. Twenty-six achieved at least grade 2 myelosuppression during carboplatin treatment. We conclude that carboplatin administered at this dose and schedule has no important activity in hormone refractory prostate cancer.
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PMID:A phase II trial of carboplatin (NSC 241240) in advanced prostate cancer, refractory to hormonal therapy. An Eastern Cooperative Oncology Group pilot study. 219 2

We report a case of clear cell adenocarcinoma arising in a paraurethral duct treated by anterior pelvic exenteration. Immunohistochemical stains for prostate specific acid phosphatase and prostate specific antigen were positive in the primary tumor and regional metastases. Focal positive staining also was noted in normal paraurethral duct epithelium. Our observations suggest that clear cell adenocarcinoma arises from the female paraurethral ducts, rather than embryonic remnants. These ducts appear to be homologous to the prostate and in some cases may be misinterpreted as urethral diverticula.
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PMID:Clear cell adenocarcinoma of the urethra: evidence for origin within paraurethral ducts. 229 40

Rectal involvement from prostate cancer occurs in 1.5-11% of cases. A rarer presentation is that of a separate metastasis to the high rectosigmoid colon causing an annular stricture. We present our experience with six such cases who presented with gastrointestinal symptoms. Two of the cases had undergone intestinal resections. All 6 patients had radiographic evidence of an annular stricture in the rectosigmoid area. Retrospective review revealed evidence of metastatic disease in all cases in the form of abnormalities in one or more of the following: intravenous urography, radionuclide bone scan, liver spleen scan, acid phosphatase, or alkaline phosphatase. The mean survival was 9.3 months. This rare presentation of prostate cancer may be difficult to distinguish from primary colorectal cancer and therefore needs to be ruled out to avoid intestinal resections.
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PMID:Separate annular strictures of the rectosigmoid colon secondary to unsuspected prostate cancer. 231 6

Pelvic lymphadenectomy is the final staging procedure before institution of therapy for patients with clinically locally confined adenocarcinoma of the prostate, a normal acid phosphatase, and a bone scan free of metastatic disease. The pathologic information it provides cannot be accurately acquired at the present time by any other method. Extraperitoneal lymphadenectomy is associated with some morbidity intraoperatively and in the early postoperative period. We enumerate our results with 284 extraperitoneal lymphadenectomies.
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PMID:Intraoperative and early complications of staging pelvic lymph node dissection in prostatic adenocarcinoma. 231 85

Endocrine-Paracrine cells (EP cells) in prostatic carcinomas were screened by immunohistochemical tests for neuron specific enolase, chromogranin, and serotonin and by Grimelius method. Formalin fixed, paraffin-embedded sections from 60 prostatic carcinomas were used. EP cells were detected in 16 cases (27%). The number of EP cells in hormone independent prostatic carcinomas were significantly larger than hormone dependent (p less than 0.05) and latent prostatic carcinomas (p less than 0.01). Five cases of prostatic carcinomas with abundant EP cell proliferation died of widespread metastases within 4 years, irrespective of hormone treatment. The pathologic finding was classified into the category of adenocarcinoma, partly showing carcinoid or small cell carcinoma-like features. EP cells were found in perineural invading cancer cells and also immunoreactive to both prostate specific antigen and prostate specific acid phosphatase. It is suggested that the proliferation of EP cells in prostatic carcinomas is related with the sensitivity to hormone treatment.
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PMID:[Expression of endocrine-paracrine cells in prostatic carcinoma]. 240 10

Metastases of 47 known prostatic carcinomas were subjected to the unlabeled immunoperoxidase procedure to localize prostate acid phosphatase (PAP) and prostate-specific antigen (PSA). PAP was found in 64% and PSA in 78% of bone marrow, lymph node, lung and liver metastases investigated. There was no significant difference between the intensity of staining in primary and metastatic neoplasms. Staining of PAP and PSA was found to be less intense in poorly differentiated metastases of prostatic adenocarcinomas. The data suggest that the demonstration of PAP and PSA is a practical and sensitive test for determining the prostatic origin of a clinically and histologically unclassifiable metastasis.
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PMID:Immunohistochemical diagnosis of the metastasizing prostatic carcinoma. 240 95

Macrophages were isolated by adherence from tumors produced by a number of murine mammary carcinoma lines and were examined by fluorescence-activated cell sorting for quantitation of leucine aminopeptidase and acid phosphatase. The tumors included three lines, 66, 67, and 168, which were originally derived from a single, spontaneously arising tumor in a BALB/cfC3H mouse and two other lines, D2A1 and D2F2, which were derived from a single tumor arising from the transplantable hyperplastic alveolar nodule line, D2. These five lines differ from one another in a number of characteristics, including the ability to metastasize spontaneously to the lung from subcutaneous implants and to form experimental metastases in lungs following intravenous injection. Line 67 is nonmetastatic under both circumstances, whereas lines 66, D2A1, and D2F2 are metastatic under the same conditions. Intermediate to these is line 168, which is nonmetastatic from the subcutaneous site but capable of colonizing the lung with an efficiency similar to 66 when injected IV. Tumor-associated macrophages (TAM) from lines 66, D2A1, and D2F2 contained the greatest amounts of leucine aminopeptidase (LAP) and those from line 67 the least, with TAM from 168 being intermediate. Conversely, the TAM from line 67 had the greatest amounts of acid phosphatase (APTase) and those from line 168 the least. In addition to differences among tumors in enzyme levels of the adherent TAM, the precentages of TAM that were adherent were also different among the tumors. Only 12% of TAM from line 67 were recovered in the adherent fraction as opposed to 35-38% of TAM from lines 66 and 168. These results confirm and extend our previous findings that TAM from metastatic tumors have increased levels of LAP compared to TAM from nonmetastatic tumors. They also demonstrate noncoordinate expression of LAP and APTase in TAM, and illustrate how a population of TAM can be homogeneous for one enzyme and heterogeneous for another. Furthermore, the difference in the percentage of macrophages that are adherent between metastatic and nonmetastatic tumors is another indication both of the heterogeneous nature of TAM and of the role of a tumor in determining the type of host infiltrate with which it is associated.
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PMID:FACS quantitation of leucine aminopeptidase and acid phosphatase on tumor-associated macrophages from metastatic and nonmetastatic mouse mammary tumors. 241 52


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