Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most reliable laboratory test for prostate cancer remains prostatic phosphatase determination. With the spectrophotometric method, however, falsely negative results are to be expected in 40% of stage D lesions. In only one third of patients with localized disease results are correctly positive. This poor specificity and sensitivity can be improved by radioimmunoassay (RIA). Using this technique the prostatogenic isoenzyme is elevated in 50% of stage A and in 80% of stage B carcinoma, suggesting RIA for screening. Erythrocyte sedimentation rate or serum iron and copper are not necessarily of prognostic value. Phosphatase determination of bone marrow aspirates also requires the RIA method if differentiation of stage C and D is to be expected. Serum hormone assays are not yet introduced into routine staging programs. Serum and urinary markers such as CEA, polyamines of LDH isoenzymes are unspecific and of uncertain value in prostatic carcinoma. Measurement of urinary hydroxyproline seems a reliable method for the search of osseous spread; other bone diseases have to be excluded. In patients with prostate cancer laboratory tests still represent adjunctive measures in connection with the clinical diagnostic armamentarium of urologists.
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PMID:[Laboratory tools in the diagnosis of prostatic cancer (author's transl)]. 38 99

Preliminary data are reported from a study of 269 cadmium-nickel battery factory workers and 94 cadmium-copper alloy factory workers. The target group comprises all workers with more than 5 years exposure to cadmium at any time since the factories started production. An internal reference group of 328 alloy factory workers without cadmium exposure was also studied. The expected number of deaths and cancers was calculated with the "life-table" method by using national average incidence rates for men in different age groups and at different calendar years. It was found that among the workers in the battery factory who started work before 1948 there was an increased general mortality in the 1950's mainly due to respiratory disease. The same group had an increased renal disease mortality. There was no increase in general cancer mortality or in general cancer incidence. The risk ratio for nasopharyngeal cancer incidence was 10 (two cases), which was statistically significant. For some other sites like prostate, lung and colon-rectum the risk ratios were also greater than 1 but not statistically significant. In the alloy factory there was a tendency for an increased mortality in prostatic cancer (four cases). After correction for the "healthy worker effect" using the reference group, the risk ratio for prostatic cancer deaths was calculated as 2.4, but this was not statistically significant. The findings in this study support the earlier reports of an association between human cadmium exposure and increased risk for prostatic cancer.
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PMID:Mortality and cancer morbidity among cadmium-exposed workers. 48 34

The effect of hyperthermia was examined on the Dunning prostate tumor model in rats. Hyperthermia was created by heating self-regulating interstitial seeds with an external oscillating magnetic field. The seed alloy was comprised of 70% nickel and 30% copper. One treatment with 50C seeds for two hours did not provide significant delay in tumor growth compared to controls. However, regimens with two treatments separated by either 48 hours or one week did cause significant delay (p = 0.0013 and p = 0.0096, respectively). These results suggest that an interstitial hyperthermia seed may provide an efficacious outpatient therapy for prostate cancer. Further, interstitial hyperthermia may be readily combined with existing radiotherapy with interstitial gold coated seeds to provide additive or synergistic anti-tumor effects.
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PMID:The effect of interstitial hyperthermia on the Dunning prostate tumor model. 155 9

Metal complexes related to the cytotoxic complexes cisplatin [cis-diamminedichloroplatinum(II)] and transbis(salicylaldoximato)copper(II) were incorporated into suitably modified luteinizing hormone-releasing hormone (LH-RH) analogues containing D-lysine at position 6. Some of the metallopeptides thus obtained proved to be highly active LH-RH agonists or antagonists. For instance, SB-40, a PtCl2-containing metallopeptide in which platinum is coordinated to an N epsilon-(DL-2,3-diaminopropionyl)-D-lysine residue [D-Lys(DL-A2pr] at position 6, showed 50 times higher LH-releasing potency than the native hormone. SB-95, [Ac-D-Nal(2)1,D-Phe(pCl)2, D-Pal(3)2, Arg5,D-Lys[DL-A2pr(Sal2Cu)]6,D-Ala10]LH-RH, where Nal(2) is 3-(2-naphthyl)alanine, Pal(3) is 3-(3-pyridyl)alanine, and copper(II) is coordinated to the salicylideneimino moieties resulting from condensation of salicylaldehyde with D-Lys(DL-A2pr)6, caused 100% inhibition of ovulation at a dose of 3 micrograms in rats. Most metallopeptide analogues of LH-RH showed high affinities for the membrane receptors of rat pituitary and human breast cancer cells. Some of these metallopeptides had cytotoxic activity against human breast cancer and prostate cancer cell lines in vitro (this will be the subject of a separate paper on cytotoxicity evaluation). Such cytostatic metallopeptides could be envisioned as targeted chemotherapeutic agents in cancers that contain receptors for LH-RH-like peptides.
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PMID:Highly potent metallopeptide analogues of luteinizing hormone-releasing hormone. 254 6

The purpose of this ongoing study is to determine whether thoracic radiotherapy for lung cancer produces an early increase in serum copper (Cu) concentration, an increase which might predict clinical outcome. Copper and iron concentrations were measured in serum obtained from nonsmall cell lung cancer patients at 0, 1, 2, 4, and 6 weeks after the start of radiotherapy. Control groups included patients irradiated for breast cancer (low dose of radiation to the lung), for endometrial, cervical or prostatic cancer (no dose to lung), and patients with congestive heart failure, pulmonary hypertension, chronic obstructive pulmonary disease (COPD), and cutaneous burns with or without smoke inhalation (no irradiation). Serum Cu concentration increased at least 10 micrograms/dl from the pretreatment level in approximately 75% of the adenocarcinoma and squamous cell lung cancer patients, but in only 1 of 4 undifferentiated lung cancer cases. In virtually all of these responders, serum Cu increased to a maximum at 2 weeks after the start of therapy, then plateaued or decreased slightly despite continuing irradiation. Within the subset of squamous cell lung cancers, there was a direct correlation between the degree of histologic differentiation and both baseline serum Cu concentration and the probability of an early increase therein. In contrast, only 33% of breast cancer patients and 15% of endometrial, cervical and prostate cancer patients exhibited an increase in serum Cu concentration at 2 weeks after the start of radiotherapy. Serum Cu concentration was within normal limits in virtually all patients with congestive heart failure, pulmonary hypertension, and COPD. Burn patients exhibited a significant reduction in serum Cu, although concomitant smoke inhalation increased serum Cu back to low-normal levels. Serum iron concentration did not change significantly in any category of patients. These data suggest that thoracic radiotherapy for well differentiated non-small cell lung cancer is accompanied by an early increase in serum Cu concentration. This increase is partly but not wholly related to lung dose in particular rather than tissue dose in general, and specifically reflects radiation-induced lung injury rather than pneumopathy in general. In lung cancer patients, the change in serum Cu concentration during the first 2 weeks of radiotherapy exhibits a sufficiently broad range (+60 to -13 micrograms/dl) to permit testing this parameter as a predictor of tumor response and pulmonary complications.
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PMID:Serum copper concentration as an index of clinical lung injury. 262 91

Recently, the study of the physiological role of the essential trace elements is being emphasized. Some environmental and disease factors has been demonstrated to perturb trace element homeostasis. A number of recent studies have described alterations in serum copper levels (SCLs) and serum zinc levels (SZLs) in human cancer patients and the relationship between the magnitude of their perturbation and disease activity. This report describes SCLs, SZLs and SCL/SZL ratios in patients with malignant neoplasms of the urogenital tract at various clinical stages and the relationship of the levels of these trace elements to disease activity. According to SCLs before treatment, patients with renal cell carcinoma appeared to be separated into two groups, normal SCL group and higher SCL group. In the higher SCL group, patients generally displayed increased erythrocyte sedimentation rate, CRP, alpha 2 globulin, beta 2 microglobulin, ferritin and CEA. In this group, SCL was a useful index of disease activity. In the normal SCL group, SCLs remained within normal limit even in patients with advanced disease. In renal cell carcinoma, SZLs did not reflect disease activity. In transitional cell carcinoma of the upper urinary tract, patients with metastasis had significantly elevated SCLs and significantly decreased SZLs, compared with normal controls or patients without metastasis. In transitional cell carcinoma of the bladder, no distinct relationships were observed between these trace elements and extent of malignancy. But there was a trend toward increasing SCLs and decreasing SZLs with progressing stage and SCL/SZL ratios fairly reflect stage of disease. Patients with prostatic cancer had nearly normal SCLs and SZLs, although there were a few exceptions. Testicular cancer patients with distant metastasis had significantly elevated SCLs and initially high SCLs decreased in patients responding to therapy and increased again in relapse. SZLs and, hence, SCL/SZL ratios had no relationship to activity of testicular cancer. Currently there is no satisfactory way of following the progress of malignancies of the urogenital tract except prostatic cancer with elevated acid phosphatase and non-seminomatous testicular tumors until the secondary tumor can be detected radiographically. Our study suggests that these trace element might be a useful indicator of disease activity of some of the urogenital malignancies.
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PMID:[Serum copper and zinc levels in patients with malignant neoplasm of the urogenital tract]. 408 94

The semicarbazide-sensitive amine oxidases constitute a group of copper-containing enzymes whose physiological function is unclear. The enzymes are present in various tissues, including blood plasma. At present, the source of the plasma enzyme in humans is not known. Results of a recent study suggested that semicarbazide-sensitive amine oxidase is expressed in the skeleton, e.g. in the spine. Using an indirect autoradiographic method in mice, we provide evidence that semicarbazide-sensitive amine oxidase is present in high abundance in bone tissue. Specific activities of semicarbazide-sensitive amine oxidase were estimated in blood samples from subjects with femoral bone fractures. Moreover, enzyme activities were also measured in patients suffering from prostate cancer with skeletal metastases. The level of specific semicarbazide-sensitive amine oxidase activity in serum was significantly elevated in patients with skeletal metastases compared with both healthy controls and patients having prostate cancer without signs of skeletal metastases. Based on the results of the present study, we propose that semicarbazide-sensitive amine oxidase in blood plasma may originate, at least in part, from the skeleton.
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PMID:Elevated activity of semicarbazide-sensitive amine oxidase in blood from patients with skeletal metastases of prostate cancer. 1036 2

Semicarbazide-sensitive amine oxidases (SSAOs) are widely expressed copper-containing enzymes. One enzyme of this family have high specific activity towards benzylamine and is present in human blood plasma. This enzyme is altered in several diseases, for instance in diabetes. Presently it is unclear where the plasma SSAO is synthesized. Previous autoradiographic studies have suggested that SSAO may be expressed in bone tissue. In the current study we have analyzed levels of SSAO in serum from cases with 'skeletal disease', i.e. patients with severe skeletal metastases of prostate cancer and subjects having recent fractures. Interestingly, subjects with metastases showed significantly elevated levels of SSAO in serum compared to individuals having prostate cancer without skeletal metastases. It is speculated that, at least in part, SSAO in the blood stream may be derived from bone tissue.
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PMID:Is semicarbazide-sensitive amine oxidase in blood plasma partly derived from the skeleton? 1106 Dec 10

Oxidative stress activates the c-Jun N-terminal kinase (JNK) pathway. However, the exact mechanisms by which reactive oxygen species (ROS) activate JNK are unclear. We found that the ability of hydrogen peroxide (H(2)O(2)) to induce JNK activation varied in different cell types. Pyrrolidine dithiocarbamate (PDTC), a presumed antioxidant, induced JNK activation on its own and enhanced JNK activation by H(2)O(2) in many cell types, including Jurkat, HEK293, and LNCaP and Tsu-Pr1 prostate cancer cells. The activation of JNK by PDTC, in the presence or absence of exogenous H(2)O(2), was dependent on its chelating ability to metal ions, most likely copper ions. Despite the strong JNK-activating ability, H(2)O(2) plus PDTC did not induce significant activation of the upstream kinases, SEK1/MKK4 and MKK7. However, the JNK inactivation rate was slower in cells treated with H(2)O(2) plus PDTC compared with the rate in cells treated with ultraviolet C (UV-C). Treatment of H(2)O(2) plus PDTC significantly decreased the expression levels of a JNK phosphatase, M3/6 (also named hVH-5), but not the levels of other phosphatases (PP2A and PP4). In contrast, UV-C irradiation did not cause the down-regulation of M3/6. These results suggest that JNK activation by H(2)O(2) plus PDTC resulted from the down-regulation of JNK phosphatases. Our data also reveal a necessity to carefully evaluate the pharmacological and biochemical properties of PDTC.
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PMID:Down-regulation of the c-Jun N-terminal kinase (JNK) phosphatase M3/6 and activation of JNK by hydrogen peroxide and pyrrolidine dithiocarbamate. 1131 66

We have identified a novel 14-exon human lysyl oxidase-like gene, LOXL4, on chromosome 10q24. The cDNA and derived amino acid sequence of LOXL4 demonstrates a conserved C-terminal region including the characteristic copper-binding site, lysyl and tyrosyl residues and a cytokine receptor-like domain. One of the four N-terminal SRCR domains contains a 13 amino acid insertion encoded by a short exon not present within the closely homologous LOXL2 and LOXL3 genes. The 3.5-kb LOXL4 mRNA is present in pancreas and testis and at lower levels in several other tissues. Fibroblasts, smooth muscle and osteosarcoma (HOS) cells express LOXL4. No expression was detected in HCT-116 and DLD-1 colon, MCF-7 breast and DU-145 prostate cancer cell lines.
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PMID:A novel human lysyl oxidase-like gene (LOXL4) on chromosome 10q24 has an altered scavenger receptor cysteine rich domain. 1169 88


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