Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the clinical and prognostic value of prostate-specific antigen (PSA) for the detection of tumor and tumor growth after therapy, 520 sera from 246 patients with prostatic carcinoma, 990 sera from patients with BPH, and 1,488 sera from patients with other urological diseases were analyzed. The values ranged from 0.1 to 1,828.9 ng/ml. 51% of all values were about 2.5 ng/ml, and 76.8% of all values about 10 ng/ml. The commercial recommendation for the cutoff values is 2.5 ng/ml (IBL, FRG). In patients with benign prostatic hypertrophy this cutoff means 61% false-positive results, which makes the test highly sensitive but unspecific. In prostatic carcinoma patients this borderline means a false-negative result in 9.75% (24 of 246). By determining the cutoff at 10 ng/ml in our series, a false-negative result appeared in 14.6%. Therefore a plea is made for the 10-ng/ml cutoff. In follow-up studies a marked decline in PSA values after transurethral resection or antiandrogen therapy (orchiectomy/Zoladex/ICI/flutamide, Essex). Generally, the greater the PSA levels the more advanced the stage of disease. These data suggest that PSA may be a useful adjuvant marker for monitoring tumor growth in patients with regionally confined tumor.
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PMID:Prostate-specific antigen in prostatic carcinoma. 169 55

The effects of luteinizing hormone-releasing hormone (LHRH) agonist (Zoladex) treatment on hormone-dependent rat prostate adenocarcinoma (R3327-H) were investigated based on changes in tumor volume and histology. Tumor-bearing rats were treated for 10 weeks with Zoladex in depot preparation by implantation every 2, 4, or 6 weeks. Tumor growth rate was similar in the castrated group and in the rats treated every 2 weeks with Zoladex. This growth rate was significantly slower than in animals treated with Zoladex every 6 weeks and the nontreated group. The growth rate in rats treated every 4 weeks appeared to be faster than that in the castrated animals (not significant). Changes in testosterone levels measured during Zoladex treatment correlated with tumor growth kinetics. Zoladex implantation yields effective and complete androgen deprivation only in the rats with two weekly depot renewal regimen. Tumor histology indicated that the stromal as well as the glandular epithelial cells responded to both castration and to Zoladex treatment. However, in tumors from rats treated with Zoladex every 4 and 6 weeks progressive increasing signs of restoration of normal elements, comparable to non-treated tumors were observed. These results strongly suggest that careful attention has to be paid to the timing of LHRH depot renewal in prostate cancer treatment.
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PMID:Renewal timing of long-acting depot luteinizing hormone-releasing hormone agonist (Zoladex) is critical in the treatment of hormone-dependent rat prostatic carcinoma (R3327-H). 296 Sep 58

Analogs of GnRH, given chronically in a continuous fashion, produce a paradoxic inhibition of pituitary gonadotropin secretion and, consequently, gonadal steroidogenesis. Thus, GnRH analogs are an attractive class of compounds for achieving a medical castration in the treatment of hormone-dependent neoplasms. In a group of 25 premenopausal patients with progressive advanced breast cancer, daily sc administration of 1-10 mg Leuprolide [D-Leu6-Pro9GnRH ethylamide (NEt)] induced objective tumor regression in 44% with a median duration of 9 months. All women treated for at least 10 weeks developed amenorrhea. Profound suppression of gonadotropins, estradiol, and progesterone secretion occurred in all patients on chronic therapy and persisted for the whole treatment period. These effects on tumor growth and ovarian hormone levels are similar to those observed after surgical ovariectomy. Other GnRH analogs such as Buserelin and Zoladex have been found to have similar antitumor and hormonal effects which are also comparable to those produced by surgical ovariectomy. The mode of drug administration is important. Consistent suppression of ovarian function has only been observed with sc injections of the analogs. Chronic intranasal therapy has been found to induce an incomplete suppression of ovarian function in most patients, probably as a result of the poor absorption of these compounds through this route (approximately 2%). Treatment of metastatic breast cancer with GnRH analogs has been associated with remarkable absence of significant toxicity. Despite some evidence in favor of a direct antitumor effect independent of suppression of ovarian function, the use of GnRH analogs in the therapy of advanced breast cancer should be restricted to premenopausal women.
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PMID:Treatment of breast cancer with gonadotropin-releasing hormone. 308 18

Experiments have been performed to clarify whether LHRH agonists might decrease growth of hormone-unresponsive prostate cancer in vivo. Male nude mice were injected s.c. with the human androgen-independent prostate tumor DU 145 cells; osmotic minipumps releasing the LHRH agonist Zoladex (LHRH-A) for 14 days were simultaneously implanted under the skin. Treatment with LHRH-A induced a significant decrease in tumor growth up to the end of the treatment. In subsequent experiment, minipumps releasing LHRH-A were implanted in nude mice either 7 or 14 days after cell inoculation. When the treatment was started 7 days after inoculation of the cells, tumor growth was significantly decreased up to 28 days; thereafter, tumor volume remained lower than in controls, although not significantly. When LHRH-A was administered beginning 14 days after cell inoculation, tumor growth was not significantly affected at any time interval considered. LHRH-A did not appear to induce apoptosis in DU 145 cells, at least on the basis of the apoptotic index and immunohistochemical staining of the p53 protein. On the other hand, treatment with LHRH-A was accompanied by a significant decrease of the concentration of epidermal growth factor receptors in DU 145 prostate cancer specimens. Our results show that the LHRH agonist used significantly inhibits the growth of DU 145 androgen-independent prostate tumor xenografts in nude mice.
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PMID:Growth-inhibitory effects of luteinizing hormone-releasing hormone (LHRH) agonists on xenografts of the DU 145 human androgen-independent prostate cancer cell line in nude mice. 959 Jan 26