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

Data are drawn from the pertinent literature supporting diethylstilbestrol for initial endocrine treatment of advanced prostatic cancer. When diethylstilbestrol is given in a dosage of 2 mg daily, the risk of cardiovascular complications is low. Bilateral orchiectomy is reserved for high-risk patients or those intolerant of estrogen. To prevent possible complications of uncontrolled tumor growth and perhaps to increase survival time, endocrine treatment of advanced prostatic cancer should be started early.
 ...
PMID:Endocrine treatment of prostatic cancer. 686 24

Shessel et al. (Invest. Urol., 17: 529-533, 1980) have reported previously that the serially transplantable Dunning R-3327-G rat prostatic, adenocarcinoma grows faster in intact versus castrated male rats. The present study has demonstrated that this is because the G tumor is composed of androgen-independent but -sensitive prostatic cancer cells. The inclusion that G tumor cells are androgen independent is based upon the observations that these cells are capable of growing following inoculation into castrated male rats and that castration of intact male rats bearing established G tumors induces neither regression of tumor volume nor cessation of the continuous growth of the tumor. The G tumor cells, while being androgen independent, are, however, highly sensitive to androgen for their maximal rate of tumor growth. This androgen sensitivity is demonstrated by the fact that the G tumor cells can be reversibly shifted to a faster or slower growth rate simply by manipulation of the host androgen status. The androgen sensitivity of G tumor growth rate is unusual in that it is not due to androgenic stimulation of cell division but to androgen-induced inhibition of G tumor cell loss (i.e., the rate of G tumor cell loss is reduced by over 50% when androgen is present). The androgen sensitivity of G tumor cell loss is also unusual in that, due to the low level of 5 alpha-reductase activity of the G tumor, the predominant intracellular androgen responsible for this inhibition in untreated intact hosts appears to be testosterone and not dihydrotestosterone (DHT). In castrated rats, however, exogenous treatment with DHT is equally as effective as exogenous testosterone in inhibiting G tumor cell loss. These results suggest that G tumor cells are sensitive to either testosterone or DHT but that in untreated intact hosts little DHT is formed by the tumor cells.
 ...
PMID:Unusual androgen sensitivity of the androgen-independent Dunning R-3327-G rat prostatic adenocarcinoma: androgen effect on tumor cell loss. 709 58

The natural history of prostatic cancer has been regarded as unpredictable for a long period of time. The discrepancy between histologically identifiable (50%) and clinically diagnosed carcinomas (8%) led to the term of 'latent' prostatic cancer and to a considerable diagnostic and therapeutic dilemma. Based on our previous studies showing that biological aggressiveness of prostatic cancer is a direct function of tumor volume and that tumor volume and serum-PSA are proportional, we evaluated two basically different groups of patients. The first group consisted of 43 patients with untreated carcinomas of the prostate followed with serial PSA determinations. The exponential (log-linear) rise in PSA led us to the conclusion of an exponential tumor growth rate. The doubling time of organ-confined tumors was three to four years and became shorter with higher clinical stages and poorly differentiated histological grades. The second group consisted of 139 patients who underwent cystoprostatectomy for bladder cancer and had no evidence for simultaneously identifiable prostatic cancer. In 55 Patients (40%) unsuspected prostatic cancer was found in the specimen; the volume distribution of these carcinomas was exponential. Eleven of the 139 men (7.9%) had a prostatic cancer > or = 0.5 cc, corresponding to the 8%-risk for a man being diagnosed within his lifetime with a clinically significant carcinoma of the prostate. We conclude that the other 44 carcinomas < 0.5 cc will never reach clinical significance due to their small size and their long doubling time; in this sense they can be considered 'latent'.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Natural follow-up of prostate cancer and consequences for early detection]. 750 45

The natural history of prostate cancer has long been regarded as unpredictable. The discrepancy between histologically identifiable (40%) and clinically diagnosed carcinomas (8%) led to the term of "latent" prostate cancer and to considerable diagnostic and therapeutic dilemmas. Based on our previous studies showing that biological aggressivity of prostate cancer is a direct function of tumor volume and that tumor volume and serum PSA are proportional, we evaluated two basically different groups of patients. The first group consisted of 43 patients with untreated carcinomas of the prostate followed with serial PSA determinations. The exponential (log-linear) rise in PSA led us to the conclusion of an exponential tumor growth rate. The median doubling time of clinically organ-confined tumors was 4 years and became shorter with higher clinical stages and poorly differentiated histological grades. The second group consisted of 139 patients who underwent cystoprostatectomy for bladder cancer and had no evidence for simultaneously identifiable prostate cancer. In 55 patients (40%), unsuspected prostate cancer was found in the specimen; the volume distribution of these carcinomas was exponential. These 139 men included 11 (7.9%) who had a prostate cancer with a volume greater than 0.5 cm3, corresponding to the 8% risk for a man being diagnosed within his lifetime with a clinically significant carcinoma of the prostate. We conclude that the other 44 carcinomas, which were less than 0.5 cm3 in volume, will never reach clinical significance because of their small size and their long doubling time; in this sense they can be considered latent.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effect of the natural history on management of adenocarcinoma of the prostate]. 751 16

Since somatostatin analogues have been shown to possess inhibitory activity on prostatic cancer cells in animal models, we studied the clinical effects of the long-acting somatostatin analogue octreotide in the treatment of advanced prostatic cancer. Five patients with metastatic prostatic cancer in relapse under hormonal treatment and with rapidly increasing levels of prostate specific antigen (PSA) received a subcutaneous infusion of octreotide in a dose of 400 to 1,000 micrograms/day for a period of 2 to 6 months. Patients were followed clinically and by monthly measurement of PSA levels. During treatment 3/5 patients showed a temporary halt in rising PSA levels, while another patient had a small decrease. This inhibitory effect however was lost after 1 to 3 months of therapy in 3 patients. The remaining patient died after 4 months before an escape of PSA levels was seen. Side effects consisted of mild diarrhoea in three patients. From this very preliminary data, it appears that octreotide in a dose of 400 to 1,000 micrograms/day may give only a moderate and temporary inhibition of tumor growth in patients with advanced prostatic cancer. Because of the limited effects the study was interrupted prematurely. Since higher doses, other somatostatin-analogues or the combination of LHRH analogues may give better results, further studies are needed to determine the potential therapeutic role of somatostatin-analogues in this group of patients.
 ...
PMID:Octreotide in advanced prostatic cancer relapsing under hormonal treatment. 751 12

The natural history of prostate cancer has been regarded as unpredictable for a long period of time. The discrepancy between histologically identifiable (40%) and clinically diagnosed carcinomas (8%) led to the term of "latent" prostate cancer and to a considerable diagnostic and therapeutic dilemma. Based on previous studies showing that biological aggressiveness of prostate cancer is a direct function of tumor volume and that tumor volume and serum-PSA are proportional, two basically different groups of patients were evaluated. The first group consisted of 43 patients with untreated carcinomas of the prostate followed with serial PSA determinations. The exponential (log-linear) rise in PSA led to the conclusion of an exponential tumor growth rate. The median doubling time of clinically organ-confined tumors was 4 years and became shorter with higher clinical stages and poorly differentiated histological grades. The second group consisted of 139 patients who underwent cystoprostatectomy for bladder cancer and had no evidence for simultaneously identifiable prostate cancer. In 55 patients (40%) unsuspected prostate cancer was found in the specimen; the volume distribution of these carcinomas was exponential. Eleven of the 139 men (7.9%) had a prostate cancer greater than 0.5 cc, corresponding to the 8% risk for a man being diagnosed within his life-time with a clinically significant carcinoma of the prostate. In conclusion, the other 44 carcinomas below 0.5 cc may never reach clinical significance due to their small size and their long doubling time; in this sense they can be considered "latent".(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The diagnostic and therapeutic window for localized carcinoma of the prostate. 752 72

Linomide, a quinoline-3-carboxamide, has the ability to inhibit the growth of prostatic cancer in vivo but not in vitro (T. Ichikawa et al., Cancer Res., 52: 3022-3028, 1992). The reason for this discrepancy is that linomide inhibits tumor growth not directly but indirectly in vivo via its ability to inhibit the angiogenic response induced within the growing prostatic cancer (J. Vukanovic, et al., Cancer Res., 53: 1833-1837, 1993). Tumor associated macrophages can stimulate angiogenesis via their ability to secrete various cytokines, particularly tumor necrosis factor alpha (TNF-alpha). Treatment of rats with linomide decreases significantly (P < 0.05), by more than 50%, the number of tumor associated macrophages within both locally invasive (i.e., from 20-40 to 10 macrophages/high power field) and highly metastatic primary prostatic cancers (i.e., from 60-70 to 15-37 macrophages/high power field). Monocytes/macrophages isolated from linomide treated rats had a decreased ability to secrete TNF-alpha when challenged in vitro with the bacterial endotoxin, lipopolysaccharide [i.e., 702 +/- 76 (SEM) ng of TNF-alpha/10(5) monocytes/macrophages from control versus 401 +/- 2 ng of TNF-alpha/10(5) monocytes/macrophages from linomide treated rats]. In addition, when rats were treated with linomide and than challenged with lipopolysaccharide in vivo, the resulting elevation in serum TNF-alpha was inhibited by approximately 50% (i.e., 4.56 +/- 1.8 ng/ml of TNF-alpha in control versus 2.9-2.2 ng/ml depending upon the dose of linomide). The ability of linomide to decrease monocyte/macrophage secretion of TNF-alpha is not immediate, however, since the secretion of TNF-alpha induced by lipopolysaccharide challenge of monocytes/macrophages isolated from untreated animals is not decreased by acute (i.e., < 4 h) linomide treatment in vitro. These results demonstrate that the ability of linomide to inhibit the secretion of TNF-alpha by monocytes/macrophages requires either additional time or host factors. To test if natural killer (NK) cells might be one of the additional host factors required for the in vivo abilities of linomide, prostatic cancer bearing rats were treated with appropriate antiserum to deplete NK cells and then tested for their response to linomide treatment. These studies demonstrated that the antitumor, antimetastatic, and antimacrophage effects of linomide were unaffected by NK cell depletion.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Linomide inhibits angiogenesis, growth, metastasis, and macrophage infiltration within rat prostatic cancers. 753 63

We used an ultrasensitive prostate-specific antigen (PSA) assay with a detection limit of 0.02 microgram/L for long-term monitoring of PSA changes in 5 patients who were cured by radical prostatectomy and in 10 patients who had failed prostatectomies; 5 patients who underwent cystoprostatectomy were also evaluated with one sample after surgery. Relapse-free periods, determined on the basis of criteria designed specifically for the ultrasensitive assay or proposed for other currently available PSA assays, were calculated for the patients with failed prostatectomies. Tumor-doubling times were also calculated, postsurgery, according to a model that assumes exponential tumor growth over time. We found that prostate cancer relapse, on average, could be diagnosed 420 or 883 days earlier with the ultrasensitive assay than with assays having detection limits of 0.1 or 0.3 microgram/L, respectively. Tumor-doubling times, calculated after radical prostatectomy, ranged from 67 to 568 days among the 10 patients. We also present evidence that even more-sensitive PSA assays might be able to further reduce the relapse-free periods in approximately 50% of the prostate cancer patients who ultimately relapse.
 ...
PMID:Ultrasensitive assay of prostate-specific antigen used for early detection of prostate cancer relapse and estimation of tumor-doubling time after radical prostatectomy. 753 72

Experimental evidence suggests that tumor growth beyond the earliest stages is dependent on angiogenesis, or neovascularization, and that angiogenesis may also promote metastasis. Recent clinical studies demonstrate that angiogenesis is a prognostic marker in breast, lung, and prostate cancer. To investigate whether tumor angiogenesis also correlates with metastasis and survival in early head and neck carcinoma, we quantified the microvascularity of 106 primary carcinomas prior to treatment and correlated the counts with eventual outcome after 3 to 15 years of follow-up. Microvessels were stained immunocytochemically for von Willebrand factor and then counted by light microscopy. Microvessels were counted per 200x and 400x fields, and their density was graded from 1 to 4, in the area of most intense neovascularization. We found that neither microvessel counts nor density grades correlated with metastatic disease, local recurrence, or survival in early head and neck carcinoma. These results are in contradistinction to those recently reported for other tumor sites.
 ...
PMID:Angiogenesis as a prognostic marker in early head and neck cancer. 754 62

The human prostate cancer cell lines, PC-3 (androgen-insensitive) and LNCaP 104-R (androgen-repressed) were inoculated subcutaneously into nude mice to produce prostate tumors. Intraperitoneal injection of green tea (-)epigallocatechin-3-gallate but not structurally related catechins, such as (-)epicatechin-3-gallate, inhibited the growth and rapidly reduced the size of human prostate tumors in nude mice. (-)Epigallocatechin-3-gallate also rapidly inhibited the growth of tumor growth formed by the human mammary cancer cell line MCF-7 in nude mice. It is possible that there is a relationship between the high consumption of green tea and the low incidence of prostate and breast cancers in some Asian countries.
 ...
PMID:Growth inhibition and regression of human prostate and breast tumors in athymic mice by tea epigallocatechin gallate. 758 63


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>