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)

Androgen binding (cytosol and nucleus) was measured in tissue obtained from 223 untreated patients with proven prostate cancer (199 primary tumor, 24 malignant lymph nodes), 19 patients with hormone refractory cancer, and 46 patients with benign prostatic hyperplasia (BPH). The mean binding in both the cytosol and nucleus was significantly higher for patients with cancer than for those with BPH. Binding appeared to correlate with tumor stage. Androgen binding in malignant nodes can differ from that in the primary tissue and can vary from node to node in the same patient. Results obtained from an assay using a single saturating concentration of R1881 correlated well with those calculated from a full six-point Scatchard analysis when an adequate amount (500 mg) of tissue was available. However, binding results obtained from a single-point analysis performed on needle biopsy specimens (about 50 mg) obtained before complete surgical removal of the prostate correlated poorly with those derived from a full six-point analysis performed on tissue (500-1000 mg) removed from the center of the malignancy. Androgen binding in nuclear extracts of histologically benign tissue adjacent to the malignancy was significantly higher than in nuclear extracts of BPH tissue. Cytosolic androgen binding in tissue removed from patients who were refractory to hormonal therapy was higher than in tissue from untreated cancer patients. The binding of estradiol by extracts of benign and malignant prostate tissue was low or absent and, thus, did not appear to be a significant phenomenon.
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PMID:Androgen receptor binding activity in human prostate cancer. 257 85

Patients with bulky prostate cancer have usually been treated by palliative measures because the likelihood of tumor control with definitive irradiation has been low and the development of distant metastases high. The addition of estrogen to irradiation has not been shown to be of value. However, we believe the method of estrogen administration may have been the cause for the apparent lack of benefit. Estrogen had been started either concurrent with irradiation or had been used for palliation and was given for long and unscheduled time periods prior to irradiation. We have used estrogen for two months prior to and concurrent with irradiation. We postulated that in those patients with estrogen responsive cancer, the reduced tumor burden prior to irradiation could enhance tumor control and survival. Between 1975 and 1980, 25 patients with bulky prostate cancer received sequential estrogen and irradiation, 12 patients irradiation alone and six patients irradiation after having become refractory to long-term estrogen use. One patient was lost to follow-up. Eighteen of 25 (72%) treated by sequential estrogen and irradiation, 14/17 (82%) with estrogen responsive cancer and 4/8 (50%) with estrogen resistant cancer had a complete tumor response. Six of 11 (55%) patients treated by irradiation alone and 2/6 (33%) treated by irradiation for estrogen refractory cancer had a complete tumor response. Disease-free survival was observed in 13/25 (52%) treated by sequential estrogen and irradiation, and 8/17 patients (47%) with irradiation. It is also possible the improved survival in the estrogen responsive group was a direct result of improved local control. Persistent local disease can act as a source for distant metastases. Distant metastases was observed in 15% of patients when the primary tumor was controlled and 30% when there was persistent or recurrent local disease. Also, progressive local disease can be an important cause of death. This was most evident in our patients with estrogen refractory cancer. Almost all patients in this group had progressive local disease that caused serious urinary bleeding and urinary infection that were considered the major cause of death. Our results suggest bulky prostate cancer should be aggressively treated when first diagnosed. The value of adjunct estrogen is unproven. Our results with the use of estrogen prior to and concurrent with irradiation is encouraging. Estrogen may shrink the cancer and allow for a more favorable geometry for external irradiation. Tumor control and survival may be thereby improved.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Improved control of bulky prostate carcinoma with sequential estrogen and radiation therapy. 674 58

The response of bone metastatic lesions to endocrine therapy was assessed by repeated magnetic resonance imaging (MRI) and an isotope bone scan after an average period of 7.0 months (2-10 months) in 12 patients with prostate cancer. MRI used both T1-weighted spin echo technique and short TI IR (STIR) sequence. Of 7 patients with hormone-dependent cancer, the bone metastatic lesions resolved or became vague in all patients on STIR image, while in only 4 and 3 on T1-weighted image and bone scan, respectively. Of 5 patients with hormone-refractory cancer, the lesions progressed on both MRI and bone scan in all patients except one who had initially had diffusely metastatic lesions of systemic bone. The results indicate that STIR image of MRI is helpful for the therapeutic evaluation of bone lesions.
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PMID:[Magnetic resonance imaging for the evaluation of prostate cancer metastatic to bone]. 763 42

The first clinical trial of high-energy shock wave (SW) combined with chemotherapy to treat metastasis of prostate cancer in the internal iliac muscle was conducted. The patient, a 57-year-old man, diagnosed as having mucin-producing, poorly differentiated adenocarcinoma of the prostate invading the bladder wall, had been treated by total cystoprostatectomy. Five months later, metastatic tumors were found in the left axillar subcutaneous tissue and the right internal iliac muscles. For the axillar metastasis we performed radiation and left subclavicular arterial infusion of cisplatin 70 mg, THP-adriamycin (THP) 50 mg and methotrexate 50 mg. For the right internal muscular metastasis, 10,000 to 20,000 shots of SW and simultaneous intravenous injection of carboplatin 100 mg and THP 10 mg were carried out. Neither of the tumors decreased in size, but on magnetic resonance images, the SW-treated tumor exhibited a central low-intensity area. The SW-treated tumor was resected and central necrosis and a collection of mucin in the central area were observed. Hormone-resistant prostate cancer is well-known to be a multidrug-resistant tumor. It is noteworthy that SW and chemotherapy induced necrosis in such a refractory cancer without any significant side effects.
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PMID:High-energy underwater shock wave treatment for internal iliac muscle metastasis of prostatic cancer: a first clinical trial. 779 Mar 15

Increasing evidence suggests that growth of the prostatic tissue is regulated by a network of hormones and growth factors, in which androgens play the prominent role. Hormonal manipulation remains the core of treatment for locally advanced and metastatic prostate cancer. Achievement of a complete androgen blockade, by surgical or medical means or a combination of both, offers superior results in palliative management of advanced disease. Management of hormonal refractory cancer, however, remains a challenge to clinicians.
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PMID:Endocrine therapy of advanced carcinoma of the prostate. 842 33

Strontium-89 chloride (Metastron) is an FDA-approved treatment for palliation of cancer pain. We evaluated blood count changes and pain relief in 28 patients with widespread painful bony metastasis treated with strontium-89 at the University of Minnesota Hospital and Clinics. Eighteen patients had prostate cancer (all hormone-refractory cancer), seven patients had breast cancer, and three patients had lung cancer, all previously treated with either radiation, chemotherapy, or a combination of the two. Serial blood counts were performed weekly up to 8 weeks and at 12 weeks after administering Metastron. Pain scale and blood values were monitored simultaneously. The mean baselines of hemoglobin (Hgb), white blood count (WBC), and platelets (Plts) were 11.4, 5900, and 258,000, respectively. The mean dose of Metastron was 3 mCi (range 2.2-4.4). The median time (range) to nadir was about 6 weeks. The percentage reductions relative to baseline were 32% (range 0-72%) for WBC; 14% (range 0-50%) for Hgb; 15% (range 0-47%) for the red blood cell (RBC) count; and 40% (range 0-85%)for Plts. We did not find a close relationship among the baseline blood count, reduction of subsequent blood counts, or previously irradiated active bone marrow volume. The median time of survival was 23 weeks (range 2-66 weeks). At 12 weeks, 29% of patients had moderate to dramatic improvement of pain, 32% had some relief of pain, and 50% had no improvement in pain. Thirty-two percent of the treated patients required additional palliative external beam radiation to their bony lesions within the study period. Our results show that Metastron for palliation for bony metastases should be used with caution because of moderate to severe bone marrow toxicity, especially in platelets, associated with its use. Careful evaluation of patients given Metastron is needed to assess accurately its full benefit.
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PMID:Strontium-89 chloride (Metastron) for palliative treatment of bony metastases. The University of Minnesota experience. 861 Jun 30

Urological complications, essentially bladder outflow obstruction and hydronephrosis, are caused by the local extension and lymphatic spread of prostate cancer. Although bladder outflow obstruction is a very common finding at diagnosis, results from clinical studies have revealed that it is not a prognostic factor for response to androgen blockade. Hydronephrosis has been shown to have an independent prognostic value for progression after hormonal treatment and correlates also with time to death from prostate cancer. Furthermore, persistent or newly developed hydronephrosis during treatment also predicts a shorter time to progression. The incidence of bladder outflow obstruction is significant in advanced prostatic cancer and may be a source of morbidity, which will impact on the patient's quality of life. Decompression of ureteric obstruction in hormone-refractory cancer decreases the length of hospital stay, thereby improving quality of life. Finally, hydronephrosis, but not bladder outflow obstruction, can be considered to be an independent prognostic variable for the response to androgen blockade. This paper reviews the incidence of urethral and ureteric obstruction in patients with advanced prostate cancer, evaluates the prognostic significance of these urinary complications and discusses the therapeutic strategies available for treating patients with this disease.
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PMID:Influence of urological complications on the prognosis of prostate cancer. 910 Dec 11

Radical prostatectomy is indicated in patients with an estimated life expectancy of 10 years and with organ defined cancer disease (T1b-T2, No, Mo). Radiotherapy is an effective alternative treatment, especially in patients with an increased comorbidity. Primary hormonal treatment is not indicated for organ-defined cancer. Prognosis of patients with locally advanced prostatic carcinoma (T3,NO,MO) is poor because of micrometastases; tumour progression will occur in 75% of patients independent of local therapy. Orchiectomy or LH-RH treatment is option of first choice in metastatic prostate cancer disease. There is no need for complete androgen deprivation. Ongoing trials measure the effect of intermittant androgen deprivation. Intention for treatment of hormone refractory cancer is improvement of quality of life. Cancer-related symptoms are pain caused by bone metastases, lymphoedemas and urinary retention. Therapeutic options are monochemotherapy, hormonal treatment, analgetic treatment besides palliative radiotherapy.
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PMID:[Therapy of prostate carcinoma. Age, general health status and stage determine choice of therapy]. 1078 86

Suramin has been shown to have an effect on bone resorption in in vitro models. It is not clear if a similar effect is seen in patients treated with suramin. The clinical effect of suramin treatment on total serum calcium was examined in two groups of patients with hormone-refractory prostate cancer. In all, 28 patients in group 1 were examined within 2 weeks before and 2 weeks after suramin treatment and 72 patients in group 2 were examined within 2 weeks before, during, and after treatment with suramin. In addition, calcium controls spiked with suramin were run in three different commercially available assays for evaluation of the effect of suramin dose on calcium determination. Group 1 patients showed a decrease in serum calcium after treatment with suramin. The mean uncorrected serum calcium level was 2.29 +/- 0.025 mmol/l before treatment and 2.09 +/- 0.025 mmol/l after treatment (P < 0.0001, paired Wilcoxon test). The mean serum calcium value corrected for albumin was 2.33 +/- 0.02 mmol/l before treatment and 2.24 +/- 0.02 mmol/l after treatment (P = 0.0022, paired Wilcoxon test). Group 2 patients also displayed a decrease in serum calcium after treatment with suramin. The mean baseline value was 2.23 mmol/l (median 2.26 mmol/l, range 1.20-2.54 mmol/l). The mean level of serum calcium corrected for albumin as determined at the end of treatment was 2.14 mmol/l (median 2.16 mmol/l, range 0.98 2.46 mmol/l). In all, 48 patients for whom pre- and post-treatment values were available for analysis displayed a median calcium decrease of 0.09 mmol/l (P = 0.0005, Wilcoxon signed-rank test for the null hypothesis of no change). For 68 patients in group 2, data on serial serum calcium measurements during treatment were available for analysis. A projected median decrease in serum calcium of 0.06 mmol/l (range 0.43 to 0.72 mmol/l) over an 8-week interval of suramin therapy was found. Overall, 47 of the 68 slopes were negative (P = 0.0022, Wilcoxon signed-rank test). Nine patients were treated with suramin for less than 6 weeks. These patients' calcium levels were significantly higher than those of 50 patients treated for longer periods (median value 2.24 versus 2.16 mmol/l, P = 0.035, Wilcoxon rank-sum test). No correlation was found between suramin dose and calcium level using the Kodak Ektachem, Hitachi 914, or Synchron Clinical System CX3 method. In conclusion, suramin treatment was consistently associated with decreases in serum calcium in two groups of patients with hormone-refractory cancer. Suramin placed in calcium controls did not affect calcium determination using three commercially available methods.
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PMID:Suramin administration is associated with a decrease in serum calcium levels. 1120 56

Although prostate cancer initially responds well to endocrine therapy, it becomes resistant to the therapy a few years later, and is called hormone-refractory cancer. In general, hormone-refractory prostate cancer is resistant to all kinds of therapy and the prognosis is extremely poor. Here we report an unusual case of a person with hormone-refractory prostate cancer, who has been surviving for more than 5 years after being diagnosed as having this type of cancer. A 75-year-old man was diagnosed with prostate cancer (poorly differentiated adenocarcinoma, T3 N0 M1, stage D2) and initial endocrine therapy combined with castration and estrogen was effective. Four years later, the tumor marker of prostate-specific antigen (PSA) increased and the cancer was thought to be hormone-independent, refractory state. Alteration of antiandrogen from chlormadinone acetate to flutamide was effective and PSA was kept at low levels for 6 months. When PSA rose again, we started oral chemotherapy with tegafur.uracil. PSA decreased to normal range (complete response) and remained stable for 10 months. After that, a rapid increase of PSA was controlled for 7 months by oral chemotherapy with estramustine phosphate sodium and VP-16. This case indicates that alteration of antiandrogens or oral chemotherapy may be useful in some cases with hormone-refractory prostate cancer.
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PMID:[Long-term survival of hormone-refractory prostate cancer: a case report]. 1127 41


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