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Biomedical subjects

K Akakura

Publications and source records attributed to K Akakura.

At least 91 records · Page 5Linked to original sources
PubMed1994

[The course and limitation of medical treatment for benign prostatic hyperplasia].

To clarify the effects and limitation of medical treatment for benign prostatic hyperplasia (BPH), 2,476 patients with BPH were analyzed in terms of symptoms, objective findings, treatment modality and whether surgery was required during the course of medical treatment. As initial therapy, 1,320 cases (53.3%) were treated with medicine and 783 cases (31.6%) underwent surgery. In the group of patients initially treated with medicine, 264 cases (20.0%) required surgery and most operations were performed within six months from the start of medical treatment. Those who required surgery had a larger prostate and more residual urine than those who continued medical treatment. This tendency was also observed in the patients treated with antiandrogen. Therefore, medical therapy might be inappropriate to treat the patients with more than 50 ml of residual urine or significantly large prostate such as goose egg sized or larger. In conclusion, medical treatment possessed potential usefulness for the management of BPH, however, there seemed to be limitation of the effects of medical treatment.

Adult↗
PubMed1994

[Measurement of serum prostatic acid phosphatase (PAP) by Delfia PAP Kit using europium and clinical evaluation in patients with prostate cancer].

Fundamental and clinical studies of serum prostatic acid phosphatase (PAP) detected by a Delfia PAP kit were performed. The system is a time-resolved fluoroimmunoassay using europium as a tracer. The lower limit of detection was 0.2 ng/ml. Sera from 54 patients with prostate cancer, 20 with benign prostatic hypertrophy, 20 with urological malignancies other than prostate cancer and 140 adult males over 46 years old were determined. From the mean + 2 S.D. of serum PAP values obtained on the adult males, 1.5 ng/ml was considered as the upper normal level of adult males. By calculating the efficiency and ROC curve using the PAP values of prostate cancer and benign prostatic cancer, 2.5 ng/ml was decided as a cut-off value of this kit. The positive rates of adult males, prostate cancer, benign prostatic cancer and urological malignancies other than prostate cancer were 0.7%, 65%, 20% and 10%, respectively. The sensitivity of stage A2, B2, C and D1 + D2 was, 0%, 0%, 64% and 83%, respectively. The efficiency of the Delfia PAP kit was 52% and that of the Markit M PA kit was 71%. The correlation between the values assayed with the Delfia PAP kit and the Dinabot PAP kit was very high; the value obtained with the Delfia PAP kit was about 80% of that obtained with the Dinabot PAP kit.

Acid Phosphatase↗
PubMed1993

Luteinizing hormone-releasing hormone agonists in prostate cancer. Elimination of flare reaction by pretreatment with cyproterone acetate and low-dose diethylstilbestrol.

BACKGROUND: In response to the first administration of a luteinizing hormone-releasing hormone (LHRH) agonist, the secretion of pituitary gonadotropin increases sharply and gives rise to a transient surge in the concentration of serum testosterone. This effect reaches a peak 4 to 7 days after the start of therapy and results in the onset of clinical symptoms and signs of tumor flare in 5% to 10% of patients. METHODS: To determine whether the effects of the LHRH-induced flare reaction are preventable, cyproterone acetate (100 mg) and low-dose diethylstilbestrol (0.1 mg) were administered daily for 4 weeks to inhibit the pituitary before the initiation of therapy with a depot LHRH agonist, goserelin acetate (3.6 mg every 4 weeks). Diethylstilbestrol was stopped after 8 weeks to eliminate associated minor toxicity while administration of cyproterone acetate was continued to suppress vasomotor symptoms. Twenty-four men with histologically confirmed prostate cancer were enrolled in the study: 6 with Stage C, 2 with Stage D1, and 16 with Stage D2 disease. RESULTS: Lead-in therapy reduced the concentration of serum testosterone into the castrate range within 1 week, and no significant change was observed in the mean level after administration of goserelin acetate. Neither was there an effect on the initial rate of normalization of serum prostate specific antigen (PSA); normal PSA values were obtained in 50% of patients after 10 weeks and in 70% after 32 weeks. In the subgroup of patients with Stage D2 disease, longer median survival was predicted by a normal serum PSA, either stable or decreasing, after 32 weeks of treatment. The regimen was well tolerated with a low incidence of hot flushes. CONCLUSIONS: These results imply that in the absence of LHRH-induced tumor flare, prognosis is related to the ability of therapy to maintain a PSA nadir in the normal range.

Acid Phosphatase↗
PubMed1993

Effects of intermittent androgen suppression on androgen-dependent tumors. Apoptosis and serum prostate-specific antigen.

BACKGROUND: Since postcastration progression of tumors to an androgen-independent state appears to be linked to the cessation of androgen-induced differentiation of tumorigenic stem cells, the authors hypothesized that the replacement of androgens at the end of a period of apoptotic regression might result in the regeneration of differentiated tumor cells with further apoptotic potential. METHODS AND RESULTS: To determine the effect of intermittent exposure of androgens on the androgen-dependent Shionogi carcinoma, the tumor was transplanted into a succession of male mice, each of which was castrated when the estimated tumor weight became about 3 g. After the tumor had regressed to 30% of the original weight, it was transplanted into the next noncastrated male. This cycle of transplantation and castration-induced apoptosis was repeated successfully four times before growth became androgen-independent during the fifth cycle. In four of Stage C and three of Stage D patients with prostate cancer, androgen withdrawal was initiated with cyproterone acetate (100 mg/d) and diethylstilbestrol (0.1 mg/d) and then maintained with cyproterone acetate in combination with the luteinizing hormone-releasing hormone agonist, goserelin acetate (3.6 mg/month). After 6 or more months of suppression of serum prostate-specific antigen (PSA) into the normal range, treatment was interrupted for 2 to 11 months. After recovery of testicular function, androgen-withdrawal therapy was resumed when serum PSA increased to a level of about 20 micrograms/l. This cycle was repeated sequentially to a total of two to four times over treatment periods of 21 to 47 months with no loss of androgen dependence. CONCLUSIONS: These results demonstrate that intermittent androgen suppression can be used to induce multiple apoptotic regressions of a tumor; they also suggest that the cyclic effects of such treatment on prostate cancer can be followed by the sequential measurement of serum PSA levels.

Adenocarcinoma↗
PubMed1991

[Response to chemotherapy in endocrine therapy-relapsed and -resistant prostate cancer].

Effects of chemotherapy to endocrine therapy (castration with estrogen/antiandrogen)-relapsed (24 cases) or endocrine therapy-resistant (14 cases) prostate cancer were compared. Pretreatment clinical stages in these groups were stage D1 (3 cases) and D2 (35 cases). Regimens of chemotherapy in this study were as follows: cis-platinum (CDDP) (1 case), phosphamide (3 cases), combination of vincristine, phosphamide and peplomycin (5 cases), combination of cyclophosphamide, adriamycin (ADM) and CDDP (8 cases) and combination of phosphamide, ADM, and CDDP (21 cases). Response to chemotherapy and subsequent survival in these two groups were examined. When evaluated at 3 months after the start of the chemotherapy, partial response and stable cases were 50% and 36% in endocrine therapy-relapsed and -resistant groups, respectively. Because the worse performance status contained more cases in the endocrine therapy-resistant group, the response was compared at the same base of performance status, and the response was almost equal in the two groups. Survival in the endocrine therapy-relapsed group was better than that in the therapy-resistant group. When compared at the same base of performance status, the difference in survival time between the two groups was not evident. In conclusion, the response of chemotherapy was similar between endocrine therapy-relapsed and -resistant patients, and performance status was a main factor influencing the prognosis of endocrine therapy-refractory prostate cancer.

Aged↗
PubMed1991

Serum gamma-seminoprotein determination in prostatic cancer.

Serum gamma-seminoprotein (gamma-Sm) was evaluated as a new marker for prostatic cancer in comparison with prostatic acid phosphatase (PAP). The sensitivity of gamma-Sm and PAP for untreated prostatic cancer was 81% and 67%, respectively. gamma-Sm showed a higher positive rate over all stages than in benign prostatic hypertrophy (BPH). There was no correlation between gamma-Sm and PAP in prostatic cancer. Improved sensitivity was obtained by simultaneous measurement of gamma-Sm and PAP. Specificity of gamma-Sm and PAP for BPH was 87% and 90%, respectively. gamma-Sm normalized after endocrine therapy for stage D2 more often than did PAP. These results indicate that gamma-Sm is another useful marker to evaluate prostatic cancer.

Acid Phosphatase↗
PubMed1990

Paracrine growth stimulation of androgen-responsive Shionogi Carcinoma 115 by its autonomous subline (Chiba Subline 2).

Shionogi Carcinoma 115 cells (SC 115 cells) and Chiba Subline 2 cells (CS 2 cells) are clones of an androgen-responsive mouse tumor cell line and its autonomous subline, respectively. Since it was reported that the growth of cells from SC 115 was regulated by an androgen-induced fibroblast growth factor (FGF)-like peptide (1), the present study was aimed at examining whether a similar growth factor was secreted by CS 2 cells in the absence of testosterone. Although SC 115 cells did not grow in the serum-free medium without androgens, SC 115 cells could proliferate in mixed culture with CS 2 cells, suggesting stimulation of SC 115 cells by CS 2 cells. It was shown that CS 2 cells secreted a growth factor without the influence of testosterone, and this factor promoted the growth of SC 115 and CS 2 cells, as well as that of BALB/3T3 cells. The factor was partially purified from serum-free conditioned medium obtained from cultures of CS 2 cells. It showed an affinity for heparin, stability to heat and acid treatments, a decrease in activity when anti-basic FGF antibody was added to cultures, and an estimated molecular weight of approximately 50,000. Therefore, the factor seemed to have the nature of an FGF-like peptide. It was concluded that, in the absence of testosterone, CS 2 cells produced an FGF-like growth factor which controlled the growth of both CS 2 cells and parent SC 115 cells, in autocrine and paracrine manners, respectively.

Animals↗
PubMed1990

[Histological effects of endocrine therapy on prostatic cancer].

Histological effects of endocrine therapy were evaluated in one hundred and four prostatic cancer patients by new criteria presented by the committee of "General Rule for Clinical and Pathological Studies on Prostatic Cancer". Route and time of biopsy, clinical stage and histological grade were related to histological effects. Biopsy specimens taken within three months from the start of the therapy tended to score rather low marks and this tendency is especially apparent with low grade cancers. Histological effects evaluated by the present method correlated well with prognosis in localized stages (stage B, C and D1). In metastatic cases, however, local effects were not related to the prognosis.

Aged↗
PubMed1990

[Spinal paralysis caused by spinal metastasis of prostatic cancer].

From 1977 to 1986, in the Chiba University Hospital, 107 cases of prostatic cancer with bone metastasis were experienced. In 10 of them spinal paralysis caused by spinal metastasis of prostatic cancer was observed. Untreated five cases received endocrine therapy. One of them also underwent spine laminectomy and spinal instrumentation and regained the ability to walk. But the other cases treated by endocrine therapy showed only insufficient improvement of paralysis. Five cases with spinal paralysis which were resistant to endocrine therapy were treated by chemotherapy or radiation to the site of bone metastasis. One of them underwent laminectomy and spinal instrumentation. However, most cases showed no improvement of paralysis. It is concluded that spinal surgery is recommended in untreated cases for the sake of quality of life, but in cases with hormone resistance spinal surgery should cautiously be applied.

Aged↗
PubMed1990

[Changes in prostatic acid phosphatase, gamma-seminoprotein and prostate specific antigen after endocrine therapy for stage D2 prostate cancer].

Prostatic acid phosphatase (PAP), gamma-seminoprotein (gamma-Sm) and prostate specific antigen (PSA) were examined on 120 cases of stage D2 prostate cancer between 1979 and 1989. All patients received endocrine therapy as the first treatment; castration and immediate administration of estrogen or antiandrogen (101), LH-RH analogs (13), estrogen (3) and antiandrogen (3). The actuarial survival rates were calculated by the cause-specific survival method. Pretreatment levels of PAP, gamma-Sm and PSA did not influence prognosis. After start of treatment, the relationship between the changes of the markers and prognosis were examined. At 1 month after the start of the treatment, normalization of PAP or gamma-Sm was not reflected in the following course. On the contrary, at 3 and 6 months, groups with normalization of PAP or gamma-Sm showed better prognosis than those with elevated levels. The same tendency of PSA was obtained at 6 months after start of treatment. In patients with normalized PAP at 3 months, abnormal gamma-Sm showed worse prognosis than normalized gamma-Sm. Therefore, the significance of determination on the two markers was manifested. As histological grade influenced the following course, poorly differentiated adenocarcinoma with normalized PAP at 3 months showed better prognosis than those with elevated levels. In conclusion, it is worthwhile to measure multiple markers for predicting the prognosis of stage D2 prostate cancer treated with endocrine therapy.

Acid Phosphatase↗
PubMed1989

Histological effects of endocrine therapy for prostatic cancer in relation to clinical course.

In order to evaluate histological changes in cases of prostatic cancer following endocrine therapy, 25 extensive specimens were removed from prostates during periods of local control, and were examined with respect to prognosis. Shortly after the commencement of the endocrine therapy, there were noticeable degenerative changes in the cancer cells as well as structural changes such as desquamation of cells and loss of cancer nests. Later than two months from the start of therapy, stromal changes such as fibrosis and scar formation appeared. Coagulation necrosis of tumor tissue, inflammatory cell infiltration and granulomatous reactions were not as prominent. Within the first two months of treatment, the endocrine therapy uniformly affected the cancer tissues to some extent. After then, some showed relapsing viable cells in a part of the tumor, being judged to be no response. The others continued to respond to the therapy. The response was estimated as marked when such therapeutic changes appeared diffusely and profoundly over the tissues removed. Patients with a marked response had a good prognosis, indicating histological evaluation after endocrine therapy to provide a prognostic factor.

Aged↗
PubMed1988

Partial purification of androgen receptor from hypertrophic human prostate.

For purification of androgen receptor from hypertrophic human prostate, solutions used for elution of androgen receptor from DNA Sepharose, affinity labeling of the receptor and ability of affinity gel to retain the receptor were examined. Elution with 20 mM pyridoxal 5'-phosphate of the receptor from DNA Sepharose was more efficient than that with diluted pyridoxal 5'-phosphate, high ionic solution or various concentrations of Mg++, 3H-dihydrotestosterone bromoacetate was applicable to covalent binding with partially purified androgen receptor regardless of the low specificity of the ligand. Affinity gel of thiopropyl-Sepharose 6B coupled to 17 alpha-(2', 3'-epoxy-propyl)-5 alpha-dihydrotestosterone was better than Affigel 102 coupled to N-[3-(3-oxo-5 alpha-androstane-17 beta-yloxycarbonyl) propionyloxy] succimide or aminoethyl-Sepharose 4B coupled to 17 alpha-carboxyethynyl testosterone with respect to the rate of retention of androgen receptor. In view of these observations, the following purification procedures were constructed: Removal of DNA Sepharose-binders from the cytosol, 40% ammonium sulfate precipitation, affinity chromatography using thiopropyl-Sepharose 6B coupled to 17 alpha-(2',3'-epoxypropyl)-5 alpha-dihydrotestosterone, and DNA Sepharose chromatography. After affinity labeling of the receptor thus obtained, the molecular weight was estimated. Some 1300-fold purification with a yield of 0.25% of the androgen receptor was achieved. The molecular weight of the receptor was mainly 45 K with 90 K in a lesser amount. The Stokes radius was calculated as 30 A.

Chromatography, Affinity↗
PubMed1988

Characteristics of progestin binder in hypertrophic human prostate.

The human prostate contains a protein which binds with progesterone in a high affinity and low capacity fashion. Characteristics of the progestin-binding protein in the prostate have been disputable; whether it is progesterone receptor or not. Therefore, the characteristics of the progestin binder in the benign hypertrophic human prostate was examined in the present study. After photoaffinity labeling with 3H-R 5020, the binder in the prostate migrated to the site of 42K on polyacrylamide gel electrophoresis under denaturing conditions, and the mobility was apparently different from that of the progesterone receptor in the human uterine endometrium. There was no protein in the prostate immunoreacted with a monoclonal antibody raised against the human progesterone receptor. It was concluded that the progestin-binding protein in the human prostate was different from the progesterone receptor observed in the female human organs.

Blotting, Western↗
PubMed1988

[Prostate specific antigen in serum of the patients with prostatic cancer].

The serum prostate specific antigen (PA) was determined with the Diagnostic Products Cooperation (DPC) PSA double antibody radioimmunoassay kit. The upper limit of the normal range was set at 4 ng/ml which was the mean + 3S.D. for males over 50 years old in a mass examination. For comparison, prostatic acid phosphatase (PAP), and gamma-seminoprotein (gamma-Sm) were determined using an Eiken kit and Chugai kit, and PA was also assayed using another kit (Eiken, Travenol). Positive rate of PA and PAP in the untreated prostatic cancer was 75 and 33% in Stage A, 100 and 0% in Stage B, 100 and 100% in Stage C, 100 and 67% in Stage D1, 100 and 80% in Stage D2 and 73 and 33% in benign prostatic hypertrophy (BPH), respectively. The level of PA determined during the follow-up of prostatic cancer showed the usefulness of simultaneous PA and PAP assays for monitoring the clinical course. The PA level using a DPC kit was highly correlated to that of PA using other kit, but the correlation with gamma-Sm and PAP was low. These results show that the DPC kit is useful for determining PA, and determination of PA and PAP is of great value both in diagnosis and in the follow-up of prostatic cancer, but the high positive rate in BPH remains a problem.

Acid Phosphatase↗
PubMed1988

[Prostatic acid phosphatase (PAP), gamma-seminoprotein (gamma-Sm) and prostate specific antigen (PA) in prostatic cancer].

The levels of prostatic acid phosphatase (PAP), gamma-seminoprotein (gamma-Sm) and prostate specific antigen (PA) were determined in the serum of 200 untreated patients 28 patients with reactivated prostatic cancer and 179 patients with benign prostatic hypertrophy (BPH) from 1979 to 1987. PAP and gamma-Sm were determined using an Eiken and Chugai kit, respectively and PA was assayed using an Eiken or Travenol kit. The sensitivity of PAP, gamma-Sm and PA respectively in the untreated prostatic cancer cases was 0, 0% and 67%, for Stage A1, 25, 17 and 100% for Stage A2, 23, 50 and 60% for Stage B, 62, 81 and 94% in Stage C, 58, 67 and 90% for Stage D1, 86, 88 and 100% for Stage D2. The specificity of PAP, gamma-Sm and PA is 89, 69 and 43%, respectively. The efficiency of PAP was the highest at all stages as a whole, but when compared at each stage, gamma-Sm was the highest at Stages B and C. The sensitivity of simultaneous assays of PAP and gamma-Sm was slightly increased, but sensitivity was not increased by simultaneous use of three markers. The efficiency of a simultaneous assay was lower than that of a single assay with PAP. However, combined determination of gamma-Sm or PA with PAP was found to be useful for monitoring the clinical course of the reactivated patients. Correlation between PAP and PA levels was high, but that between gamma-Sm and PA levels was low. There was no correlation between PAP and gamma-Sm levels. In conclusion, PAP is the most valuable marker for prostatic cancer, and gamma-Sm is of value for use in combination with PAP. However, an additional PA assay was not found to be of advantage.

Acid Phosphatase↗