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Biomedical subjects

K Akakura

Publications and source records attributed to K Akakura.

102 records · Page 6Linked to original sources
PubMed1988

[Comparison of 3 assay kits of prostate specific antigen in serum of prostatic cancer].

The serum prostate specific antigen (PA) of the patients with prostatic cancer were determined with 3 assay kits, the Diagnostic Products Cooperation (DPC) kit, the Eiken kit and the Dainippon Pharmaceutical Co. (MARKIT F) kit. The first 2 assay kits involve radioimmunoassay and the latter EIA. For comparison, prostatic acid phosphatase (PAP) and gamma-seminoprotein (gamma-Sm) were determined using an Eiken kit and Chugai kit. Efficiency of the DPC kit, Eiken kit and the MARKIT F kit for untreated prostatic cancer was 26, 25 and 36%, respectively. The PA level measured using the Eiken kit and the MARKIT F kit both well correlated to the PAP level, but with the DPC kit correlation was slightly low. The PA level measured using the 3 different kits correlated poorly with the gamma-Sm level. The PA values obtained with 3 different assays from patients with prostatic cancer were highly correlated, but showed great differences in the values measured. When the standards used in the DPC kit were analyzed by the Eiken kit, the DPC standards as measured by the Eiken kit had only about half of their assigned values. The same standards were analyzed by the MARKIT F kit, the standards yielded measured values about one third of their assigned values. When the standards used in the MARKIT F kit were analyzed by the Eiken kit, the MARKIT F standards yielded measured values about 2.5 fold of their assigned values. The differences between the values obtained with the 3 assay kits presented a serious problem in clinical use of PA. Standardization of these assay kits will be awaited.

Acid Phosphatase↗
PubMed1988

[Treatment of prostatic cancer with slow-release formulation of luteinizing hormone releasing hormone (LH-RH) analog].

A slow-release formulation of the luteinizing hormone releasing hormone (LH-RH)analog(TAP-144-SR) was administered in 6 cases of prostatic cancer. Five were untreated cases, 3 of moderately-differentiated and 2 of poorly-differentiated cancers (four D2 and one C, NX), the other (D2) was under control by another LH-RH analog. The plasma level of luteinizing hormone and follicle stimulating hormone fell below normal, and the plasma testosterone was less than 1 ng/ml by four weeks after start of treatment. According to the National Prostatic Cancer Project Criteria, 2 of the untreated cases showed a partial response and 3 of the untreated ones showed a stable response, one of which underwent transurethral resection later. The pretreated case still continued controlled more than 4 months. No side effect was noticed.

Acid Phosphatase↗
PubMed1988

[Treatment of prostatic cancer].

Since more than half of stage A-C prostatic cancers show pelvic lymph node metastasis (D1, pN1-3), a staging operation is required at the start of treatment. Most pN0 and pN1 (stage A2BC) cases have been treated with radiation, and good results have been obtained. Endocrine therapy, consisting of orchiectomy and immediate administration of a large dose, followed by an intermediate dose of estrogen or antiandrogen, was applied to pN2-4 and D2 cancer cases. Five-year survival was approximately 40%, and side effects were less marked than those reported in western countries. Factors affecting prognosis during endocrine therapy were grade, acid phosphatase response, and tissue androphilic protein. For D2 with risk factors, chemoendocrine therapy was applied, but no improvement in survival was observed.

Androgen Antagonists↗
PubMed1988

[Trends in patterns of care for prostatic cancer in Japan: statistics of 9 institutions for 5 years].

Five hundred and sixty-five patients with prostatic cancer, who first visited 9 institutions in Japan between 1981 and 1985, were analyzed. The peak of age distribution was in the seventies. As clinical symptoms, disturbance on micturition was the most frequent and pain caused by metastasis was a complaint in approximately one tenth of the cases. Alkaline phosphatase measurement, prostatic biopsy, intravenous pyelography, bone scintigraphy, cystourethrography, and measurements of serum prostatic acid phosphatase and serum acid phosphatase were performed on more than 80% of the patients. The clinical stage was stage A1 in 6.2%, A2 in 3.7%, B in 14.9%, C in 20.7%, D1 in 7.4%, and D2 in 43.7%. According to the histological grade, well, moderately and poorly differentiated adenocarcinoma were observed in 20.4, 33.3 and 32.7%, respectively. Increased ratio of high grade to low grade was noticed in the lower age group as well as in the advanced stage. In this series, endocrine therapy was still accepted in most of the patients. Almost all were treated with hormonal medication and half of them had undergone bilateral orchiectomy. Surgery, radiation, chemotherapy or multidisciplinary therapy were attempted judging from the clinical stage and histological grade. However, old age restricted the therapeutic modality. Actuarial survival rate at 5 years for stage A1, A2, B, C, D1 and D2 was 89.2, 66.1, 72.7, 51.0, 47.5 and 28.0%, respectively. In the patients with stage D2, the 5-year actuarial rate of poorly differentiated adenocarcinoma was lower than that of well or moderately differentiated adenocarcinoma, even though more intensive therapy was given to the former.

Adenocarcinoma↗
PubMed1988

[Prostatic carcinoma. I: Androgen dependency of prostatic carcinoma].

Endocrine therapy, which consists of orchiectomy followed by administration of large doses of estrogen, then a reduced amount of estrogen, has been applied as the main treatment for stage D2 prostatic cancer. Alternatively, anti-androgen is used for elderly patients or those with cardiovascular disorders. Survival rate with endocrine therapy at 5 and 10 years was 35% and 16%, respectively. Therefore, in Japan, a better survival is shown than that reported in western countries using much smaller doses of estrogen. Most of the side effects caused by estrogen are not serious. Side effects caused by anti-androgen are few except for loss of libido. At the start of treatment, more than 80% of patients showed a response, but gradually relapse occurred and only 20% were well controlled 5 years after the start. Factors influencing the survival were pathological grade, response to endocrine therapy judged by the level of prostatic acid phosphatase 4 weeks after the start, and R1881 (methyltrienolone)-binding protein observed histochemically. The latter protein was also correlated with the grade and response to endocrine therapy. Relapse after endocrine therapy might be attributable to adaptation or mutation progressing to androgen-independent cells. Using SC 115, an androgen-dependent mouse tumor, these two types of relapse were demonstrated. Gradual progression to undifferentiated cancer was noticed between pretreatment biopsy and autopsy. Relapse in human prostatic cancer may thus be partly due to genetic change to a resistant clone.

Androgen Antagonists↗
PubMed1987

[Prostatic specific antigen in the serum in prostatic cancer].

Prostatic specific antigen (PA) level was determined with a Wako test kit (Japan) for prostatic cancer and others. The incidence of abnormal values of PA in untreated prostatic cancer, was 50, 50, 80, and 100% for stage A1, C (pN0, NX), D1 and D2 cancers, respectively. Grade was not related to the level of PA. Prostatic hypertrophy, prostatitis and urinary stone showed a false positive rate of 52, 18 and 0%, respectively. The level of PA was not correlated to those of prostatic acid phosphatase (RIA). In 31% of the cases, the elevated PA decreased 4 weeks after start of endocrine treatment. Elevated PA in low grade cancer was not normalized as much as that in high and moderate grade cancers. The positive rate of PA in the serum of reactivated patients was significantly higher than that of the patients with cancer under good control by endocrine treatment.

Acid Phosphatase↗
PubMed1987

[A case of renovascular hypertension due to chondrosarcoma arising from lumbar vertebrae].

A 35-year-old man visited our clinic with the chief complaint of headache and an upper abdominal mass. Renal vein renin activity, drip infusion pyelogram, GT scan and selective renal angiogram demonstrated a retroperitoneal tumor and right renovascular hypertension. Thus tumor extirpation and right nephrectomy were performed. After nephrectomy, blood pressure was corrected within the normal range. Histologically the tumor was diagnosed to be chondrosarcoma and there was no lesion in the wall of the right renal artery. This case had secondary chondrosarcoma arising from the first and second lumbar vertebrae and produced renovascular hypertension due to compression of the tumor.

Adult↗
PubMedDate not supplied

Acquired expression of hst-1 in an autonomous subline (Chiba subline 2) derived from androgen-responsive mouse mammary tumor (Shionogi carcinoma 115).

Since growth of Shionogi Carcinoma 115 (SC 115) and its autonomous subline (CS 2) were regulated by fibroblast growth factor-like peptide, expression of int-2 and hst-1 was examined in these cell lines. Hybridization of genomic DNA with long terminal repeat of mouse mammary tumor virus (MMTV) revealed the same pattern of restriction fragments, showing the same integration of MMTV. Although weak expression of int-2 was noticed in the two cells, clear expression of hst-1 was seen only in CS 2 cultured with/without testosterone. It is suggested that autonomous growth of androgen-unresponsive CS 2 is connected with expression of hst-1.

Animals↗
PubMedDate not supplied

Changes in cell proliferation and apoptosis during local progression of prostate cancer.

To determine the changes in biological features of the prostate during the course of local recurrence of prostate cancer after endocrine therapy, histologic grade, proliferating activity and apoptotic indices were examined in prostate specimens obtained before treatment and at recurrence. A total of 16 patients, who had received endocrine therapy and eventually recurred in the prostate, were evaluated. Histologic grade was determined by the method of Gleason and the number of proliferating cells and apoptotic cells were counted. Tumors with a high grade Gleason score remained at a high grade. A statistically significant increase in the number of Ki-67 positive cells was observed from pretreatment biopsy to local recurrence. On the other hand, the apoptotic index decreased during progression. Patients with a higher number of Ki-67 positive cells before the initial treatment had a poorer prognosis than those with a lower number of Ki-67 positive cells. In conclusion, prostate cancer shows an increase of malignant potential as assessed by the number of Ki-67 positive cells, whilst the decrease in apoptosis might play some role in the course of progression.

Apoptosis↗