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Biomedical subjects

M Sakurai

Publications and source records attributed to M Sakurai.

At least 739 records · Page 41Linked to original sources
PubMed1987

Shedding of leukemia-associated P24 antigen by lymphoblastoid cell lines.

We report the development of a unique enzyme-linked immunosorbent assay (ELISA) which makes possible the detection of leukemia-associated P24 antigen, utilizing its ability to bind the Ricinus communis agglutinin (RCA1) and a monoclonal antibody, SJ-9A4 simultaneously. Using the RCA1/SJ-9A4-ELISA, P24 antigen, as few as 50 X 10(3) cells from a common acute lymphoblastic leukemia (C-ALL) cell line could be detected. The presence of D-galactose gave complete and specific inhibition of P24 antigen binding to RCA1. Matched concentrations of D-glucose and D-sucrose had no effect on binding. The release of the P24 antigen into the culture medium by a C-ALL cell line maintained at 37 degrees C could be detected; however, no P24 antigen was present in the culture medium when the cells were maintained at 4 degrees C. Sequential analysis of the culture medium for soluble P24 antigen revealed that release of the P24 antigen associated with cell growth. Molecular sieve chromatography of concentrated culture medium indicated that shed P24 antigen was eluted in the macromolecule fraction. P24 antigen was detected in the cerebrospinal fluid (CSF) of four patients with P24 positive ALL at the time of relapse of the central nervous system (CNS) and was undetectable while in complete remission. The CSF from three patients with P24 negative ALL and three patients with aseptic meningitis had no detectable activity.

Antibodies, Monoclonal↗
PubMed1987

[The changes in serum neuron-specific enolase in patients with small cell lung cancer].

Serum neuron-specific enolase (NSE) was measured in 48 newly diagnosed untreated patients with small cell lung cancer (SCLC) by radioimmunoassay. Serum NSE level elevated (greater than or equal to 15 ng/ml) in 50% of all patients. The positive ratio of NSE in patients with extensive disease (64%) was significantly higher than those in the patients with limited disease (30%) (p less than 0.05). The positive ratio of NSE in the patients with one metastatic site was 50%, that with two or more metastatic sites was 100% (p less than 0.05). No significant correlation was found between serum NSE levels and metastatic site as well as between serum NSE levels and response to the chemotherapy. In the patients with extensive disease, survival time was shorter in the patients with positive NSE levels than the patients with normal NSE levels. These findings indicate that serum NSE may be a useful marker for staging, monitoring and prognosis in patients with SCLC.

Carcinoma, Small Cell↗
PubMed1987

[Recent status of the diagnosis and treatment of bone metastasis in patients with advanced lung cancer].

The incidence and prognosis of patients with bone metastasis in primary advanced lung cancer were studied retrospectively. Between Jan. 1980 and Dec. 1985, 289 cases entered various kinds of chemotherapy protocol studies. Patients with bone metastasis of non-small cell lung cancer (NSC) comprised 44% (86/192), and those with small cell lung cancer (SC) comprised 43% (42/97). Histologically, 48% of adenocarcinoma, 50% of large cell carcinoma and 31% of squamous cell carcinoma showed bone metastasis. 8 percent of NSC bone meta (+) cases had an initial symptom of bone metastasis. Bone scan and bone X-ray were complementary and useful for diagnosis of bone metastasis, and sequential examinations tended to reduce the incidence of false-positive cases. Vertebral column, rib, pelvis and femur were the most common sites. Over 70% of the bone metastasis were in multiple skeletal systems, and 90% showed multiple-site involvement for both NSC and SC. Radiation therapy effectively reduced severe pain but paralysis was hard to control. In very few cases surgical treatment was indicated because of multiple bone metastasis, and systemic dissemination. Bone scan in 12% of SC patients showed apparent improvement with systemic chemotherapy. Among the M1 group of adenocarcinoma, median survival was 9 months in bone (+) cases, 11 months in bone (-) cases, 2 year survival was 8%, and 24%, and 3-year survival 2% and 22%, respectively. Among the bone(+) group and bone(-) group in ED cases of SC, median survival was 10 months vs. 11 months, and 2-year survival rates were both 13%. 22 percent (8/36) of squamous cell carcinomas without bone metastasis showed hypercalcemia (5.5 mEq/l). In patients with advanced lung cancer the major goal of treatment is recovery of the performance status of the patient and the relief of pain. In the case of SC, intensive systemic chemotherapy should be conducted as an adjuvant to local therapy.

Adenocarcinoma↗
PubMed1987

Human c-erbB-2 remains on chromosome 17 in band q21 in the 15;17 translocation associated with acute promyelocytic leukemia.

Using the human c-erbB-2 cDNA as a probe, we applied in situ hybridization techniques to acute promyelocytic leukemia cells with a 15;17 chromosome translocation, t(15;17)(q;22;q21), and were able to localize the c-erbB-2 gene on chromosome 17 to band q12 or q21 and on the proximal side of the breakpoint in the translocation. From this finding and previous observations by others, we presume that the gene and the breakpoint are both in band q21.1 of chromosome 17. We suggest possible involvement of the c-erbB-2 gene in the development of the t(15;17)-associated acute promyelocytic leukemia.

Chromosome Mapping↗
PubMed1987

[Direct and indirect antitumor effect of murine recombinant interferons].

The antitumor effects of murine recombinant interferons (beta) and (gamma) against B-16 melanoma and B16-F10 melanoma were examined. In a pharmacokinetic study, intraperitoneal injection of Mu-rIFN (gamma) produced higher and longer detectable IFN activity than administration of Mu-rIFN (beta) in both plasma and organs. In clonogenic assay, Mu-rIFN (gamma) at 1,000 units/ml showed 80% inhibition of colonies of B16-F10 melanoma. However, Mu-rIFN (beta) hardly inhibited the colony formation of B16-F10 melanoma. Furthermore, both IFNs had different characteristics from each other in the augmentation of NK cell and macrophage activities. In the experimental metastasis of B-16 melanoma, the inhibitory effect of Mu-rIFN (beta) on the pulmonary metastasis was mediated by the host defense mechanism, and NK cells and macrophages were important for the inhibition. Mu-rIFN (gamma) showed a stronger effect against B16-F10 melanoma in the inhibition of the growth of sc implanted tumor and artificial metastasis.

Animals↗
PubMed1987

[Chromosomal investigation in infertile cases of azoospermia].

Chromosomal examination in 85 patients with azoospermia revealed 62 patients (73%) with the karyotype 46, XY and 23 patients (27%) with other abnormal karyotypes. In this population, there were 17 patients with 47, XXY. Other anomalies were: 46, XYp+, 46, XXp+, 46, XYp-, 45, X, t (Ynf; 21), 45, XY, t (13q 15q), and 46, XY, r (18). Serum LH and FSH levels were high and testosterone level was low in the patients with 47, XXY compared with the other 6 patients (p less than 0.01). Also the mean value of testicular volume was low in the patients with 47, XXY (p less than 0.05).

Adult↗
PubMed1987

Prediction of hematologic toxicity of carboplatin by creatinine clearance rate.

Twenty-six patients with histologically proven lung cancer, treated with carboplatin at the National Cancer Center Hospital between October 1985 and October 1986, were retrospectively analyzed to determine the hematologic toxicity of carboplatin (CBDCA) and to develop guidelines for dose modification. A total of 34 courses of CBDCA were administered, of which 21 were adequate for assessment of the myelosuppression in relation to the renal function. One of three doses of CBDCA was administered by iv drip infusion over one hour (450 mg/m2, 19 courses; 400 12; 300, 3). Myelosuppression was dose-limiting, with thrombocytopenia being more sensitive than leukopenia, neutropenia or anemia. No significant correlation of the absolute count of platelets, white blood cells, polymorphoneutrophils, or hemoglobin with patient's creatinine clearance (Ccr) and dose of CBDCA administered was found. However, the percent reduction in platelets, white blood cells, polymorphoneutrophils, or hemoglobin correlated well with the relative dose of CBDCA [RD = total dose of carboplatin administered (mg/m2)/pretreatment Ccr/m2]. As thrombocytopenia was dose-limiting, we have developed an equation for modification of the dose of CBDCA from the relationship between the relative dose and percent reduction at platelet count nadir: Dosage (mg/m2) = (Ccr/m2/5.34) x [(1-desired platelet count nadir/pretreatment platelet count) x 100-12.9]. After consideration of the range of thrombocytopenia, we have further developed a simple equation to use CBDCA easily and safely: Dosage (mg/m2) = (1/10) x Ccr/m2 x desired % reduction in platelet count nadir = 10 x Ccr/m2 x (1-desired platelet count nadir/pretreatment platelet count. The clinical validity of these two equations is now being evaluated in prospective studies.

Adult↗
PubMed1987

In vitro growth inhibition of cisplatin-resistant human lung cancer cell lines by recombinant human tumor necrosis factor and/or recombinant human interferon-gamma by virtue of collateral sensitivity.

The colony-inhibitory effects of recombinant human tumor necrosis factor (rH-TNF) and recombinant human interferon-gamma (rH-IFN-gamma) were evaluated in four human lung cancer cell lines and their cisplatin-resistant sublines. The cell lines tested were PC-7 and PC-9 (adenocarcinoma), H69 and N231 (small cell lung cancer) and four cisplatin-resistant sublines, PC-7/1.0, PC-9/0.5, H69/0.2 and N231/0.2, which were 20.0, 7.1, 4.8 and 8.4 fold resistant to cisplatin, respectively, compared to the respective parental cell line in terms of IC50 in a soft agar colony assay. All parental cell lines were resistant to rH-TNF and rH-IFN-gamma, alone or in combination. However, two resistant sublines showed sensitivity to rH-TNF and rH-IFN-gamma. Colony formation by PC-9/0.5 was significantly inhibited, in the absence or presence of cisplatin, by 10(2) U/ml of rH-TNF (less than 50% of control) and the inhibition was synergistic with that produced by 10(3) or 10(4) U/ml of rH-IFN-gamma. RH-IFN-gamma inhibited the colony formation of H69/0.2 only at the highest concentration tested (10(4) U/ml) (less than 50% of control) and the combined effect with rH-TNF was additive. These results suggest that rH-TNF and rH-IFN-gamma may have some potential in overcoming cisplatin resistance by virtue of collateral sensitivity.

Cisplatin↗
PubMed1987

A case report of adenocarcinoma of the lung in which a partial response was achieved by carboplatin.

A 56-year-old housewife was incidentally discovered to have an abnormal shadow in the right B6 area upon a chest X-ray film being taken. A transcutaneous lung biopsy of the mass revealed adenocarcinoma of the lung (WHO classification). A brain computed tomography (CT) scan demonstrated multiple brain metastasis. Following whole brain irradiation, carboplatin (CBDCA) (450 mg/m2) was administered by intravenous drip infusion on March 7, 1986. After three weeks of initial treatment with CBDCA, the size of the tumor in the primary site was found to have decreased on the chest X-ray film by more than 50%, following which, similar doses of CBDCA were administered twice, and reduced (330 mg/m2) doses three times every three to four weeks. She showed a partial response and, for seven months after the beginning of the CBDCA treatment, no progression was seen on the chest X-ray film. It is suggested that there is a need for further phase II studies of CBDCA against non-small cell lung cancer.

Adenocarcinoma↗
PubMed1987

[A randomized controlled trial of acute and delayed cisplatin-induced emesis with metoclopramide, dexamethasone and prochlorperazine].

Forty patients with advanced lung cancer who had received chemotherapy containing cisplatin (80 mg/m2) were accrued for a randomized controlled trial to evaluate the additional effect of prochlorperazine on the combination of high-dose metoclopramide and dexamethasone for the treatment of acute cisplatin-induced emesis. The effect of intravenous metoclopramide and dexamethasone in emesis occurring more than 24 hours after cisplatin administration was also evaluated. Excellent emetic control (no emesis during 24 hours after cisplatin administration) was achieved in 70% (14/20) and 76% (16/21) of the patients who received the combination of prochlorperazine, metoclopramide and dexamethasone and the combination of metoclopramide and dexamethasone, respectively. The overall toxicities associated with both regimens were not serious and were similar. Patients treated with metoclopramide and dexamethasone on days 2-7 experienced less delayed emesis, nausea and anorexia compared with those treated with a placebo (delayed emesis, 25% versus 50%, respectively, p = 0.105; more than 4 days of nausea, 10% versus 35%, respectively, p = 0.059; less than 3 days of anorexia, 80% versus 50%, respectively, p = 0.048). It was concluded that metoclopramide and dexamethasone showed an excellent antiemetic effect on acute drug-induced emesis, as well as on delayed emesis, induced by cisplatin.

Adult↗
PubMed1987

[Pharmacokinetic and clinical studies on flomoxef in the pediatric field].

The new antibiotic flomoxef (FMOX, 6315-S) was administered to 38 children. The results obtained are summarized as follows. 1. In 3 cases of children administered with FMOX (20 mg/kg) by intravenous drip infusion for 30 minutes, the mean T1/2 (beta) was 0.96 hour and the mean 6-hour urinary excretion was 95.5%. 2. The antibiotic was administered to a total of 38 patients with bronchopneumonia, lacunar tonsillitis, upper respiratory tract infection complicated with brain tumor, otitis media, urinary tract infection, purulent meningitis, subcutaneous and hyponychial abscess, cervical lymphadenitis, or bacterial enteritis. The treatment was markedly effective in 24 cases, effective in 13, fair in 1, and ineffective in none. The efficacy rate was 97.4%. From our results, this drug appears to be particularly effective to bronchopneumonia, upper respiratory tract infection and urinary tract infection. 3. None of the children showed clinical symptoms indicating side effects of the drug. These results showed that FMOX is a drug that can be safely used in the pediatric field as well as for adults.

Age Factors↗
PubMed1987

[Cefmenoxime or piperacillin plus amikacin. A prospective randomized comparison of empiric antibiotic therapy of febrile granulocytopenic cancer patients].

Cefmenoxime plus amikacin was compared in a prospective randomized trial with our standard regimen of piperacillin plus amikacin as an empiric therapy for fever in patients with granulocytopenia. Initial profound granulocytopenia (fewer than 100/mm3 mature granulocytes) was present in approximately 45% of the patients in trial of both treatment groups. Of 53 microbiologically and clinically documented infections treated with piperacillin plus amikacin, 36 (68%) showed improvement. Of 48 microbiologically and clinically documented infections treated with cefmenoxime plus amikacin, 23 (48%) showed improvement. The response rate for gram-negative infections treated with cefmenoxime plus amikacin was lower than that for infections treated with piperacillin plus amikacin. Toxicity was minimal, with an equivalent incidence of skin rash, diarrhea and hepatic dysfunction. Although clinical efficacy of the combination of piperacillin plus amikacin may be superior to cefmenoxime plus amikacin therapy, this study demonstrated no statistically significant differences.

Adolescent↗
PubMed1987

[Phase I-II study of recombinant interleukin-2].

A phase I-II study of recombinant interleukin 2 (rIL-2) (Shionogi Pharmaceutical Co.) was conducted against carcinoma of the lung (20 cases) and stomach (1 case) as well as metastatic pulmonary tumor (17 cases). The cytotoxicity of lymphocytes against K562, PC-9, PC-14 and Daudi cells was examined before and 1, 2, 3, 5, 7, 14, 21 and 28 days after rIL-2 administration. The subsets of lymphocytes and pharmacokinetics of rIL-2 were also analyzed. Four administration methods were used. 2-h drip infusion of 6.7 X 10(5) U/m2/day (A1: 6 cases) or 2.2 X 10(6) U/m2/day (A2: 8 cases) for 5 consecutive days, subcutaneous injection of 6.7 X 10(5) U/m2/day (B: 3 cases) for 28 consecutive days, 4-h continuous drip infusion of 3.3 X 10(5) U/m2/day (C1: B cases), 6.7 X 10(5) U/m2/day (C2: 7 cases) or 1.1 X 10(6) U/m2/day (C3: 5 cases) for 28 consecutive days, and (D) 24-h continuous drip infusion of 6.7 X 10(5) U/m2/day (D: 6 cases) for 5 consecutive days every week, repeating four cycles of the course. We discussed whether or not the problems of the phase I study with BRMs could be solved.

Drug Administration Schedule↗
PubMed1987

Synergistic effect of recombinant interleukin-2 on the inhibition of growth of adenocarcinoma 755 by mitomycin.

The increase in life-span (ILS) of tumor-bearing mice caused by recombinant interleukin-2 (RIL-2) was studied in the solid tumor adenocarcinoma 755 system. With long-term treatment (Days 5-12), RIL-2 (10(5) U/mouse) showed a weak effect (24% ILS), but short-term RIL-2 treatment (Days 5-8 or 9-12) had hardly any effect. Mitomycin, at 2 mg/kg (maximum nontoxic dose), caused 35% ILS with Days 5-8 treatment and only 12% ILS with Days 9-12 treatment. Sequential treatment with mitomycin (Days 5-8) and RIL-2 (Days 9-12) markedly enhanced antitumor activity (88% ILS). This value is significantly greater than that of mitomycin alone or RIL-2 alone (P less than 0.01). Furthermore, mitomycin followed by RIL-2 markedly augmented killing activity of spleen cells that are cytotoxic in vitro. These results indicate that RIL-2 markedly affects the inhibition of growth of a tumor treated with an antitumor agent.

Adenocarcinoma↗