M Sakurai

Saitama Cancer Center, Saitama, Saitama, Japan

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Publications (253)805.09 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: We studied chromosomes in bone marrow (BM) or peripheral blood cells of nine patients with haemophagocytic lymphohistiocytosis (HLH); three of them had a family history of HLH and four others underwent concurrent Epstein-Barr virus (EBV) infection. In addition to a large population of normal mitotic cells, karyotypically abnormal clonal cells were found in two patients, abnormal clonal cells and a nonclonal (single) abnormal cell in one, and nonclonal abnormal cells in three. All the six patients with chromosome abnormalities died of progressive disease; one of them also had EBV infection and EBV-associated clonal proliferation. Two of three patients with EBV infection and only normal mitotic cells in BM completely recovered from the disease. Although HLH did not show histological and/or haema-tological evidence of a neoplastic disease, clonal chromosome abnormalities and the fatal clinical outcome found in some of the patients suggest that the disease may be heterogenous and include malignancy. HLH patients with karyotypically abnormal clonal cells in BM should warrant more intensive chemotherapy than that presently being applied to them and should be considered as candidates for BM transplantation.
    British Journal of Haematology 03/2008; 90(1):48 - 55. DOI:10.1111/j.1365-2141.1995.tb03379.x · 4.71 Impact Factor
  • A Ooi · T Ohkubo · M Higashigawa · H Kawasaki · H Kakito · Y Kagawa · M Kojima · M Sakurai ·
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    ABSTRACT: Several 5-fluorouracil (5-FU) derivatives, 1-hexylcarbamoyl-5-fluorouracil (HCFU), 5'-deoxy-5-fluorouridine (5'-DFUR) and UFT (mixed compound of tegafur and uracil), have been developed and clinically widely used. However, comparative pharmacokinetic studies of the parent compound and other fluorinated drivatives have not been precisely reported. The dosage of the oral clinical use for human cancer of 5-FU, HCFU, 5'-DFUR and UFT as tegafur (FT) is 200-300mg/d, 600mg/d, 800-1,200mg/d and 300-600mg/d respectively. These amounts of the drugs are almost equimolar. Previously, we reported the effect of oral equimolar administration of each four drugs on thymidilate synthase activity, deoxyribonucleotide metabolism and cell cycle progression in L1210 ascites tumor. (1,2) In this study, we examined the antitumor effect and 5-FU concentration in the plasma, intestine and tumor after oral equimolar administrations of each drug using BDF1 mice bearing L1210 ascites tumor. In our study, UFT showed the best life prolongation among these four drugs. The intestine 5-FU level was highest by treatment with 5-FU during the initial 4 h. The plasma 5-FU level was highest by treatment with HCFU for 4 h. But the tumor 5-FU level was highest by treatment with UFT over the 24 h. In spite of the high plasma 5-FU concentration after the treatment with HCFU, the 5-FU concentration in the tumor was below the detectable level until 24 h. These findings suggested that the highest specific accumulation of 5-FU in tumor cells may explain the best therapeutic results of UFT.
    Biological & Pharmaceutical Bulletin 12/2001; 24(11):1329-31. · 1.83 Impact Factor
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    ABSTRACT: Monocytes as antigen-presenting cells play an important role in host defence. There are several cytokines affecting monocyte function. We demonstrate that both adult and cord blood monocytes constitutively express hepatocyte growth factor (HGF) receptor, MET. HGF significantly down-regulated MET expression of adult blood monocytes, compared with cord blood monocytes, when cultured either in RPMI-1640 containing 10% FBS or serum-free medium. Surface levels of MET correlated with c-met mRNA levels both in adult and cord blood when cultured. MET expression was down-regulated by treating with actinomycin D or cycloheximide. HGF stimulated DNA synthesis of adult monocytes, but not cord blood. HGF enhanced antigen-presenting capacity of adult blood monocytes but not cord blood monocytes. HGF up-regulated HLA class I expression in adult monocytes but not in cord blood monocytes. The current results suggest that the failure of cord blood monocytes to respond to HGF may be responsible, in large part, for their functional immaturity.
    Clinical & Experimental Immunology 09/2001; 125(2):222-8. DOI:10.1046/j.1365-2249.2001.01591.x · 3.04 Impact Factor
  • H Hayakawa · Y Komada · M Hirayama · H Hori · M Ito · M Sakurai ·
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    ABSTRACT: Anthracyclines are effective anticancer drugs for childhood cancer with dose-limiting cardiotoxicity. Children who have received anthracyclines thus need periodical cardiac evaluation. The plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have been shown to increase in proportion to severity of cardiac dysfunction. We examined whether plasma levels of ANP and BNP, in addition to echocardiographic evaluation, can be used as specific markers for doxorubicin-induced cardiotoxic effects in children. Consecutively, 34 patients (18 boys and 16 girls) who had previously received doxorubicin-containing chemotherapy were enrolled in this study. Plasma ANP and BNP were assayed simultaneously at the time of first cardiac function evaluation by echocardiography. Of the 34 patients, 8 (23.5%) had left ventricular dysfunction as assessed by echocardiography. Both ANP and BNP plasma levels in these patients were significantly elevated in comparison with healthy controls (P < 0.01) or patients with normal cardiac function (P < 0.05). It should be also noted that ANP and BNP levels were correlated significantly with cardiac systolic function, but not with diastolic function. These results suggest that plasma ANP and BNP levels could be markers for doxorubicin-induced cardiotoxicity in children. Measurement of natriuretic peptide levels during treatment may allow earlier-identification of individuals at risk for severe cardiac damage.
    Medical and Pediatric Oncology 07/2001; 37(1):4-9. DOI:10.1002/mpo.1155
  • Y Mitani · M Ueda · R Komatsu · K Maruyama · R Nagai · M Matsumura · M Sakurai ·
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    ABSTRACT: Primary pulmonary hypertension (PPH) is associated with specific structural alterations, including cellular intimal thickening, intimal fibrosis, and plexiform lesions. To determine the phenotypes of smooth muscle cells (SMCs) in such lesions, the authors conducted an immunohistochemical analysis of lung tissues from two patients with PPH, using two antimuscle actin antibodies, HHF35 and CGA7, and two anti-SMC myosin heavy chain markers, anti-SM1 and anti-SM2 antibodies and related antibodies. Cells that stained positive (+) with HHF35, CGA7, anti-SM1, and anti-SM2 were considered to be SMCs of a mature state. Conversely, those that stained positive with HHF35 and anti-SM1, but weakly positive (+/-) or negative (-) with CGA7 and anti-SM2, were considered to be SMCs exhibiting an immature state. Cellular intimal thickening was composed of SMCs of an immature phenotype (HHF35+, CGA7+/-, SM1+, SM2+/-), accompanied by the expression of fibronectin and the presence of macrophages; intimal fibrosis contained mature SMCs (HHF35+, CGA7+, SM1+, SM2+); and plexiform lesion consisted of proliferative endothelial cells (von Willebrand factor-positive cells, proliferating cell nuclear antigen-positive cells) and underlying immature SMCs (HHF35+, CGA7-, SM1+, SM2-) associated with fibronectin expression and macrophage infiltration. These findings suggest that smooth muscle cells with specific phenotypes may contribute to the development of specific vascular lesions in primary pulmonary hypertension.
    European Respiratory Journal 03/2001; 17(2):316-20. DOI:10.1183/09031936.01.17203160 · 7.64 Impact Factor
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    Y Mitani · J Maruyama · A Yokochi · K Maruyama · T Yoshimoto · M Naruse · M Sakurai ·
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    ABSTRACT: Natriuretic peptides (NPs), such as atrial natriuretic peptide (ANP), C-type natriuretic peptide (CNP), and adrenomedullin (ADM), are endogenous vasodilators acting via specific receptors. This study addressed the question of how pulmonary artery (PA) responses to these peptides and the gene expression of their receptors are modulated in pulmonary hypertension rat models exposed to chronic hypoxia. In this study, isometric tension was measured in PA rings exposed to these NPs and 8-bromoguanosine 3', 5'-cyclic monophosphate (8-bromo-cGMP). It was compared with messenger ribonucleic acid (mRNA) levels of NP-A and -B receptors, which bind to ANP and CNP, respectively, as determined by ribonuclease (RNase) protection assay. Chronic hypoxia increased the maximal relaxation elicited by ANP, but the responses to CNP and 8-bromo-cGMP were unchanged. Chronic hypoxia did not change NP-A and -B receptor mRNA levels. The results showed that pulmonary artery response to atrial natriuretic peptide is selectively enhanced, possibly via a post-transcriptional modulation of its receptor in chronically hypoxia rats. These pharmacological characteristics of atrial natriuretic peptide are consistent with the hypothesis that the atrial natriuretic peptide system is protective against the progression of pulmonary hypertension.
    European Respiratory Journal 03/2000; 15(2):400-6. DOI:10.1034/j.1399-3003.2000.15b29.x · 7.64 Impact Factor
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    ABSTRACT: Many protocol studies have shown that low dose 6-mercaptopurine (6MP) in maintenance chemotherapy for childhood acute lymphoblastic leukemia (ALL) can be utilized to cure the disease. Mitotic or reproductive cell death has been recognized after G2 arrest when cells are treated with antitumor agents. The precise mechanism of mode of action of 6MP still remains unclear. We found delayed cytotoxic effect of 6MP in P388 murine leukemic cells. Morphological study showed that 6MP induced delayed death was characterized by an enlargement of cell size and multinucleated nuclei. Agarose gel electrophoresis of fragmented DNA from cells treated with 6MP showed the typical ladder pattern. These findings were compatible with mitotic death. Our results make us hypothesize that the delayed cytotoxicity of 6MP is one of the drug induced mitotic deaths caused by DNA damage due to incorporation of 6-thioguanine (6TG) into DNA as thioguanine nucleotide (TGN). Mitotic death may be a mechanism for killing the cycling cells from residual leukemic cells in G0 or long G1 phases in the treatment of childhood ALL.
    Journal of experimental & clinical cancer research: CR 10/1999; 18(3):417-24. · 4.23 Impact Factor
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    ABSTRACT: Histone H3 (H3) phosphorylation at Ser(10) occurs during mitosis in eukaryotes and was recently shown to play an important role in chromosome condensation in Tetrahymena. When producing monoclonal antibodies that recognize glial fibrillary acidic protein phosphorylation at Thr(7), we obtained some monoclonal antibodies that cross-reacted with early mitotic chromosomes. They reacted with 15-kDa phosphoprotein specifically in mitotic cell lysate. With microsequencing, this phosphoprotein was proved to be H3. Mutational analysis revealed that they recognized H3 Ser(28) phosphorylation. Then we produced a monoclonal antibody, HTA28, using a phosphopeptide corresponding to phosphorylated H3 Ser(28). This antibody specifically recognized the phosphorylation of H3 Ser(28) but not that of glial fibrillary acidic protein Thr(7). Immunocytochemical studies with HTA28 revealed that Ser(28) phosphorylation occurred in chromosomes predominantly during early mitosis and coincided with the initiation of mitotic chromosome condensation. Biochemical analyses using (32)P-labeled mitotic cells also confirmed that H3 is phosphorylated at Ser(28) during early mitosis. In addition, we found that H3 is phosphorylated at Ser(28) as well as Ser(10) when premature chromosome condensation was induced in tsBN2 cells. These observations suggest that H3 phosphorylation at Ser(28), together with Ser(10), is a conserved event and is likely to be involved in mitotic chromosome condensation.
    Journal of Biological Chemistry 10/1999; 274(36):25543-9. DOI:10.1074/jbc.274.36.25543 · 4.57 Impact Factor
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    ABSTRACT: Granisetron has been used widely for the prevention and treatment of nausea and vomiting associated with anticancer drugs in adult patients with cancer. This multi-center open study was conducted to study the efficacy, safety and usefulness of granisetron in children with cancer. Among 166 evaluable patients, the efficacy rate (percentage of "remarkably effective" or "effective") was 84.9% and the usefulness rate (percentage of "extremely useful" or "useful") was 87.3%. No serious adverse effects were observed. As granisetron 40 micrograms/kg had an excellent antiemetic effect and a high degree of safety against nausea and vomiting associated with anticancer drugs, it was shown to be useful for children with cancer.
    Gan to kagaku ryoho. Cancer & chemotherapy 09/1999; 26(9):1295-304.
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    ABSTRACT: Of 29 infants with acute myeloid leukemia (AML), 14 (48%) had various 11q23 translocations. MLL rearrangements were examined in 21 of the 29 patients, and 11 (52%) showed the rearrangements. 11q23 translocations and/or MLL rearrangements were found in 17 (58%) of the 29 patients. While all but one of the 17 patients with 11q23/MLL rearrangements had M4 or M5 type of the FAB classification, the 12 patients without such rearrangements had various FAB types, including M2, M4, M4EO, M6 and M7. Of the 12 patients with other chromosome abnormalities or normal karyotypes, two had inv(16) ort(16;16), one had t(1;22)(p13;q13), and two had a novel translocation, t(7;12)(q32;p13). The breakpoint on 12p of the t(7;12) was assigned to intron 1 or the region just upstream of exon 1 of the TEL/ETV6 gene by fluorescence in situ hybridization. The event-free survival at 5 years for the 17 patients with 11q23/MLL rearrangements was 42.2%, and that for the 12 patients without such rearrangements was 31.3% (P = 0.5544). 11q231MLL rearrangements have been frequently reported and a poor prognosis in infant acute lymphoblastic leukemia implied. Our study showed that while 11q23/MLL rearrangements were also common in infant AML, AML infants with such rearrangements had a clinical outcome similar to that of AML infants without such rearrangements.
    Leukemia 08/1999; 13(7):1013-7. DOI:10.1038/sj.leu.2401439 · 10.43 Impact Factor
  • Y Komada · T Matsuyama · A Takao · T Hongo · Y Nishimura · K Horibe · M Sakurai ·
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    ABSTRACT: This randomised study was performed to assess the anti-emetic efficacy and tolerability of two-dose regimens of granisetron in children with leukaemia. 49 children with leukaemia were treated with three consecutive courses of high-dose methotrexate or cytarabine regimen. During the first course, patients were evaluated regarding the emetogenicity of each regimen. They were randomised in a crossover manner to receive 20 or 40 micrograms/kg of granisetron before the second and third course of chemotherapy. Neither emesis nor severe appetite loss were observed in over 80% of patients within the first 24 h in all treatment groups. There was no significant difference in the anti-emetic efficacy between the two-dose regimens of granisetron. However, complete protection was achieved less frequently on days 2 and 3. Older children and girls appeared to be less well protected. No adverse events attributable to granisetron were observed. Granisetron dose regimens of 20 and 40 micrograms/kg are, comparably, well tolerated and effective in controlling chemotherapy-induced emesis in the first 24 h, though this protection fails thereafter, particularly in older patients and girls.
    European Journal of Cancer 08/1999; 35(7):1095-101. DOI:10.1016/S0959-8049(99)00071-4 · 5.42 Impact Factor
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    ABSTRACT: Of 40 Wilms tumors with chromosome abnormalities, 6 were hypodiploid, 10 were pseudodiploid, 7 were hyperdiploid with 47 to 49 chromosomes, and 17 were hyperdiploid with 50 or more chromosomes, mostly including +12. WT1 deletions/mutations were found in one hypodiploid, eight pseudodiploid, and one hyperdiploid (47-49 chromosomes) tumor, but in none of the hyperdiploid (> or =50 chromosomes) tumors. Of the 10 tumors with WT1 abnormalities, 6 had a homozygous WT1 deletion, 1 had a nonsense WT1 mutation and loss of heterozygosity at 11p, 1 had an intragenic hemizygous WT1 deletion without detectable WT1 mutation, and 2, which occurred in Wilms tumor-aniridia-genitourinary abnormalities-mental retardation syndrome patients, had a hemizygous deletion and a missense or frameshift mutation of WT1. Six of the nine tumors with homozygous or hemizygous WT1 deletions had chromosome aberrations involving chromosome band 11p13 in one of the two chromosomes 11. While one hypodiploid and one pseudodiploid patient died of the disease, and one hyperdiploid (47-49 chromosomes) patient was alive in nonremission, all hyperdiploid (> or =50 chromosomes) patients had no evidence of disease at the last follow-up. Our data show that chromosome aberrations are closely correlated to WT1 abnormalities and suggest that hyperdiploid (> or =50 chromosomes) Wilms tumors may be characterized by the absence of WT1 abnormalities and possibly also by a favorable prognosis.
    Genes Chromosomes and Cancer 06/1999; 25(1):26-32. DOI:10.1002/(SICI)1098-2264(199905)25:1<26::AID-GCC4>3.0.CO;2-Z · 4.04 Impact Factor
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    ABSTRACT: A fusion transcript of AF10 and CALM was isolated recently from the U937 cell line with t(10;11)(p13;q21). We performed reverse transcription-polymerase chain reaction and sequencing analysis on the t(10;11) leukemia samples obtained from four patients and one cell line, and we identified reciprocal fusion transcripts of AF10 and CALM in all the samples. The fusion transcripts in the five samples showed four different breakpoints in AF10 and three different breakpoints in CALM. In addition, the fusion transcripts in one sample showed a nucleotide sequence deletion in AF10, and those in two samples showed a nucleotide sequence deletion in CALM; the deletions were thought to be caused by alternative splicing. The variety of breakpoints and splice sites in the two genes resulted in five different-sized AF10-CALM mRNAs and in four different-sized CALM-AF10 mRNAs. Clinical features of 11 patients, including 6 of our own and 5 reported by others, in whom the fusion of AF10 and CALM was identified, are characterized by young age of the patients, mixed-lineage immunophenotype with coexpression of T-cell and myeloid antigens, frequent occurrence of a mediastinal mass, and poor clinical outcome.
    Genes Chromosomes and Cancer 05/1999; 25(1):33-9. DOI:10.1002/(SICI)1098-2264(199905)25:1<33::AID-GCC5>3.0.CO;2-3 · 4.04 Impact Factor
  • T Sugimoto · Y Komada · M Sakurai · Y Horii · R Morishita · R Nagai · K Takahashi · Y Asada ·
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    ABSTRACT: Human neuroblastoma (NB) cell lines have at least three morphological appearance of neuroblastic (N-type), substrate-adhessive (S-type) and intermediate(I) cells. Our previous study revealed S-type cells expressed alpha-smooth muscle actin, desmin and/or basic-calponin, indicating the plausible smooth muscle cell characteristics of S-type cells. In this study, a new human NB cell line, MP-N-MS, was established from bone marrow metastasis of a one year and six-month old girl with advanced NB, originating from right adrenal gland. Morphology of this cell line is composed of S-type cells. MP-N-MS was identified as a NB cell line by surface membrane antigen analysis and MYCN gene amplification. EWS-FLI1 and EWS-ERG chimeric products, observed in Ewing family tumors, were not detected by RT-PCR (reverse transcriptase-polymerase chain reaction). In cytoskeletal protein analysis, alpha-smooth muscle actin and basic calponin of smooth muscle cell markers were detected. Furthermore, smooth myosin of SM1 isoform was identified in MP-N-MS cell line by immunofluorescence, Western blot and RT-PCR, whereas smooth myosin of SM2 was detected by RT-PCR. MP-N-MS is the first cell line, showing SM1 and SM2 isoforms. The presence of smooth muscle myosin of SM1 and SM2 isoforms in MP-N-MS demonstrated the mature smooth muscle phenotype of this NB cell line, and the ability of NB cells to differentiate into smooth muscle cell.
    Human Cell 04/1999; 12(1):47-56. · 1.41 Impact Factor
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    Y Mitani · J Maruyama · K Maruyama · M Sakurai ·
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    ABSTRACT: In chronic exercise-trained animals, acetylcholine (ACh)-stimulated endothelial nitric oxide (NO) release is enhanced in the systemic circulation. The purpose of the present study was to determine whether chronic exercise training also enhances NO-mediated relaxation in rat pulmonary artery. Sprague-Dawley rats were randomly divided into groups of exercise-trained and sedentary control rats. The exercise-trained rats ran on a motor-driven treadmill at 30 m x min(-1) up a 15 degree incline 10-60 min x day(-1), 5 days per week for 10 weeks, and had less body weight, lower serum total cholesterol and triglyceride levels than sedentary rats. Contraction induced by potassium chloride and prostaglandin (PG)F2alpha were similar between isolated conduit pulmonary arterial rings from sedentary and exercise-trained rats. There were no differences between PGF2alpha-precontracted rings from sedentary and exercise trained rats in both ACh and sodium nitroprusside-induced relaxations. The NO synthase inhibitor, nitro-L-arginine, suppressed ACh-induced relaxation in both sedentary and exercise-trained rats. These results suggested chronic exercise training did not alter the acetylcholine-induced endothelial NO production and release and the sensitivity of vascular smooth muscle cell to NO in isolated conduit pulmonary artery of rat.
    European Respiratory Journal 04/1999; 13(3):622-5. DOI:10.1183/09031936.99.13362299 · 7.64 Impact Factor
  • J Chipeta · Y Komeda · X L Zhang · M Sakurai · E Azuma ·

    Blood 03/1999; 93(3):1120-2. · 10.45 Impact Factor
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    ABSTRACT: The mass screening (MS) of neuroblastoma has been undertaken in Japan by measuring urinary catecholamine metabolites in infants at the age of 6 months. To clarify the biological characteristics of MS-positive (MS+) tumors in infants and MS-negative (MS-)/late-presenting tumors in young children, metaphase cytogenetic and/or interphase 2-color FISH analyses using terminal 1p and pericentromeric 1q probes were performed on 246 (186 MS+ and 60 MS-) patients with neuroblastomas. The 246 tumors were classified into 4 groups on the basis of the constitution of chromosome 1; 22 tumors had disomy 1 with no 1p deletion (Dis1Norm1p); 41 tumors had disomy 1 or tetrasomy 1, all with the 1p deletion (Dis1Del1p); 164 tumors had trisomy 1, pentasomy 1, or a mixed population of cells with trisomy 1 and cells with tetrasomy 1, none with 1p deletion (Tris1Norm1p); 19 tumors with the same copy numbers of chromosome 1 as the Tris1Norm1p group, had 1p deletion (Tris1Del1p). mycn amplification was absent in the Dis1Norm1p and Tris1Del1p groups, frequent in the Dis1Del1p group (24/41), and rare in the Tris1Norm1p group (3/164) (p < 0.0001). Event-free survival at 5 years was lowest [19.5%; 95% confidence interval (CI), 5.1-33.9] in the Dis1Del1p group, highest in the Tris1Norm1p (96.3%; 95% CI, 93.5-99.2) and Tris1Del1p (94.7%; 95% CI, 84.7-104.8) groups, and intermediate but varied (54.5%; 95% CI, 33.7-75.4) in the Dis1Norm1p group (p < 0.0001). Of the MS+ tumors, 90% were Tris1Norm1p or Tris1Del1p, and 55% of the MS- tumors were Dis1Del1p. The finding that the Dis1Del1p tumors were frequent in MS- but not in MS+ tumors suggests the limited efficacy of the MS program into reducing mortality from neuroblastoma.
    International Journal of Cancer 02/1999; 80(1):54-9. DOI:10.1002/(SICI)1097-0215(19990105)80:1<54::AID-IJC11>3.0.CO;2-G · 5.09 Impact Factor
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    ABSTRACT: It has been reported that aclarubicin inhibits etoposide (VP-16) induced cytotoxicity in human lung cancer cell lines (1, 2). However, it still remains unclear how aclarubicin (ACR) inhibits etoposide-induced cytotoxicity. We report here that the combination of ACR and VP-16 showed antagonistic cytotoxic effect in P388 murine leukemic cells. DNA unwinding assay showed that 1000 ng/ml ACR significantly reduced VP-16 induced early DNA double strand(ds) breaks compared to that of VP-16 alone at a concentration of 10 microM. However, ACR did not inhibit VP-16 induced early DNA double strand breaks at a concentration of 100 ng/ml, a clinically achievable concentration. Furthermore, DNA repair occurred within two hours after removing VP-16 even if ACR was co-cultured at concentrations of 100 and 1000 ng/ml. DNA agarose gel electrophoresis and detection of sub-G1 fraction by flowcytometer showed that 100 ng/ml of ACR inhibited VP-16 induced DNA ladder formation and formation of sub-G1 fraction. Radioactive precursor incorporation studies showed that VP-16 inhibited DNA synthesis rather than RNA synthesis. On the other hand, ACR selectively inhibited RNA synthesis at a concentration of 100 ng/ml. The VP-16 induced increment of [3H]-L-leucine uptake was canceled by addition of 100 ng/ml of ACR. These data suggest that ACR inhibited VP-16 induced apoptosis by the inhibition of RNA synthesis along with protein synthesis, but not early DNA double strand breaks and DNA repair at a concentration of 100 ng/ml in P388 murine leukemic cells.
    Journal of experimental & clinical cancer research: CR 01/1999; 17(4):435-42. · 4.23 Impact Factor

  • H Inaba · H Kawasaki · S Nakamura · H Yamamoto · Y Kaneko · N Satake · Y Komada · M Ito · M Sakurai ·
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    ABSTRACT: We report a case of a 20-year-old Japanese female with recurrent anaplastic large cell lymphoma (ALCL) associated with Sjögren's syndrome (SjS). She was first diagnosed to have ALCL presenting with axillary lymphadenopathy, which within a month underwent spontaneous remission, at the age of 12 years. Eight years later she developed left inguinal lymphadenopathy with clinical overt sicca symptoms associated with elevated serum IgG, interleukin (IL)-1beta and IL-6 levels. Lymph node biopsy was now diagnostic of ALCL characterized by large pleomorphic CD30+ blast cells with the specific chromosomal abnormality, t(2;5)(p23;q35). In contrast to this the salivary gland and renal biopsy revealed infiltration of small lymphocytes, morphologically and cytogenetically distinct from the ALCL cells. Interestingly, SjS symptomatology correlated with disease activity of ALCL and based on an association with elevated IgG and IL-6 levels, suggesting that the concurrence of these two diseases could be more than coincidental. To the best of our knowledge, this is the first reported case of ALCL presenting concurrently with SjS.
    Leukemia and Lymphoma 01/1999; 32(1-2):183-8. DOI:10.3109/10428199809059260 · 2.89 Impact Factor

Publication Stats

4k Citations
805.09 Total Impact Points


  • 1978-2008
    • Saitama Cancer Center
      • Saitama Cancer Center Hospital
      Saitama, Saitama, Japan
  • 2001
    • Mie-chuo Medical Center
      Matsusaka, Mie, Japan
  • 1990-2001
    • Social Insurance Chukyo Hospital
      Nagoya, Aichi, Japan
  • 1987-1999
    • Mie University
      • • Department of Pediatrics
      • • School of Medicine
      Tu, Mie, Japan
  • 1991
    • Kyoto Prefectural University of Medicine
      • Department of Pediatrics
      Kyoto, Kyoto-fu, Japan
    • Noguchi Memorial Institute for Medical Research
      Akra, Greater Accra, Ghana
  • 1989
    • Tokyo Dental College
      • Department of Dental Anesthesiology
      Tiba, Chiba, Japan