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Biomedical subjects

M Sakurai

Publications and source records attributed to M Sakurai.

At least 685 records · Page 38Linked to original sources
PubMed1988

[Clinical evaluation of gamma-seminoprotein as a serum marker of prostate carcinoma].

The serum levels of gamma-Seminoprotein (gamma-Sm) were determined by enzyme immunoassay in 77 patients with prostatic cancer (30 untreated and 47 treated), 44 patients with benign prostatic hypertrophy and 12 patients with prostatitis. Serum levels of gamma-Sm in each disease were as follows; untreated prostatic cancer 23.2 +/- 18.3 ng/ml (positive rate 93%), treated prostatic cancer 4.7 +/- 8.3 (positive rate 25.5%), benign prostatic hypertrophy 3.6 +/- 3.3 (positive rate 23.7%), prostatitis 2.0 +/- 2.0 (positive rate 7.7%). Serum gamma-Sm levels in prostatic cancer were higher in advanced stage but relatively low in poorly differentiated adenocarcinoma. We consider that the level of serum gamma-Sm is a useful tumor marker as well as prostatic acid phosphatase (PAP) in diagnosis and follow-up of the patients with prostatic cancer.

Acid Phosphatase↗
PubMed1988

Incorporation of N4-behenoyl-1-beta-D-arabinofuranosylcytosine into DNA as 1-beta-D-arabinofuranosylcytosine.

BHAC is a newly synthesized lipophilic derivative of ara-C. To clarify its pharmacological mode of action, P388 murine leukemic cells were incubated with two different types of 14C-labeled BHAC, [cytosine-2-14C]BHAC and [acyl-1-14C]BHAC, and DNA was extracted with phenol. The phenol-extracted DNA was then hydrolyzed by nuclease P1 and analyzed with high-performance liquid chromatography (HPLC). The radioactivity of DNA, from the cells incubated with [cytosine-2-14C]BHAC, was detected as ara-CMP. But the radioactivity of DNA, from the cells incubated with [acyl-1-14C]BHAC, was hardly detected. On the other hand, the main radioactivity of the acid soluble fraction was determined as ara-CTP. On the basis of our results, BHAC is not phosphorylated directly to produce N4-behenoyl-ara-CTP, but is mainly converted to ara-C which subsequently produces ara-CTP, the active metabolite of the drug, and which is then incorporated into DNA.

Animals↗
PubMed1988

Chromosome translocations involving band 7q35 or 7p15 in childhood T-cell leukemia/lymphoma.

In a chromosome study in childhood T-cell leukemia/lymphoma, we found t(7;11)(q35;p13) in 2 patients, t(7;14) (q35;q11) in one patient, and t(7;14)(p15;q32) in 1 patient. Southern blotting and in situ chromosomal hybridization studies in one patient with the t(7;11) demonstrated that both alleles of the T-cell antigen receptor beta-subunit gene (TCRB) were rearranged, and that one TCRB allele had relocated from 7q35 to the fusion point in band p13 of the involved chromosome 11 (11p-). These findings suggest that juxtaposition of TCRB with the putative oncogene tcl-2 located in band 11p13 may be a critical step toward development of this T-cell leukemia/lymphoma. In the other two translocations, all breakpoints were sites for lymphocyte function genes, ie, 7q35 for TCRB, 14q11 for T-cell antigen receptor alpha-subunit gene (TCRA), 7p15 for T-cell antigen receptor alpha-subunit gene (TCRG), and 14q32 for immunoglobulin heavy-chain gene (IGH). Thus, the findings in these cases allow us to expand the above hypothesis and propose that the juxtaposition of TCRB or TCRG with tcl-2, TCRA, or IGH through chromosomal translocation may activate a mechanism for the genesis of T-cell leukemia/lymphoma with these chromosome translocations.

Adolescent↗
PubMed1988

The non immunogenicity of CALLA in leukemic children.

The sera from 55 children with acute lymphoblastic leukemia (ALL) treated with active immunotherapy were examined for the presence of antibodies against common ALL antigen (CALLA). A solid phase indirect radioimmunometric assay (IRA) was developed which enabled the detection of anti-CALLA antibody in patients' sera, utilizing the ability of affinity-purified CALLA to bind Ricinus communis agglutinin and anti-CALLA antibody simultaneously. Using IRA, anti-CALLA antibody activity could not be detected in a majority of patients. We concluded that the patients did not raise comparable antibodies against CALLA, indicating this antigen is not immunogenic for ALL patients.

Antibodies, Neoplasm↗
PubMed1988

A novel translocation, t(9;17)(q34;q23), in aggressive childhood lymphoblastic lymphoma.

In a chromosome study of childhood lymphoblastic lymphoma, we found a novel translocation, t(9;17)(q34;q23), in three patients. They presented with mediastinal mass and no bone marrow involvement. Despite intensive chemotherapy, one patient had no response, the other two relapsed after a brief remission, and all progressed to death. The 9;17 translocation may have a clinical implication for lymphoblastic lymphoma patients in predicting a poor prognosis. Since, in addition to our cases, involvement of the 9q34 breakpoint, together with 2q33, 14q11, or 7q34, has been reported in the literature in four lymphoblastic lymphoma patients, a gene located in 9q34 and referred to as tcl-3 may participate in the genesis of the T cell malignancies carrying these translocations. Furthermore, as is the case in other lymphomas, the reciprocal breakpoint, 17q23, might be the site of a yet unidentified T cell function gene.

Adolescent↗
PubMed1988

Clinical characteristics of infant acute leukemia with or without 11q23 translocations.

Of 34 infants less than 1 year of age with acute leukemia, 20 had an 11q23 translocation (group I), 8 had t(4;11), 5 had t(11;19), 3 had t(1;11), 2 had t(10;11), 1 had t(9;11), and the other had an 11q+ chromosome. Nine had other chromosome changes (group II), including t(1;19), t(8;14), 5q- chromosome, or +8 in one each, and a translocation involving 7p22 in two. The other five had normal diploidy in their leukemic cells (group III). Thus, the 11q23 translocation was seen in 50% of the leukemic infants, and in as high as 75% of the infants less than 6 months old. While the 7p22 translocations were both seen in those less than 6 months, the four chromosome abnormalities without 11q23 translocation mentioned above and normal diploidy were found only in those 6 months old or more. The group I patients had higher leukocyte counts than the group II (p less than 0.05) or group III (p less than 0.01) patients. Of the 20 group I patients, 16 were classified as having ALL, and 4 were classified as having ANLL. Eleven of 15 ALLs with the 11q23 translocation showed an Ia+, CALLA-, and B4+ (8 of 9 examined) immunophenotype. Coexpression of lymphoid and myeloid Ags was seen in four ALLs and two ANLLs with the 11q23 translocation. The survival of group II patients (median, 9 months) was significantly shorter than that of group I (median, 19 months) (p less than 0.05) or group III (median, 44 months) (p less than 0.01) patients; the difference in the survival between group I and group III patients was not significant. It is noteworthy that 5 of the 20 group I patients have survived 20 months or more without relapsing.

Antigens, Differentiation↗
PubMed1988

Discontinuing chemoimmunotherapy in childhood acute lymphoblastic leukemia.

We examined the results of discontinuing therapy in Japanese children with acute lymphoblastic leukemia. Of the 209 patients in chemoimmunotherapy study, 120 (57.4%) had all chemotherapy stopped after 3 years of complete remission, and 72 (34.4%) reached the point of discontinuing immunotherapy after 5 years of complete remission. Of the 120 children removed from chemotherapy, 14 (11.7%) have relapsed, mainly in the extramedullary sites (5 testis, 5 bone marrow, 3 central nervous system, 1 bone); relapses occurred 1-23 months after cessation of chemotherapy (median 11 months). Boys had a higher post-chemotherapy relapse rate than girls (0.21 vs. 0.08, P less than 0.05). None of the 72 children removed from immunotherapy have yet relapsed. Long-term remission and possibly cure can be expected in approximately one half of newly-diagnosed Japanese patients. Moreover, the active immunotherapy could be of benefit to elimination of bone marrow relapses after cessation of chemotherapy in children with acute lymphoblastic leukemia.

Adolescent↗
PubMed1988

[Primary carcinoma of the male urethra: report of two cases].

Two cases of primary carcinoma of male urethra are reported. Case 1: A 31-year-old male, who complained of urethral bleeding, was admitted to our clinic in April, 1982. A rice size papillary tumor was found at the fossa navicularis in the glans, and resected by electric knife. Histologically, the tumor was well differentiated squamous cell carcinoma. Case 2: A 37-year-old man, who complained of urethral bleeding, was admitted to our clinic in July, 1985. A tumor was found at the fossa navicularis in the glans and resected. Histologically, the tumor was well differentiated squamous cell carcinoma confined to mucosa. These two cases have not shown any signs of recurrence. Including these cases, 135 cases of primary carcinoma of urethra in the literature in Japan are reviewed.

Adult↗
PubMed1988

[Experiences with sultamicillin granules in pediatric patients].

Sultamicillin (SBTPC) is a combination drug of sulbactam (SBT) and ampicillin (ABPC) in an ester bonding at 1:1 ratio. SBT, a new semisynthetic beta-lactamase inhibitor restores and extends the spectrum of ABPC against resistant strains of bacteria. SBTPC granules were administered to 26 pediatric patients with infections, and clinical efficacies were studied in 23 patients. The clinical efficacy rate was 95.7% and the drug was evaluated to be highly effective for the treatment of infectious diseases in the pediatric field. SBTPC was safe and well tolerated.

Age Factors↗
PubMed1988

Characteristic karyotypic pattern in T-cell lymphoproliferative disorders with reactive "angioimmunoblastic lymphadenopathy with dysproteinemia-type" features.

We report the clinical, histological, immunophenotypic, and cytogenetic findings in ten patients with T-cell lymphoproliferative disorders demonstrating reactive "angioimmunoblastic lymphadenopathy with dysproteinemia (AILD)-type" features. Fifteen available specimens were diagnosed as atypical hyperplasias (four) or malignant lymphomas (11). The latter were classified as AILD-type (five), T-zone (four), lymphoepithelioid (one), and low-grade, unclassified lymphoma (one). Despite the histologic differences, all these lesions shared minor nuclear atypicalities and reactive AILD-type features such as prominent vascularity, plasma cells, eosinophils, macrophages, and residual germinal centers. All lesions were immunophenotyped as predominantly T cell. The chromosome pattern was characterized by the frequent presence of karyotypically unrelated abnormal clones and/or cells with nonclonal chromosome abnormalities, a large population of normal mitotic cells, and a high incidence of trisomies 3 and 5. Sequential cytogenetic and histologic studies in five patients revealed that atypical hyperplasia and lymphoma with AILD-type features shared the same cytogenetic characteristics, ie, an unstable coexistence of normal mitotic cells and small-clonal and/or nonclonal abnormal cells, and that histologic transformation from low-grade lymphoma to immunoblastic lymphoma was accompanied by a selective proliferation of abnormal clonal cells. The AILD-type histology and the characteristic karyotypic pattern may be the expression of a specific pathogenesis and may warrant the separation of these neoplasias from other peripheral T-cell lymphomas.

Adult↗