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Biomedical subjects

N Maseki

Publications and source records attributed to N Maseki.

At least 73 records · Page 4Linked to original sources
PubMed1988

Trisomy 11 in chronic myelomonocytic leukemia: report of two cases and review of the literature.

Two cases of chronic myelomonocytic leukemia (CMMoL) with trisomy 11 as the sole chromosome abnormality are reported. A simple trisomy 11 also has been reported in 11 patients with myeloproliferative disorders, including CMMoL and acute nonlymphocytic leukemia (ANLL) in the literature. From data on these 13 patients, leukemia with trisomy 11 may be characterized by a nonlymphoid origin and myelomonocytic features. Patients with this abnormality were mostly elderly, and often had a preleukemic phase and a short survival. We propose that trisomy 11 and nonlymphocytic leukemia with myelomonocytic features may be a new association in human neoplasia.

Aged↗
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

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

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↗
PubMed1987

Chromosome abnormalities in malignant lymphoma in patients from Saitama.

Clonal chromosome abnormalities were found in 89 (97%) of 92 patients with non-Hodgkin's malignant lymphoma including immunologically determined 34 B- and 25 T-lymphomas; only 3 of 19 T-lymphoma patients examined had serum adult T-cell leukemia/lymphoma-associated antigen antibody. Association of 8q24 translocations with small non-cleaved cell (P less than 0.01) and that of t(14;18) (q32;q21) with follicular histology (P = 0.03) were significant. Several other abnormalities were also found to be correlated with histological or immunological phenotypes: trisomy 5 with diffuse, mixed cell lymphoma (P = 0.03); a break at 3q21 with diffuse, large cell lymphoma (P = 0.04); gain of chromosome 18 or X and rearrangements of 13q with immunoblastic lymphoma (P = 0.02, 0.03, and 0.03, respectively); and rearrangements of 7q with diffuse large cell histology (P = 0.02) and T-cell phenotype (P = 0.02). Multiple clones were more frequently seen in T-cell lymphoma than in B-cell lymphoma (P = 0.01). Structural changes of the long arm of chromosome 4 or 15 and a break in 6p21 were also associated with T-lymphoma (P = 0.03, respectively). Since the frequency of T-lymphoma is significantly higher and that of t(14;18) is significantly lower in the adult T-cell leukemia/lymphoma nonendemic area of Saitama in Japan than in Minnesota in the United States (P less than 0.01), factors affecting the lymphoma-genesis may be different or operating in different intensities in different areas.

Adolescent↗
PubMed1987

Hemophagocytic syndrome complicating T-cell acute lymphoblastic leukemia with a novel t(11;14)(p15;q11) chromosome translocation.

A case of hemophagocytic syndrome that developed in a patient with T-cell acute lymphoblastic leukemia (ALL) with a novel chromosome translocation involving 14q11 is reported. A 15-year-old boy with T-cell ALL in relapse showed leukemic cells with an abnormal karyotype of 46,XY,-15,t(11;14)(p15;q11), +der(15)t(15;?)(p11;?). Pancytopenia and extensive hemophagocytosis by macrophages in the bone marrow were observed after reinduction chemotherapy and again at the terminal stage. At autopsy, infiltration of such cells was also found in other organs. The findings suggested occurrence of hemophagocytic syndrome probably associated with cytomegalovirus (CMV) infection. The t(11;14)(p15;q11) may be a novel translocation specific for T-cell ALL, and conceivably, the association of T-cell ALL with the histiocytosis in this patient may not have been coincidental.

Adolescent↗
PubMed1987

Different karyotypic patterns in early and advanced stage neuroblastomas.

Of 23 untreated and 7 treated (relapsed) neuroblastomas, 14 (11 untreated, 3 treated) had modal chromosome numbers in the diploid (45 to 51), 9 (8 untreated, 1 treated) in the triploid (60 to 77), and 6 (3 untreated, 3 treated) in the hypotetraploid (81 to 88) range, and one (untreated) had hypertetraploidy (100). The near-or-pseudodiploid and hypotetraploid tumors were characterized by numerous structural abnormalities, most frequently of 1p, and frequent presence of double minutes or homogeneously staining regions. The near-triploid tumors were characterized by three almost complete haploid sets of chromosomes, and few structural abnormalities. N-myc amplification was found in five of the near-or-pseudodiploid or hypotetraploid tumors but in none of the near-triploid tumors. Most near-triploid tumors were found in infants at stage I or II, and the near-or-pseudodiploid or hypotetraploid tumors in children at stage II or IV mostly 1 year old or older. Among the untreated patients, all 8 with a near-triploid tumor were alive with no evidence of the disease, and the 11 with a near-or-pseudodiploid tumor had a median survival of only 376 days (P less than 0.05), 7 of the 11 being dead. Thus, the near-triploid patients had well recognized favorable prognostic factors and an excellent prognosis, and the near-or-pseudodiploid patients had unfavorable prognostic factors and a dismal prognosis. The hypotetraploid tumors seemed to have karyotypic and clinical features in common with the near-or-pseudodiploid tumors. We presume that the near-triploid tumors and the near-or-pseudodiploid or hypotepraploid tumors may constitute distinctly different subcategories within neuroblastomas.

Age Factors↗
PubMed1987

Chromosome studies of hematopoietic colonies for distinct diagnosis of megakaryoblastic crisis of chronic myelogenous leukemia: a case report.

Chromosome studies of cells from megakaryocytic colonies (CFU-Meg) as evidenced by a megakaryocyte-specific monoclonal antibody, TP80, from a patient with chronic myelogenous leukemia (CML) in the blast crisis (BC) revealed the same aberrant karyotype, 52,XY,+9,+9,+18,+19,+21,+22,t(9;22)(q34;q11),t(9;22), as that having newly appeared in the peripheral blood. Cells from erythroid bursts (BFU-E) showed only the standard 46,XY,t(9;22) karyotype, and cells from granulocyte/macrophage colonies (CFU-GM) had either of these karyotypes. These results demonstrated that the whole megakaryocytic line and part of the granulocyte/macrophage line had been involved in the BC while the erythroid line totally belonged to the original clone. Chromosome analysis coupled with immunophenotyping of hemopoietic colonies was useful for a definite diagnosis of megakaryoblastic crisis of CML in this patient.

Adult↗
PubMed1987

Nonrandom additional chromosome changes in acute nonlymphocytic leukemia with inv(16)(p13q22).

Five patients with acute nonlymphocytic leukemia and inv(16)(p13q22), all with additional chromosome changes, are reported. Three were diagnosed as having acute myelomonocytic leukemia (FAB-M4), and the other two as having acute monocytic leukemia (FAB-M5b). All five patients had abnormal eosinophils in the bone marrow at diagnosis. Two had a deletion of the long arm of chromosome #7, del(7)(q31), and a trisomy of chromosome #22. These changes have been reported frequently in acute nonlymphocytic leukemia with inv(16), but are extremely rare in leukemias with other specific rearrangements including t(9;22), t(8;21), and t(15;17). Our findings and review of the literature indicate that inv(16) is observed not only in acute myelomonocytic leukemia but also in acute monocytic leukemia, and that del(7q) and +22 are nonrandomly associated with inv(16) as additional abnormalities. No significant differences in the clinical features seem to exist between the patients with only inv(16) and those with inv(16) and additional chromosome changes, except for the lower white blood cell count in the latter group.

Adolescent↗
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

[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↗
PubMed1986

Myeloblastoma with an 8;21 chromosome translocation in acute myeloblastic leukemia.

An 8;21 chromosome translocation was found in cells from myeloblastomas of two acute myeloblastic leukemia (AML) patients. In one patient, a sudden onset of paraplegia, which was caused by an epidural myeloblastoma in the thoracic vertebral canal, was the initial symptom of the disease and that of the first relapse. In the other, myeloblastomas, which occurred in the breasts during a hematologic remission, heralded the first relapse. Karyotypes of tumor cells obtained from both patients showed the t(8;21) and additional chromosome abnormalities. These findings, together with earlier experience and reports in the literature, indicate that myeloblastoma may be unique to the 8;21 translocation, and that certain chromosomal abnormalities additional to the t(8;21) may be necessary for the tumor formation.

Adolescent↗