PubMed Health⌕ Search

Biomedical subjects

K Yumura

Publications and source records attributed to K Yumura.

At least 19 recordsLinked to original sources

[CD5+, CD7+, and CD19+ non-Hodgkin's lymphoma in a child].

The 9-year-old boy was admitted to Shizuoka Children's Hospital because of cervical lymphoadenopathy. Complete blood count showed normal RBC and platelet counts. WBC was 2700/microliters with no tumor cells. Bone marrow aspirate showed normocellularity with 34% tumor cells. Lymph node biopsy from his right neck was performed and the patient was diagnosed as non-Hodgkin's lymphoma (lymphoblastic type). Surface marker analysis disclosed that the tumor cells were positive for CD5, CD7, CD19, CD38, CD71, and Ia antigen. Chromosomal analysis of the cervical lymph node revealed 46, XY, t(7;14) (p15;q32). Molecular investigation with appropriate probe showed germ-line configurations of IgH gene, TcR beta gene, and TcR gamma gene, and one rearranged band of TcR delta gene. Monoclonality of tumor cells was demonstrated from chromosomal analysis and molecular study. CD7 and CD19 are not lineage specific antigens because CD7 is expressed on immature AML cells and CD19 is expressed on T ALL cells or AML cells. Moreover, TcR delta rearrangement is considered to occur at early phase of hematolymphoid cells. Based on these data, tumor cells of this patient is considered to originate from immature lymphoid cell, so-called lymphoid stem cell.

Antigens, CD19↗

Aggressive natural killer cell leukaemia/lymphoma: report of four cases and review of the literature. Possible existence of a new clinical entity originating from the third lineage of lymphoid cells.

The morphologic, immunologic, genotypic and functional properties of peripheral blood and bone marrow cells or cultured cells from four patients with a clinically aggressive non-T, non-B natural killer cell leukaemia/lymphoma (ANKL/L) are described. The leukaemic cells possessed medium to large granules in the cytoplasm, antigens against CD38, CD2, OKIa 1 and NKH-1 CD56) monoclonal antibodies on their cell-surface, and also showed natural killer (NK) activity. In addition, these ANKL/L belonged to neither T- nor B-cell lineage, proved by studying clonal gene rearrangement for the T beta, T gamma and T delta receptors, and immunoglobulin. After comparing them with the seven cases of ANKL/L reported in other institutions, with regard to immunophenotype, genotype and function, we conclude that ANKL/L originating from a third lineage of lymphoid cells is a distinct clinical entity.

Adolescent↗

Rearrangement of variable region T cell receptor gamma genes in acute lymphoblastic leukemia. V gamma gene usage differs in mature and immature T cells.

Using probes recognizing variable regions (V gamma) and joining regions (J gamma) of the T cell receptor (TCR) gamma gene, we have analyzed the usage of V gamma genes in 24 patients with T cell acute lymphoblastic leukemia (ALL) and 36 patients with B-precursor ALL. In CD3- T-ALL derived from immature T cells, V gamma genes more proximal to J gamma were frequently rearranged; V gamma 8, V gamma 9, V gamma 10, and V gamma 11 were used in 19 of 24 rearrangements. In contrast, CD3+ T-ALL derived from a more mature stage of T cell ontogeny, showed a high frequency of rearrangements involving V gamma genes distal to J gamma; V gamma 2, V gamma 3, V gamma 4, and V gamma 5 were used in 17 of 25 rearrangements. In B-precursor ALL, no notable bias of V gamma gene usage was observed. This probably reflects the possibility that TCR genes may not rearrange according to a T cell hierarchy when under control of a B cell gene program. Furthermore, deletions of those V gamma genes located 3' to rearranged V gamma genes were observed in all patients analyzed. This supports the theory that loop deletion is a major mechanism for TCR-gamma gene rearrangement.

Antigens, Differentiation, T-Lymphocyte↗

A novel leukemia cell line, MR-87, with positive Philadelphia chromosome and negative breakpoint cluster region rearrangement coexpressing myeloid and early B-cell markers.

We developed a Philadelphia chromosome (Ph) positive cell line, designated MR-87, from a 4-year-old boy with Ph+-acute leukemia. MR-87 cells grew in single cell suspensions with a doubling time of 120 to 144 hours. Both MR-87 and original leukemia cells were positive for myeloperoxidase (MPO) and myeloid antigen CD13. These cells exhibited the early B-cell phenotype, ie, terminal deoxynucleotidyl transferase+, Ia+, CD19+, and CD10+. Rearrangement of the immunoglobulin heavy chain was confirmed in both. Approximately 80% of MR-87 cells coexpressed CD13 and lymphoid antigens CD10 or CD19, as confirmed by a two-color analysis. Simultaneous expression of MPO and CD19 on a single MR-87 cell was demonstrated at ultrastructural level. Thus, MR-87 is a Ph+ leukemia cell line exhibiting a hybrid phenotype. The breakpoint cluster region (bcr) was not rearranged in the MR-87 cells and subsequent analysis using antisera revealed that these cells expressed a novel protein, P190c-abl, which was immunoprecipitated with anti-abl and anti-phosphotyrosine antibodies. The MR-87 line will be most useful for investigating the biology and pathogenesis of Ph+ bcr- acute leukemia.

Antigens, Differentiation, B-Lymphocyte↗

Concomitant rearrangements of T-cell beta- and gamma-chain genes in childhood T-lineage leukemia/lymphoma.

Similar to the immunoglobulin (Ig) gene rearrangements in B-lineage cells, identification of T-cell receptor (TCR) gene rearrangements is a novel clonal marker and necessary to establish a T-cell lineage. The function of T-cell gamma-chain (T gamma) gene is still unknown, but because of its shared properties with T-cell alpha-chain (T alpha) and T beta genes, we analysed T gamma gene organization in 10 patients with T-lineage leukemia/lymphoma as well as in non-T lineage leukemias. All 10 cases of T-lineage leukemia/lymphoma, whose phenotypes were different, demonstrated T gamma gene rearrangements as well as T beta gene rearrangements. In contrast, among the non-T-lineage leukemias, the emergence of T beta and/or T gamma gene rearrangements was varied. Based on these findings, concomitant rearrangements of T beta and T gamma genes are characteristic in childhood T-lineage leukemia/lymphoma regardless of their phenotypic differences. Furthermore, no obvious developmental hierarchy was observed between T beta and T gamma gene arrangements in these leukemia/lymphoma cells.

Antibody Diversity↗

Remarkable depression of CD4+2H4+ T cells in severe chronic active Epstein-Barr virus infection.

In order to better understand the features of chronic active Epstein-Barr (EB) virus infection, we employed two-colour immunofluorescence staining with monoclonal antibodies and flow cytometry analysis to study the lymphocyte phenotypes of two patients with severe symptoms of this disorder as well as four patients with mild symptoms. We found an increased number of activated T cells, as characterized by CD4+Ia+, CD8+Ia+, or CD4+Tac+ phenotypes, and a markedly decreased CD4+2H4+ T cell subpopulation, previously characterized as a suppressor-inducer subset, in the patients with severe symptoms. In contrast, the four patients with mild symptoms showed only a slightly elevated number of activated T cells and a normal CD4+2H4+/CD4+ ratio. These phenotypic differences may suggest heterogeneity in this disorder. Also, a failure in the suppressor-inducer population could contribute to changes in the host-virus relationship and the degree of the decrease in this population may correlate directly with the severity of the disease.

Antigens, Surface↗

Heterogeneity of acute undifferentiated leukemia at the immunoglobulin and T-cell receptor genes level.

Phenotypic markers of leukemic cells from 76 children with acute leukemia were examined. Of these cases, 7 were diagnosed as acute undifferentiated leukemia (AUL) whose leukemic cells were negative for myeloperoxidase and did not react with lineage-specific or lineage-associated monoclonal antibodies. Then, we analyzed the configuration of both immunoglobulin (Ig) and T-cell receptor beta-chain (T beta) gene in these 7 AUL cases. Three cases had no rearrangement of Ig or T beta genes which was suggestive of non-lymphoid origin of these cases. In contrast, 4 cases showed rearrangements of Ig and/or T beta genes. One of these 4 cases demonstrated T beta gene rearrangement with retention of the germline configuration of Ig genes. Two cases with both Ig and T beta gene rearrangements also showed kappa-chain gene rearrangements. These findings indicate the heterogeneity of AUL at the DNA level, and may cast new light on the early differentiation of hematopoietic progenitor cells.

Acute Disease↗

Further heterogeneity of childhood common acute lymphoblastic leukemia.

In an attempt to look further at the problem of heterogeneity, we have studied the immunoglobulin (Ig) gene organization in leukemic cells from 20 children with acute lymphoblastic leukemia (common ALL). Nineteen cases were divided into two subgroups: 12 cases with rearrangement of the Ig heavy (H) chain genes and 7 cases with rearrangement of both the Ig H and light (L) chain genes. No Ig gene rearrangement was found in one case. These findings indicate that there is more heterogeneity among patients with common ALL than has previously been believed.

Antigens, Neoplasm↗

Volume regulation in leukemic and lymphoma cells in children and determination of cell lineage.

Among normal lymphocytes, T cells can readjust their volume rapidly following initial swelling in a hypotonic medium, whereas B cells do not have this ability. Based on this finding, we examined the volume regulation of malignant cells from 40 patients with lymphocytic and nonlymphocytic malignancies. The T lineage cells were able to regulate their volume in response to hypotonic stress, whereas B lineage cells were not able to do so. In contrast to lymphoid lineage cells, nonlymphocytic leukemia cells as well as undifferentiated cells did not show a consistent tendency in their volume regulation. These results showed that the difference in the ability to regulate cell volume in response to hypotonic stress is available as a marker for identifying the cellular lineage of lymphoid malignancies.

Acute Disease↗