PubMed Health⌕ Search

Biomedical subjects

T Tauchi

Publications and source records attributed to T Tauchi.

At least 73 records · Page 4Linked to original sources
PubMed1991

Establishment of a novel heterotransplantable acute lymphoblastic leukemia cell line with a t(17;19) chromosomal translocation the growth of which is inhibited by interleukin-3.

A cell line, designated HAL-01, was established from the blood cells of a patient with acute lymphoblastic leukemia (ALL) with a myeloid-associated marker. Both the cell line and the patient's fresh leukemia cells had the chromosomal translocation t(17;19)(q21;p13). Morphologically and cytochemically, the cells were lymphoid in appearance. Immunophenotyping of the donor's leukemia cells revealed that they express B lineage antigens (CD10+, CD19+, CD20+, CD22+); the myeloid-associated antigen (CD13) detected in the donor's leukemia cells was not expressed by the established cell line. The HAL-01 cells have a rearrangement of the immunoglobulin heavy chain gene, while the T-cell receptor beta-chain genes remain in the germline configuration. The gene encoding the binding proteins for the kappa-light chain enhancer (kappa E2), which is involved in pre-B-ALL cells with the t(1;19) (q23;p13) translocation, is not rearranged in the cell line. The HAL-01 cells were transplantable into the peritoneum of untreated nude mice where they grew as an ascites tumor. The growing tumor cells also infiltrated lymph nodes, liver, spleen, kidney, and bone marrow without exhibiting a particular change in the morphology of the neoplastic cells. Clonogenic assay in methylcellulose culture demonstrated that the proliferation of the HAL-01 cells was suppressed by interleukin-3 (IL-3) in a dose-dependent fashion, with maximum inhibition occurring at concentrations greater than 100 U/ml. Treatment with IL-3 reduced the number of viable cells as well as induced morphological changes without concomitant changes in cytochemical reactions or immunophenotypic expression. Reduction of 3H-thymidine incorporation by exposure of IL-3 was blocked by the pretreatment of neutralizing anti-IL-3 antibody, but not by neutralizing anti-TGF-beta antibody. Thus, HAL-01 is a unique ALL cell line exhibiting proliferative suppression by IL-3 that may prove useful in studying the interactions of cytokines in ALL.

Adolescent↗
PubMed1991

[Immunogenotypic and clonal culture studies in Philadelphia chromosome-positive acute leukemia].

Molecular analysis and blast colony assay were performed on patients with Philadelphia chromosome-positive acute leukemia (Ph+ AL). All patients were diagnosed as ALL- L2 and 3 were My+ ALL. Nine of the 12 cases had rearranged immunoglobulin heavy chain, and 4 had rearranged TCR beta. TCR gamma rearrangement was noted in 3 patients, and TCR delta involvement was also noted in 6 patients. Clonal culture analysis revealed that leukemia cells of M-BCR rearranged Ph+ AL cases had a potential to proliferate by myelopoietic CSFs and ILs, however, M-BCR nonrearranged Ph+ AL did not. These results indicate biological and immunogenotypic heterogeneity of Ph+ AL.

Acute Disease↗
PubMed1991

Treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia: a pilot study which raises important questions.

Acute lymphoblastic leukemia (ALL) patients with a Philadelphia chromosome (Ph+ ALL) were treated with a combination of antineoplastic drugs recommended for both myeloid and lymphoid leukemia (BHAC-DMPV: behenoylcytosine arabinoside, daunorubicin, 6-mercaptopurine, prednisolone, and vincristine). Ph+ ALL patients with chromosome breaks which occur within the major breakpoint cluster region (M-BCR rearranged Ph+ ALL) were treated with natural interferon-alpha (IFN-alpha) after entering complete remission. In this study, four of seven patients with Ph+ ALL had M-BCR rearrangement, and all achieved complete remission with karyotypic normalization. Subsequent cytogenetic analysis during complete remission in two ALL patients with M-BCR rearrangement revealed that the percentage of bone marrow cells with the Ph chromosome increased, while the bone marrow maintained remission status. This cytogenetic-hematological discrepancy led us to consider that M-BCR rearranged Ph+ ALL might be a variant of chronic myelogenous leukemia, therefore, three Ph+ ALL patients with M-BCR rearrangement were treated with IFN-alpha after achieving complete remission. In contrast, only one of three patients with M-BCR non-rearranged Ph+ ALL obtained complete remission.

Adult↗
PubMed1990

CD4+ and CD56+ acute monoblastic leukemia.

We report here a patient with acute monoblastic leukemia whose leukemia cells had CD4 (T4) and CD56 (NKH-1) antigens, in addition to CD36 (OKM5) antigen. The leukemia cells did not have NK or ADCC activities. They showed no rearrangements of immunoglobulin heavy (IgH) chain and T cell receptor (TCR)-beta chain genes, indicating that the leukemia cells were nonlymphoid. The presence of this case suggests that leukemia cells could be originated from monocytes with NK-associated antigen without IgH or TCR rearrangements.

Adolescent↗
PubMed1990

ETS1 gene in myelodysplastic syndrome with chromosome change at 11q23.

We examined the c-ets1 gene (located at 11q23) in two myelodysplastic syndrome (MDS) patients displaying a chromosome change at band 11q23 to ascertain any association between this oncogene and the chromosome change. Besides the chromosome change at 11q23, the two MDS patients also showed other numerical and structural changes. Bone marrow cells from the first case showed a translocation between chromosomes 11 and 22, t(?;11;22)(?;p11 or q11----q23;q11), resulting in a Ph-like chromosome. Neither a transposition nor a rearrangement of the c-ets1 gene was detected. Bone marrow cells of the second case showed unidentified chromosomal material attached to bands 11q23 and 6q27. Southern blot study, however, revealed that these cells carried an amplified c-ets1 gene associated with the chromosomal rearrangement. In both MDS cases studied, the amount of c-ets1 related message was the same whether amplification of the c-ets1 gene was present or not, and the level of the c-ets1 gene in MDS cells was very low.

Aged↗
PubMed1990

Philadelphia chromosome-positive chronic myelogenous leukemia with deleted fusion of BCR and ABL genes.

In the great majority of patients with chronic myelogenous leukemia (CML) the reciprocal translocation between chromosomes 9 and 22, t(9;22)(q34;q11), resulting in the Philadelphia (Ph) chromosome produces fusion DNA sequences consisting of the 5' part of the major breakpoint cluster region-1 (M-BCR-1) and the ABL protooncogene which encodes for the P210BCR-ABL phosphoprotein with tyrosine kinase activity implicated in the pathogenesis of CML. Molecular analysis was performed on 25 patients with Ph-positive CML using 2 breakpoint cluster region (bcr) probes within the M-BCR-1 DNA sequences, and two of them did not contain either detectable rearranged DNA homologous to the 5' side bcr probe or ABL-related fusion mRNA. The chromosomal in situ hybridization technique revealed that these two Ph-positive CML cases did not carry DNAs homologous to the 5' bcr or ABL probes on the Ph chromosome. Furthermore, one of the two Ph-positive CML cases did not show either rearranged DNA or regions homologous to the 3' bcr probe on a 9q+ chromosome, while the other CML case showed a rearrangement detected by the 3' bcr probe and transposition of the 3' bcr homologous to the 9q+ chromosome. Thus, the possibility is raised that the BCR/ABL fusion DNA has been deleted in rare CML cases, and that the deletion possibly occurred in a stepwise manner following the formation of the Ph chromosome at any stage of the disease.

Adult↗
PubMed1990

Immunoglobulin and T cell receptor gene rearrangements in Philadelphia chromosome-positive leukemia: a different involvement pattern in blast crisis and acute leukemia.

We have analyzed the configuration of the immunoglobulin heavy (IgH) chain gene and the T cell receptor (TCR) chain (beta, gamma, and delta) genes in a group of 22 leukemia patients with the Philadelphia (Ph) chromosome. The group consisted of 14 patients with chronic myelogenous leukemia in blast crisis (CML-BC) and eight with Ph-positive acute leukemia (Ph + AL); these diagnoses were based on hematologic and cytogenetic features. In CML-BC patients, an IgH joining region rearrangement was detected only in patients with CD10 expression; TCR-beta, -gamma, or -delta rearrangements were associated with IgH involvement. In contrast, five of the eight Ph+ AL patients had breaks within the major breakpoint cluster region (M-BCR), and four of them had IgH involvement. Of the remaining three Ph+ M-BCR nonrearranged AL patients, only one showed IgH rearrangement. In addition, TCR-beta involvement was sometimes detected in Ph+ AL patients (two of the eight patients) with or without rearranged M-BCR, and no PH+ AL case displayed rearranged TCR-gamma. These findings suggest that genotypic changes in CML-BC are usually associated with phenotypic results of the neoplastic cells: the expression of CD10 in CML-BC patients is accompanied by the involvement of IgH with frequent TCR rearrangements which possibly are due to the common recombinase activity. On the other hand, the mechanism of the involvement of IgH in Ph+ AL patients without rearranged M-BCR seems different from that observed in Ph+ leukemia patients with rearranged M-BCR, although TCR involvement could occur whether or not the leukemia cells had a rearranged M-BCR in Ph+ AL patients.

Adolescent↗
PubMed1989

[Refractory idiopathic thrombocytopenic purpura which responded to protein A column].

Currently, there is no satisfactory therapy available for patients with chronic idiopathic thrombocytopenic purpura (ITP) who are unresponsive to conventional therapeutic modalities. In this report, we describe a patient with chronic refractory ITP treated with immobilized protein A in an extracorporeal system. The patient was a 74 years old male diagnosed as ITP in 1980. Despite steroid therapy, the disease progressed and the patient exhibited ecchymosis and gum bleeding which was unresponsive to intravenous gammaglobulin therapy. Severe gastrointestinal bleeding was evident and administration of danazol was discontinued due to liver dysfunction. The patient was treated with extracorporeal protein A immunoabsorption. The patient's whole blood (200-300 ml per treatment) was separated into plasma and cellular components and the plasma was passed through an immunoabsorption column containing 200 mg of covalently bound protein A. The treated plasma and cellular components were returned to the patient. After 4 immunoabsorption treatments, the platelet counts elevated and there was evidence of improvement in gastrointestinal bleeding. This report indicates that protein A immunoabsorption therapy should be considered in patients with chronic refractory ITP.

Aged↗