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T Shikano

Publications and source records attributed to T Shikano.

At least 55 records · Page 3Linked to original sources
PubMed1991

[Cytogenetic studies on 53 childhood acute nonlymphocytic leukemia].

Cytogenetic study in 53 children (aged less than 15 years) with acute non-lymphocytic leukemia (ANLL) were studied. The cytogenetic findings were compared with those of ANLL patients (136 aged less than 19 years and 747 aged over 20 years) in the Fourth International Workshop on Chromosomes in Leukemia (IV IWCL) and also with those of childhood acute lymphoblastic leukemia (ALL) cases (previously reported as our 124 ALL case). Of the ANLL patients, 77.4% had acquired chromosomal clonal abnormalities. As abnormalities, t(15;17), all cases which were seen in M3 or M3V cases, t(8;21), which was seen in M1 or M2, and rearrangements of 11q23, which were seen in M5, were more frequently seen than was reported at the IV IWCL (20.8%, 17.0% and 7.5% vs 6.3%, 6.3% and 3.2% respectively). 5q-, monosomy 7, t(6;9) and t(9;22), which have been noted previously in this disease, were not seen. Besides structural abnormalities, some cytogenetic differences in numerical abnormality between ALL and ANLL were observed as follows: 1) Hyperdiploidy of greater than 51 chromosomes noted in ALL was not found in ANLL. 2) Isolated trisomy 8 was frequently found in ANLL, but not in ALL. 3) Loss of a sex chromosome was frequently found in ANLL, but not in ALL. Our study revealed a different frequency of non-random chromosome abnormality in children with ANLL as compared with that of adults, and clarified the differences in numerical abnormalities, as well as structural abnormalities, between ALL and ANLL.

Adolescent↗
PubMed1991

[Significance of the 14q32 translocations in childhood acute lymphoblastic leukemia].

To assess the frequency and significance of 14q32 translocation abnormalities in childhood acute lymphoblastic leukemia (ALL) and the differences between the clinical and cytogenetic features of patients with the 8; 14 translocation and those of patients with other 14q32 translocations, we analyzed our experience with 124 consecutive cases with completely banded karyotype. Eight cases (6.5%) with 14q32 translocation were identified :5 with the 8; 14 translocation and 3 with other 14q32 translocations. As compared with ALL children lacking 14q32 translocations, these 8 cases had a higher serum lactic dehydrogenase (LDH) level, more L3 (FAB classification), and a poorer outcome. On the other hand, in comparison with ALL patients with other 14q32 translocations, patients with the 8:14 translocation were likely to be younger (median age 4.5 years vs 10.4 years), to have a higher serum LDH level (median 5832 IU/l vs 504 IU/l), to have more L3 (3/5 vs 0/3), to have a higher induction failure rate (4/5 vs 1/3), and to have more partial duplication of the long arm of chromosome 1 (4/5 vs 0/3). These results helped clarify the characteristic features of ALL children with 14q32 translocations and showed that ALL children with the 8 ; 14 translocation have different clinical and cytogenetic findings from those of ALL children with other 14q32 translocations.

Adolescent↗
PubMed1991

[Nonoliguric acute renal failure complicated with tumor lysis syndrome in chronic myelocytic leukemia in lymphoid crisis].

A case of nonoliguric acute renal failure complicated with tumor lysis syndrome is described. The patient is a 14-year-old boy who was diagnosed chronic myelocytic leukemia 17 months ago. On lymphoid crisis, he received vindesine-prednisolone therapy and acute renal failure occurred. Urine output was kept enough volume (2,500-4,000 ml/day), but blood urea nitrogen and serum creatinine levels rose and hyperkalemia, hyperphosphatemia and hypocalcemia were observed. Tumor lysis syndrome in patients with chronic myelocytic leukemia is rare, and acute renal failure with tumor lysis syndrome is oliguric or anuric in most patients. At therapy of lymphoproliferative disease, nonoliguric acute renal failure may occur. Physicians who treat patients with lymphoproliferative disease should pay attention to blood urea nitrogen and serum creatinine levels even if urine output is satisfactory.

Acute Kidney Injury↗
PubMed1990

Karyotypic changes from initial diagnosis to relapse in childhood acute leukemia.

Cytogenetic study was performed at both diagnosis and relapse in 31 children with acute leukemia who had initially abnormal karyotypes, 21 with acute lymphocytic leukemia (ALL) and 10 with acute nonlymphocytic leukemia (ANLL). Seventy percent of the patients showed karyotypic changes between diagnosis and relapse. The ALL patients showed karyotypic changes more often than the ANLL patients (76 vs. 40%)(chi-square test, p less than 0.05). All the initially abnormal patients with karyotypic changes exhibited structural changes, most frequently chromosome 1 abnormalities, especially in ANLL, and 6q-, 7p-, 9p- in ALL. Half of the patients, with structural karyotypic change had two or more clonally related cell lines at relapse. On the other hand, only 20% of the patients with karyotypic changes showed numerical changes. All but one of the initially abnormal patients showed karyotypic changes involving the original cytogenetically abnormal clone. Our study demonstrated that sequential cytogenetic studies may provide a better understanding of the nature of leukemia relapse.

Acute Disease↗
PubMed1990

[Hyperdiploidy (greater than 50 chromosomes) has the most favorable prognosis among the major karyotypic subgroups of childhood acute lymphoblastic leukemia].

Thirty-four children, including nine relapsed cases with acute lymphoblastic leukemia (ALL) having hyperdiploidy (greater than 50 chromosomes) were studied on clinical and cytogenetic characteristics. The majority of children initially with hyperdiploidy (greater than 50 chromosomes), who showed favorable prognostic features such as lower leukocyte counts, lower serum lactic dehydrogenase levels, ages between 2 and 10 years, or the presence of common ALL antigen, had the most favorable outcome among childhood ALL (5-year survival rate was 100%). Even nine children, who showed poor prognostic features such as ages over 10 years, leukocyte counts over 2 X 10(4)/mm3 or lymphomatous signs, had also the same favorable outcome. There were no differences in clinical features between 6 patients with additional chromosomal structural abnormalities and 19 patients without them. Duplication of the long arm of chromosome 1 was frequently observed as additional chromosomal structural abnormalities. Patients with hyperdiploidy (greater than 50 chromosomes) observed at relapse, who had the same favorable clinical features as those at diagnosis, had a poorer prognosis. These findings show that initial hyperdiploidy (greater than 50 chromosomes) is an independent favorable prognostic sign in childhood ALL and additional chromosomal structural abnormalities may not indicate a poor prognosis among childhood ALL with hyperdiploidy (greater than 50 chromosomes). On the other hand, relapsed children with hyperdiploidy (greater than 50 chromosomes) have not a favorable outcome after the onset of relapse.

Child↗
PubMed1989

Chromosomal and immunophenotypic patterns in T cell acute lymphoblastic leukemia (T ALL) and lymphoblastic lymphoma (LBL).

In this study of 33 T cell acute lymphoblastic leukemia (T ALL) and 17 lymphoblastic lymphoma (LBL) patients, no relevant differences between the two groups were observed in clinical characteristics, response to therapy, and survival. We found translocations involving 14q11, 7q35, or 7p15, where T cell receptor alpha and delta, beta, and gamma subunit genes reside, in 20 patients (40%). Most of these translocations were seen with equal frequency in T ALL and LBL, indicating that, in a large proportion, the two diseases are different manifestations of the same lymphoblastic disorder. However, other translocations, such as t(9;17)(q34;q23), occurred only in LBL, perhaps pointing to the existence of subsets of LBLs that are distinct from T ALL. On the basis of karyotype, 50 patients could be classified into three groups: 20 patients with 14q11, 7q35, or 7p15 translocations (group A); 20 with other translocations, and/or deletions (group B); and 10 with normal diploidy (group C). There was no difference in survival time between any two of the three groups.

Adolescent↗
PubMed1989

[Correlation of karyotype with clinical features in childhood acute lymphoblastic leukemia].

The karyotype of 124 children with acute lymphoblastic leukemia (ALL), who were diagnosed on the basis of the FAB classification, were studied according to numerical, structural abnormalities and the presence or absence of translocations. Clonal chromosome abnormalities were found in 85 (68.5%) of the 124 patients. Firstly, chromosome abnormalities were classified according to modal number. Twenty-four patients with ALL had hyperdiploidy (51-66 chromosomes). They had favorable prognostic factors, including low leukocyte count, age between 2 and 10 years and a low level of serum LDH. They had the most favorable outcome. Thirty-nine patients with normal karyotype had a relatively favorable outcome. In contrast 8 patients with near hyperdiploidy (47, 48 chromosomes), 47 with pseudodiploidy, and 4 with hypodiploidy (45 chromosomes) had a poor outcome. Secondly, chromosome abnormalities were also classified according to specific structural abnormalities. The 1; 19 translocation, which is associated with the pre-B phenotype, was found in 13 patients. Their outcome was better than has hitherto been reported. The abnormality of the short arm of chromosome 12 was found in 11 patients, who had a good outcome. The chromosome abnormality of the breakpoint in the T-cell receptor gene locus, containing bands 14q11 and 7q35, was found in 7 patients. Four patients had mediastinal tumors and the T phenotype. Their outcome was intermediate. The 14q32 translocation was found in 8 patients. The 8; 14 translocation was closely associated with L3 (FAB) and the B phenotype, but another 14q32 translocation was not. Their outcome was poor. The 11q23 translocation was found in 4 Patients, who had null cell blasts. Three of the 4 had unfavorable prognostic factors, including both a high leukocyte count and age under one year. They had a poor outcome. The partial deletion of the long arm of chromosome 6 was found in 4 patients. The structural abnormality of the short arm of chromosome 9 was found in 4 patients with absence of T cell phenotype. Two patients had a mass. Prognosis of the patients with 6q- and 9p abnormalities was unclear because of the small number of cases. Thirdly, chromosome abnormalities were also classified according to the presence or absence of translocations. The chromosomal translocations, which have an adverse effect in ALL (p = 0.004), were ones of the strongest predictor of treatment outcome. This study demonstrated that chromosome modal number, specific structural abnormalities and the presence or absence of translocations were significantly correlated with clinical features and survival rates of Japanese childhood ALL.

Age Factors↗
PubMed1989

[Clinical and laboratory studies in seven patients with pre-B cell leukemia in children].

We have experienced and treated seven patients of pre-B cell leukemia in childhood. Clinical, cytological and ultrastructural characteristics of them were studied. Most of them had higher counts of white blood cells, hepatosplenomegaly, high value of lactic dehydrogenase and various karyotype abnormalities at onset. The chromosomal translocation t (1; 19) that is supposed to be specific to pre-B cell ALL was found in four of seven of our cases. In the seven patients, survival was studied in comparison to that of 27 common ALL patients at our hospital that are common in childhood acute leukemia. Although no difference in remission duration and survival time between pre-B cell ALL patients and common ALL group, there have been seen the tendency that remission and survival were of shorter duration for patients with pre-B cell ALL.

Child↗
PubMed1989

[BCR rearrangement and cytogenetic findings in Philadelphia-positive chronic myelocytic leukemia in children].

Eight children with Philadelphia (Ph1) chromosome positive chronic myelocytic leukemia (CML) were available for cytogenetic studies and breakpoint cluster region (bcr) rearrangement analysis as compared to the features of adults with Ph1-positive CML. In chronic phase additional abnormalities other than Ph1 chromosome were found in none of our cases. On the other hand, in blastic crisis all of 6 cases had additional chromosomal abnormalities like as i(17q), double Ph1 and +8. The frequency of the appearance of additional chromosomal abnormalities, especially i(17q), is higher in children than in adult cases. In the DNA of 7 of 7 examined patients, rearrangement of bcr could be demonstrated by Southern blot analysis. These findings were similar to those observed in adults. An analysis of the location of the bcr breakpoint indicated that 5' breakpoints were found in four cases who were long-term survivors, and two of the other cases had blastic crisis from the onset of the disease. These findings showed the cytogenetic findings of children with Ph1+CML were different from those of the adult cases in the frequency of the appearance of the additional chromosomal abnormalities, and the location of the bcr breakpoint in children cases might be different from that in the adult cases and influence its prognosis.

Adolescent↗
PubMed1988

Possible association of human growth hormone treatment with an occurrence of acute myeloblastic leukemia with an inversion of chromosome 3 in a child of pituitary dwarfism.

An 11-yr-old girl, who had been treated with human growth hormone (h-GH) for 31 months, developed acute myeloblastic leukemia with an inv(3)(q21q26). Since GH has been suggested to influence the genesis of leukemia, and the inversion 3 has been reported only in adult leukemia patients, the GH treatment may have caused the development of leukemia or accelerated the proliferation of the leukemia cells.

Child↗
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

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↗
PubMed1986

Balanced and unbalanced 1;19 translocation-associated acute lymphoblastic leukemias.

The authors studied clinical and immunologic characteristics of six children with 1;19 translocation-associated acute lymphoblastic leukemia (ALL); two of the six had the balanced type, t(1;19)(q23;p13), three had the unbalanced type, -19,+der(19)t(1;19)(q23;p13) with a resultant partial 1q trisomy, and the other had a mosaicism of cells with the balanced type and those with the unbalanced one, t(1;19)/-19,+der(19)t(1;19). Leukemic cells of all three patients, in which intracytoplasmic immunoglobulin was determined, were proved to show pre-B phenotype. Of the six patients, three had an initial leukocyte count of greater than 50 X 10(9)/l, and were classified in the high-risk group. Three patients relapsed after a brief remission and died. The mosaicism observed suggested that at least in some patients the leukemic cells with -19,+der(19)t(1;19) might derive from those with t(1;19) as a step in the course of clonal evolution. Our data and a review of the literature indicate that there may be no differences in the clinical and immunologic characteristics between the patients with the balanced translocation and those with the unbalanced one, and that the leukemia with the 1;19 translocation may join with other translocation-associated ALLs, with which the patients are known to have poor prognosis.

Adolescent↗
PubMed1986

Clinical and hematologic characteristics in acute leukemia with 11q23 translocations.

We studied the clinical, morphological, and immunologic characteristics of 11 patients with 11q translocation-associated acute leukemia. There were three patients with t(9;11)(p22;q23), one with a variant of the t(9;11), three with t(11;19)(q23;p13), two with t(1;11)(p32;q23), one with t(10;11)(p15;q22or23), and one with t(11;17) (q23;q25). The breakpoints in chromosome 11 clustered in band q23. The morphological feature was FAB-M5 in two patients, FAB-M2 in one, FAB-L1 in six, and lymphoblastic lymphoma in one. The remaining patient underwent morphological changes from FAB-L1 seen at the time of diagnosis to M5b at relapse. Immunologic marker studies in ten patients revealed that one had T cell type; another pre-B cell type; three CALLA- Ia- non-T, non-B type; two CAL-LA- Ia+ non-T, non-B type; two monocytic type (positive Fc-receptor); and the remaining one underwent phenotypic changes from CALLA+ Ia+ non-T, non-B type to monocytic type. The patients were usually young; five were under 1 year and two were 9 and 13 years. Hyperleukocytosis was observed in eight of the ten patients with acute leukemia, and two of the eight died of intracranial hemorrhage within two days of admission, associated with disseminated intravascular coagulation. These findings indicate that leukemia with the 11q23 translocation share certain characteristics in common, irrespective of the recipient chromosome, even though the latter may have some influence on the morphological and immunologic phenotype. Our data provide a hypothesis that multipotent stem cells are involved in the genesis of the 11q translocation-associated leukemia.

Age Factors↗