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Biomedical subjects

A Iwabuchi

Publications and source records attributed to A Iwabuchi.

At least 37 records · Page 2Linked to original sources
PubMed1994

Telomere shortening associated with disease evolution patterns in myelodysplastic syndromes.

We identified the telomere length at different hematological phases in 16 patients with myelodysplastic syndromes (MDS), showing disease evolution with a conventional Southern blot hybridization using the (TTAGGG)4 probe. The MDS patients studied were classified into three groups according to the pattern of telomere length reduction. The first group had telomere shortening at the time of disease diagnosis. In four of the six MDS patients in this group, the disease progressed within 6 months postdiagnosis and each of them survived for less than 1 year. Moreover, in this group four patients showed a 5q anomaly with or without additional changes, and 50% of patients in this group had complex chromosome abnormalities. The patients in the second group showed reductions in telomere length after disease progression; two of these three patients showed gradual disease progression and had one or two chromosome abnormalities. The third group comprised the remaining seven MDS patients; they showed no telomere reduction by disease evolution. Two patients in this group experienced rapid disease progression. These results may indicate that telomere reduction is linked to disease evolution in some MDS patients, perhaps as a result of genomic instability because patients with complex chromosome abnormalities were clustered in the first group. However, because some MDS patients show disease progression without telomere reduction, genetic changes, including point mutations of certain gene(s), may also contribute to disease progression. We further noted that telomere shortening at the time of MDS diagnosis might indicate a poor MDS prognosis.

Acute Disease↗
PubMed1994

Percentages of bone marrow blasts and chromosomal changes in patients with refractory anemia help to determine prognoses.

We statistically analyzed the hematologic findings of patients with refractory anemia (RA) to identify parameters associated with a poor prognosis. We first separated the RA patients into two groups: one group with disease progression and one without. The patients with disease progression were predominantly male and had a significantly higher percentage of bone marrow (BM) blasts at the time of diagnosis (3.06 +/- 1.29% vs. 1.44 +/- 1.38%, P < 0.005). This finding was confirmed when the patients were separated into the two groups; those who survived and those who expired (BM blasts: 2.68 +/- 1.59% vs. 1.37 +/- 1.27%, P < 0.005). The survival probabilities were calculated depending on whether or not the RA patients had > or = 3% BM blasts. The RA patients with > or = 3% BM blasts had a significantly worse prognosis (P < 0.01) than the patients with < 3% BM blasts. Notably, the RA patients with > or = 3% BM blasts did not show any significant differences in the incidence of disease progression, mortality rate, or survival probability, when compared with the patients with RA with an excess of blasts (RAEB). The present findings indicate that RA patients are heterogeneous with regard to prognosis, and the RA patients with > or = 3% BM blasts might have a poorer prognosis than those with fewer BM blasts. Thus we propose a general approach in predicting the prognosis of RA patients: those with complex chromosomal changes will expire shortly. Secondly, when the patients do not have any complex changes, the prognosis might be linked to the percentage of BM-blasts at the MDS diagnosis.

Anemia, Refractory↗
PubMed1993

Two additional cases of acute myeloid leukemia with t(7;11)(p15;p15) having low neutrophil alkaline phosphatase scores.

We report two additional patients with acute myeloid leukemia (AML) and a translocation between chromosomes 7 and 11: t(7;11)(p15;p15). One patient was diagnosed as having AML-M2 and the other as AML with myelofibrosis. Both patients had low-level neutrophil alkaline phosphatase (NAP) scores. In the literature, only 15 AML patients with t(7;11)(p15;p15) have been reported; nine of them had an AML-M2 morphology, and all had a decreased NAP score. Moreover, mean survival of the reported AML patients with t(7;11)(p15;p15) was 15 months, although 85% of them obtained complete remission, indicating that this type of leukemia frequently tends to relapse. These findings indicate a strong association between the chromosome abnormality and hematologic manifestations of this disease.

Acute Disease↗
PubMed1993

Clinical and cytogenetic significance of myelodysplastic syndromes with disease evolution.

We performed a retrospective study of 83 patients with myelodysplastic syndrome (MDS) to clarify the clinical and cytogenetic implications of disease evolution. Twenty-three patients showed disease progression; six of the 11 patients whose disease evolved within 100 days showed complex cytogenetic aberrations and most of them died within 300 days. Of the patients who survived more than 300 days, those with high bone marrow (BM) blast percentages experienced significant disease progression, but we noted no cytogenetic indicators for disease evolution at the later phase. Sixty percent of patients showing karyotypic evolution without disease evolution had deletion-type chromosome changes. The most frequent anomaly in patients with disease evolution who survived more than 300 days was an additional numerical change, whereas patients with disease evolution who survived less than 300 days showed karyotypic instability. It was difficult to predict disease progression for patients whose disease evolved more than 300 days after diagnosis, but in some patients the presence of additional numerical changes was related to disease progression. The cutoff level of early disease evolution was 100 days after diagnosis, and most patients with complex abnormalities survived less than 300 days with or without disease evolution.

Adult↗
PubMed1993

Influence of gastrointestinal microflora on digestibility and biological value of protein in rats.

The influence of the gastrointestinal microflora on the digestibility and biological value of casein was investigated in germ-free (GF) and conventionalized (Cvd) Fischer 344/Yit rats fed an 8% casein diet. There was no significant difference in the true digestibility of casein between GF and Cvd rats, but the apparent digestibility was higher in Cvd than in GF rats. The biological value of casein was significantly higher in GF than in Cvd rats. In the casein diet period, body weight gain was almost the same in GF and Cvd rats, but food intake was significantly greater in Cvd than in GF rats. The excretion of fecal N was similar in GF and in Cvd rats whereas more urinary N was excreted in Cvd than in GF rats. In the protein-free diet period, metabolic fecal N per 100 g of food intake was significantly higher in GF than in Cvd rats, but there was no difference in the excretion of endogenous urinary N per 100 grams of body weight between the GF and Cvd rats. The results indicate that the presence of a gastrointestinal microflora does not influence the true digestibility, but increases the apparent digestibility and decreases the biological value of casein at an 8% level in the diet.

Animals↗
PubMed1993

Acute myeloid leukemia with concomitant expression of T-/B-lymphoid antigens and immunogenotypic alterations exhibiting t(7;12)(q32;q24).

We report here a patient with acute myeloid leukemia (AML) expressing both T- and B-lymphoid-associated antigens. The leukemia cells in this case had rearrangements of not only immunoglobulin heavy-chain but also T-cell-receptor beta- and delta-chain genes. Although a relatively large number of AML patients with lymphoid markers have been reported, only about a dozen AML patients expressing both T- and B-lymphoid markers have been reported so far.

Antigens, CD↗
PubMed1993

[A case of vivax malaria with thrombocytopenia suggesting immunological mechanisms].

Recently, it has been shown that the thrombocytopenia that complicates some malarial infections is caused by immune mechanisms. We report a case of malaria associated with thrombocytopenia and increased platelet-associated IgG (PAIgG). In this case, anti-malarial therapy reduced the level of PAIgG to normal levels in association with normalization of the platelet count. This case suggests the immunological mechanisms of thrombocytopenia in malaria.

Adult↗
PubMed1992

Cytogenetic and clinical findings of myelodysplastic syndromes with a poor prognosis. An experience with 97 cases.

BACKGROUND: Clinical and cytogenetic analyses were performed in 97 patients with myelodysplastic syndromes (MDS) to evaluate risk factors for poor prognosis. METHODS/RESULTS: Among them, 22 patients survived for less than 1 year: 10 of these had complex chromosomal abnormalities (complex aberrations), but only 5 of the remaining 75 patients who survived longer than 12 months did. Leukemia did not develop in approximately half of the patients who died within 1 year. The occurrence rate of leukemic transformation appears to depend on MDS subtypes rather than cytogenetic changes. In contrast, the percentage of patients who survived for less than 1 year is related to chromosomal changes, especially to complex aberrations. Of particular interest in this study is that 7 of 11 patients with MDS who had myelofibrosis survived for less than 1 year, and 5 of 7 patients with secondary MDS were included in this group showing a poor prognosis. By hematologic analysis, significant differences were found in the hemoglobin values and platelet counts of patients who survived for less than 1 year. CONCLUSIONS: From this analysis, three major risk factors for a poor prognosis were identified: complex aberrations, a history of chemotherapy or radiation therapy (secondary MDS), and development of myelofibrosis. The survival probability in the patients with MDS having at least one of these three factors was significantly low when compared with that in patients without these factors, indicating that cytogenetic analysis in combination with observance of certain clinical manifestations is important in therapeutic management of patients with MDS.

Anemia, Refractory, with Excess of Blasts↗
PubMed1992

Trisomy of chromosome 8 in myelodysplastic syndrome. Significance of the fluctuating trisomy 8 population.

Chromosome analyses were performed in five patients with myelodysplastic syndrome (MDS) who showed trisomy of chromosome 8 during the course of their disease. Four of these patients showed trisomy 8 at the diagnosis of MDS, and the remaining one had trisomy 8 when the leukemia phase developed. The proportion of bone marrow (BM) cells with trisomy 8 in the four patients who showed trisomy 8 at MDS diagnosis fluctuated, and this fluctuation was not related to the percentage of blasts in the BM or to progression of the disease. However, in two patients, metaphase cells with trisomy 8 disappeared when their anemic state improved, although leuko-thrombocytopenia was still present, suggesting that the decrease in the number of BM cells with trisomy 8 reflects hematologic features in some MDS patients. These findings indicate that trisomy 8 in our MDS patients was possibly not the primary event in the genesis of the disease, and that there may have been competition between a normal karyotype clone and a trisomy-8-positive clone. Our results further suggest that the presence of a clone with trisomy 8 is not always a sign of disease progression or of poor prognosis in MDS patients.

Adult↗
PubMed1991

Clinical and cytogenetic characteristics of myelodysplastic syndromes developing myelofibrosis.

Myelofibrosis occurs in various hematologic neoplasias, including myelodysplastic syndrome (MDS), with a relatively low incidence. To gain insight into the clinical and cytogenetic implications of MDS patients in whom myelofibrosis develops, statistical analysis was done on 82 primary MDS patients with successful cytogenetic results. Seven patients had myelofibrosis during the course of the disease (8.5%, Group I), 34 had abnormal karyotypes without myelofibrosis (41.5%, Group II), and the other 41 had abnormal karyotypes without myelofibrosis (50%, Group III). All of the MDS patients except one with myelofibrosis had cytogenetic abnormalities, and four of them had multiple chromosome abnormalities. In univariant analysis, MDS patients with myelofibrosis showed no significant differences in age, sex, or peripheral blood data. In contrast, patients with chromosome abnormalities evolved into myelofibrosis with a high incidence compared with those with normal karyotypes (14.6% versus 2.4%, P = 0.054). The occurrence of myelofibrosis was higher during the first 6 months after the diagnosis of MDS than in the next 6 months (6.1% versus 0%, P = 0.045). Most of the MDS patients survived for less than 10 months after myelofibrosis was evident. Furthermore, survival was significantly shorter in Group I compared with Groups II (P less than 0.05) and III (P less than 0.01). Among the MDS patients in whom myelofibrosis developed, some were associated with acute megakaryoblastic leukemia, indicating a heterogeneity of clinical features in MDS with myelofibrosis.

Adult↗
PubMed1990

Change in a complex translocation involving band 7q34 and 9p- in a case of T-cell lymphoblastic lymphoma.

The authors report a case of T-cell type non-Hodgkin's lymphoma (NHL) in which neoplastic cells possessed a three-way translocation involving chromosomal bands 3q21, 7q34, and 22q11, as well as partial monosomy of the short arm of chromosome 9. In the literature, most reported cases of 7q32-q36 abnormalities had T-cell type leukemia/lymphoma and were younger than 20 years. Two NHL cases, including the current case, were diagnosed as having lymphoblastic lymphoma with a leukemic transformation. The neoplastic cells of the reported cases commonly showed CD2 (E-rosette receptors) and CD38. All 17 patients but three manifested a mediastinal mass at diagnosis and seven had central nervous system lesions or pleural infiltration. Furthermore, five of the 19 reported cases also showed 9p- change.

Adult↗
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

In vitro cytogenetic effects of recombinant human hematopoietic growth factors on cells derived from myelodysplastic syndromes.

Chromosomes of bone marrow cells obtained from nine patients with myelodysplastic syndrome (MDS) were assessed after in vitro co-culture (48 hours culture) with recombinant human granulocyte colony-stimulating factor (rhG-CSF), recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF), or recombinant human erythropoietin. Three of the nine MDS cases showed no cytogenetic abnormalities with or without any recombinant human hematopoietic growth factors; one MDS patient with a t(3;4) did not show any change in the proportion of cells with this cytogenetic change. The remaining five cases exhibited changes in the frequency of subclones after the treatment. An increasing number of metaphase cells with less complex chromosome abnormalities was observed in two of the five cases by treatment with rhG-CSF; one of them also showed an increasing number of cells with normal karyotypes. After rhGM-CSF treatment, cells with nonclonal hyperdiploid abnormalities appeared in one MDS patient. After erythropoietin treatment, an increasing number of cells with a prototypic change was observed in one MDS patient, whereas one patient showed an increasing number of cells with an additional chromosome abnormality. These observations indicate that hematopoietic growth factors possibly modify the constitution of marrow cells with multiple chromosome abnormalities and the degree is different in each MDS patient. Furthermore, a chromosome analysis using an in vitro culture system with human recombinant hematopoietic growth factors may be able to detect metaphase cells with additional chromosome abnormalities in some MDS patients.

Cells, Cultured↗
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↗
PubMed1989

Myelodysplastic syndrome with trisomy 11 associated with polycythemia vera.

A 52-year-old male with myelodysplastic syndrome (MDS) who had a prior history of polycythemia vera is reported. Chromosome analysis revealed that the bone marrow and blood cells at the MDS phase contained trisomy of chromosome 11 as the sole cytogenetic change. Trisomy 11 is rarely found in hematologic neoplasia, and all of the reported cases with trisomy 11 were diagnosed as having nonlymphocytic neoplasia. In this report, a correlation between the chromosome change and leukemia/MDS developed in polycythemia vera is discussed.

Blood Cell Count↗