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T Nimura

Publications and source records attributed to T Nimura.

At least 19 recordsLinked to original sources
PubMed1997

Translocation (8;12;21)(q22.1;q24.1;q22.1): a new masked type of t(8;21)(q22;q22) in a patient with acute myeloid leukemia.

The translocation t(8;21)(q22;q22) is found in 40% of cases of acute myeloid leukemia (AML) designated as the subtype M2 in the French-American-British (FAB) classification. The 8;21 translocation is clinically of interest because patients with this subtype have a good prognosis. We describe a masked type of the translocation, t(8;12;21)(q22.1;q24.1;q22.1). The translocation was first interpreted as t(8;12)(q22;q24) based on cytogenetics, but was reevaluated as a result of Southern blot and fluorescence in situ hybridization (FISH) analyses.

Acute Disease↗
PubMed1997

Prediction of delayed ischemic injury with diffusion-weighted MRI following temporary middle cerebral artery occlusion in rats.

Early reductions in the apparent diffusion coefficient of water (ADC) during focal cerebral ischemia are often reversible with reperfusion. With sustained ischemia, the magnitude of the ADC reduction generally increases with time, which could reflect increased severity of ischemic damage. Thus, a threshold in ADC reduction may exist beyond which damage can not be reversed with reperfusion. The goal of this study was to determine if such a threshold exists that is independent of the duration of ischemia in a rat model. Rats were subjected to either 30, 60, or 90 min of temporary middle cerebral artery occlusion. ADC maps acquired just before and 30 min after reperfusion were compared to histology performed after a 72 h survival period to determine the relationship between ADC reduction and final ischemic injury. Significant variability in tissue recovery was observed for the 30 min group. Regions with ADC reductions of up to 45% often recovered, while some regions not exhibiting any change in ADC during occlusion showed ischemic injury at 72 h. Similar observations were made in cortical regions of the 60 min group. In the caudate-putamen, reduced ADC was often associated with ischemic injury. For the 90 min group, results for the caudate-putamen were similar to those for the 60 min group, while reduced ADC was a much better predictor of final ischemic injury in cortical regions than it was in both the 30 and 60 min groups. Thus, no single threshold of ADC reduction that was independent of the duration of ischemia was associated with irreversible injury.

Animals↗
PubMed1997

BCL6 rearrangement in a patient with mantle cell lymphoma.

We describe a patient with mantle cell lymphoma (MCL) associated with BCL6 gene rearrangement. MCL is a distinct subtype of non-Hodgkin's lymphoma characterized by CD5+, CD10-, CD20+, t(11;14)(q13;q32) and PRAD1/cyclin D1 overexpression. Although rearrangement of the BCL6 gene is the most frequent genetic change among diffuse lymphomas and some follicular lymphomas this is the first report of a patient with MCL associated with BCL6 rearrangement.

Aged↗
PubMed1996

Duplication of chromosome 9 carrying a BCR/ABL chimeric gene in Philadelphia chromosome negative chronic myeloid leukemia.

We investigated a patient with Philadelphia chromosome (Ph) negative but BCR positive chronic myeloid leukemia (CML) by fluorescence in situ hybridization (FISH). In the chronic phase one chromosome 9 contained a BCR/ABL fusion gene instead of chromosome 22. Although in blast crisis, both chromosomes 9 had BCR/ABL fusion genes. This could be caused by duplication of the rearranged chromosome 9, which may have a significance similar to a double Ph chromosome. This may suggest that the critical event in CML is the formation of a BCR/ABL chimeric gene regardless of its locus in the genome.

Chromosome Aberrations↗
PubMed1996

11q23 aberration is an additional chromosomal change in de novo acute leukemia after treatment with etoposide and mitoxantrone.

We report on 2 patients with acute leukemia who had an 11q23 chromosomal aberration as an additional change after treatment with etoposide and mitoxantrone, agents that affect topoisomerase II (Topo II). One patient with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (L2) received chemotherapy, including 1,000 mg of etoposide and 75 mg of mitoxantrone. She relapsed 10 months later. Analysis at time of relapse showed a chromosomal aberration of del(11)(q23) as an additional cytogenetic change. The other patient was diagnosed with acute monoblastic leukemia (M5a) and received two autologous peripheral blood stem-cell transplantations. Her cumulative doses of etoposide and mitoxantrone were 6,000 mg and 42 mg, respectively. She also relapsed, and analysis at that time revealed del(11)(q23) as an additional chromosomal aberration. The mixed lineage leukemia/myeloid-lymphoid leukemia (MLL) gene was not rearranged in either case, making these cases distinct from previously described therapy-related leukemias caused by Topo II inhibitors. Based on these two cases, it may be that Topo II inhibitors can cause clonal evolution affecting chromosome band 11q23.

Adult↗
PubMed1996

Translocation (9;11;22)(p22;q23;q11). A new type of complex variant translocation of t(9;11)(p22;q23) with MLL rearrangement.

We describe a patient with acute monocytic leukemia (M5a, FAB classification) associated with a new type of variant translocation (9;11). Southern blot analysis showed the rearrangement of the MLL (ALL-1/HRX) gene at 11q23. Fluorescence in situ hybridization (FISH) with painting probes of chromosomes 9, 11, and 22 revealed the translocation as t(9;11;22) (p22;q23;q11). This is more evidence that the production of chimeric mRNA following the translocation of the LTG9 (MLLT3/AF9) gene at 9p22 to 11q is a critical event in this leukemia subtype.

Adult↗
PubMed1996

Translocation (3;14)(q27;q11): a new variant translocation in a patient with non-Hodgkin's lymphoma of B-cell type with BCL6 rearrangement.

We report a 65-year-old woman with non-Hodgkin's lymphoma (NHL) carrying a t(3;14)(q27;q11) and BCL6 rearrangement in the affected cells. She had generalized lymphadenopathy and the bone marrow was infiltrated by lymphoma cells at presentation. Histological diagnosis was "malignant lymphoma, diffuse, large cell" type according to an International Working Formulation. Chromosome analysis revealed a t(3;14)(q27;q11), which is a new variant translocation of t(3;14) (q27;q32). Southern blot analysis showed rearrangement of BCL6, JH, and TCR beta but not of TCR delta. Cosmid probe of BCL6 hybridized to 14q11 and 3q27 by fluorescence in situ hybridization (FISH). Although the band 14q11 is a locus of T-cell receptor alpha- and delta-chains (TCR alpha/delta), lymphoma cells expressed B-cell, IgGk phenotype. The findings suggest that a novel proto-oncogene in the vicinity of TCR alpha/delta is involved in this translocation.

Aged↗
PubMed1996

Heme oxygenase-1 (HO-1) protein induction in rat brain following focal ischemia.

The induction of the heme oxygenase-1 (HO-1) protein, also called HSP32, was compared to HSP70 heat shock protein induction following focal ischemia. Adult Sprague-Dawley male rats (n = 14) were subjected to either 30 min or 2 h of focal cerebral ischemia using the suture, middle-cerebral-artery (MCA) occlusion model. Controls (n = 4) had sham surgery. Following 24 h of reperfusion, subjects were killed and their brains stained immunocytochemically for HO-1 and the HSP70 heat shock proteins. One day following 30 min of ischemia, HO-1 and HSP70 staining in striatum occurred mainly in endothelial cells in infarcts and in glial cells surrounding the areas of infarction. Following the 30 min ischemia HO-1 was not induced in cortex whereas HSP70 was induced in cortical neurons in the MCA distribution. One day following 2 h of MCA ischemia, both HO-1 and HSP70 were induced in neurons in cortex in the MCA distribution. HO-1, however, was induced in glial cells throughout ipsilateral cortex, inside as well as outside the MCA distribution. This suggests that translation and/or transcription of the HO-1 and HSP70 genes are blocked in neurons and glia destined to die within infarcts, whereas translation of these stress genes continues in the endothelial cells. The duration of ischemia required to induce HSP70 in cortical neurons appears to be less than that required to induce HO-1 in cortical glia. Prolonged spreading depression and/or diffuse hemispheric ischemia may induce HO-1 in glia throughout the ipsilateral cortex via immediate early gene activation of the AP-1 site in the HO-1 promoter. Since HO-1 degrades heme, a pro-oxidant, to antioxidant molecules, the induction of HO-1 may augment oxidative defense mechanisms compromised by cerebral ischemia.

Animals↗
PubMed1996

A new non-random chromosomal translocation t(3;6)(q27;p21.3) associated with BCL6 rearrangement in two patients with non-Hodgkin's lymphoma.

We describe two cases of non-Hodgkin's lymphoma associated with t(3;6)(q27;p21.3) and BCL6 rearrangement. The first case was in a 78-year old woman, whose performance status (PS) was 1, the serum lactate dehydrogenase (LDH) level was elevated, and the Ann Arbor stage was IIIA with no extra nodal lymphomatous site. The pathological diagnosis from a biopsy of the inguinal lymph node was 'malignant lymphoma (ML), follicular, small cleaved' according to the Working Formulation. Complete remission was achieved. Although she had relapse in 1992, remission was obtained again. The second case was in a 62-year old man, whose PS was 1, the serum LDH was normal, and Ann Arbor stage was IVA with the involvement of the small intestine. Histological diagnosis of the cervical lymph node was 'ML, diffuse, large cell'. Complete remission was obtained without relapse. The 3q27 translocations, found in 20-30% of non-Hodgkin's lymphoma, are unique in having multiple chromosomal translocation partners. Chromosome band 6p21.3 is one of these partner sites that may be the site of a novel gene. The two cases presented here show that this translocation is a non-random chromosomal change involving 3q27 and BCL6. Since t(3;6) was the sole karyotypic abnormality in one case, this translocation may play a role in lymphomagenesis.

Aged↗
PubMed1995

Bone and brain involvement in a case of diffuse large B cell lymphoma associated with t(2;3)(p12;q27).

We report a 57-year-old male with non-Hodgkin's lymphoma (NHL) associated with t(2;3)(p12;q27). The patient showed bone lesions at presentation and brain involvement at relapse in addition to systemic lymph node swelling. Histological diagnosis was malignant lymphoma, diffuse, large cell, immunoblastic, plasmacytoid. Chromosome analysis revealed t(2;3) which is a variant type of t(3;14)(q27;q32). Fluorescence in situ hybridization (FISH) analysis disclosed splits of signals of BCL-6 gene. Among the cases reported in the literature, the common feature of t(2;3)(p11 or p12;q27) was diffuse, large cell lymphoma of B cell, kappa phenotype and four patients immunosuppressive state before lymphoma.

Bone Neoplasms↗
PubMed1994

Translocation (8;17)(p21;q21), a possible variant of t(15;17), in acute promyelocytic leukemia.

We report a 64-year old man with typical features of acute promyelocytic leukemia (APL) [M3, French-American-British (FAB) classification] in whom a variant, t(8;17)(p21;q21), was detected. This is the second case of the same variant translocation to be reported. The breakpoint on 17q was similar to those described in cases with a standard translocation 15;17. Consequently, this chromosome break or rearrangement at band 17q21, rather than the recipient site of translocation of the deleted material, appears to be of crucial importance in the genesis of APL.

Chromosomes, Human, Pair 15↗
PubMed1994

Risk factors for hepatosplenic abscesses in patients with acute leukemia receiving empiric azole treatment.

The authors retrospectively evaluated 63 febrile neutropenic episodes in 33 consecutive patients with leukemia who received empiric azole treatment for refractory or relapsing fever that occurred despite broad-spectrum antibiotics. In 8 patients (24%), hepatosplenic abscesses (HSA) developed. To identify the risk factors for the development of HSA, the authors compared various characteristics of febrile episodes in those with and without HSA. The risk factors included relapsed status of leukemia (P = 0.04) and Candida colonization of surveillance cultures from the throat (P = 0.03) and stool (P = 0.03). However, the duration of neutropenia, gastrointestinal symptoms, types of chemotherapy, and leukemia subtypes were not correlated with the development of HSA. Based on these results, the authors identified the high risk group for the development for HSA as patients with relapsed leukemia with fungal colonization of gastrointestinal tract during neutropenia despite empiric antifungal treatment with azoles.

Abscess↗
PubMed1993

Ph+ acute myelogenous leukemia with t(7;11)(p15;p15) and clonal evolution in relapse after bone marrow transplantation.

A 20-year-old female with Ph+ acute myelogenous leukemia (M2) associated with t(7;11)(p15;p15) is reported. Bone marrow aspirates were hypercellular with leukemic cells including Auer rods. Chromosome analysis showed t(7;11) and the Ph chromosome. After complete remission, normal karyotype was restored. Normal male karyotypic cells replaced the bone marrow following allogeneic bone marrow transplantation from her brother. On day 358, cytogenetic study at relapse revealed 14q+ as an additional change and clearly showed that the abnormal clone was derived from the patient, because metaphases with XX were all of abnormal karyotype and those with XY were normal.

Adult↗
PubMed1993

Acute myelogenous leukemia associated with a mediastinal tumor.

We describe a 45-year-old female who developed acute myelogenous leukemia (AML) associated with a mediastinal mass. The patient achieved a complete remission accompanied by resolution of the mediastinal mass following intensive chemotherapy alone. A review of the literature disclosed ten AML patients with a mediastinal tumor; all five patients who had mediastinal granulocytic sarcoma treated by local irradiation prior to developing AML, eventually relapsed as frank leukemia and died soon afterwards. On the other hand, three of the other five patients who simultaneously developed both a mediastinal tumor and overt AML achieved complete remission with combination chemotherapy. In conclusion, intensive chemotherapy should be considered for a patient with granulocytic sarcoma of the mediastinum, irrespective of the concomitant leukemia.

Antineoplastic Agents↗
PubMed1993

[Long term follow-up of three cases of acute myeloid leukemia associated with inv(16)(p13q22)].

Three cases of acute myeloid leukemia associated with inv(16(p13q22) were followed up for over 5 years. This chromosome aberration is generally thought to be a good prognostic factor. However, it is also reported that these patients are apt to relapse and have relatively high frequency of central nervous system (CNS) involvement. The first patient (M4Eo), who died of gastric cancer about 5 years after the initial treatment without frank relapse, did not have prophylactic therapy for CNS involvement. The second patient (M5b) developed meningeal leukemia and myeloblastoma of the brain, showing similar findings on CT scan to cases reported by Holms et al. He was treated successfully with whole brain irradiation and intrathecal injection of ara-C and MTX, and intracranial tumor disappeared on CT and MR imaging. He has been enjoying a good quality of life without any complication for over ten years after the initial diagnosis. The third patient (M4Eo) relapsed once but reentered complete remission with relative ease and we used an intrathecal injection prophylactically. This case has been followed up as an outpatient for more than 5 years since onset. On the basis of these findings, it may be concluded that these leukemia patients with inv(16)(p13q22) have good prognosis and can be cured with chemotherapy.

Acute Disease↗