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M Daibata

Publications and source records attributed to M Daibata.

At least 19 recordsLinked to original sources
PubMed2006

Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of acute biphenotypic leukemia.

A 47-year-old Japanese woman was diagnosed as having acute biphenotypic leukemia with association of t(9;22)(q34;q11). Cholestatic liver dysfunction arose, and she died of cachexia and intracranial hemorrhage. Autopsy showed unusual hepatic fibrosis. In the liver, bridging infiltration, bridging necrosis and bridging fibrosis by leukemic cells were seen. It seemed that the degree of fibrosis was associated with the number of aggregates of infiltrating leukemic cells. The fibrotic foci were predominantly composed of reticulin and collagen fibers, and distortion of the lobules was observed. Immunohistochemically, dense bundles of alpha-smooth muscle actin (ASMA)-positive stromal cells, namely activated hepatic stellate cells (HSCs), were observed in the immature fibrotic foci as well as along the sinusoids densely infiltrated by leukemic cells. No cells positive for TGF-beta1 or PDGF-BB were identified. In conclusion, extensive intrahepatic involvement by neoplastic cells in adult acute biphenotypic leukemia may cause the unusual "disorganized" hepatic fibrosis.

Becaplermin↗
PubMed2006

Different breakage-prone regions on chromosome 1 detected in t(11;14)-positive mantle cell lymphoma cell lines and multiple myeloma cell lines are associated with different tumor progression-related mechanisms.

To better define secondary aberrations that occur in addition to translocation t(11;14)(q13;q32) in mantle cell lymphomas (MCL) and in multiple myelomas (MM), seven t(11;14)-positive MCL cell lines and four t(11;14)-positive MM cell lines were analysed by fluorescence R-banding and spectral karyotyping (SKY). Compared with published data obtained by G-banding, most chromosome aberrations were redefined or further specified. Furthermore, several additional chromosome aberrations were identified. Thus, these cytogenetically well defined t(11;14)-positive MCL and MM cell lines may be useful tools for the identification and characterization of genes that might be involved in the pathogenesis of MCL and MM, respectively. Since MCL and MM were found to have different alterations of chromosome 1, these were investigated in more detail by fluorescence in situ hybridization (FISH) and multicolor banding (MCB) analyses. The most frequently altered and deletion-prone loci in MCL cell lines were regions 1p31 and 1p21. In contrast, breakpoints in MM cell lines most often involved the heterochromatic regions 1p12-->p11, and the subcentromeric regions 1q12 and 1q21. These data are in accordance with previously published data of primary lymphomas. Our findings may indicate that different pathways of clonal evolution are involved in these morphologically distinct lymphomas harboring an identical primary chromosome aberration, t(11;14).

Cell Line, Tumor↗
PubMed2001

Lactate dehydrogenase production and release in a newly established human myeloma cell line.

Aggressive multiple myeloma with high serum lactate dehydrogenase (LDH) often has unusual clinical features and is considered to be a distinct clinical entity of multiple myeloma. A myeloma cell line, designated Maska-98, was established from the bone marrow of a patient with aggressive myeloma with extremely high serum LDH that was resistant to conventional chemotherapy. Maska-98 cells had morphological features of immature plasma cells, and immunophenotypic analysis showed that the cells expressed the plasma cell-associated surface antigens including CD38, 49d, and 56, but no T- or B-cell antigens, such as CD2, 3, 4, 8, 19, and 20. Maska-98 cells contained cytoplasmic immunoglobulin (IgG lambda). By utilizing this cell line we demonstrated that the myeloma cells produce and release a large amount of LDH, since (i) abundant LDH was found in the culture supernatant of Maska-98, (ii) immunocytochemical analysis showed that cytoplasm of the cells was strongly stained with anti-LDH monoclonal antibody, and (iii) Maska-98 cells expressed a greater amount of LDH mRNA than the T-cell line TALL-1, as shown by reverse transcription-polymerase chain reaction. As far as we know, there is no report of a myeloma cell line producing excess LDH. Therefore, Maska-98 would provide a novel source for further studies of the pathogenesis of aggressive multiple myeloma with high serum LDH.

Antibodies, Monoclonal↗
PubMed2001

Detection of human herpesvirus 6 and JC virus in progressive multifocal leukoencephalopathy complicating follicular lymphoma.

Progressive multifocal leukoencephalopathy (PML), a demyelinating infectious disease caused by JC virus (JCV), occurs almost exclusively in immunocompromised patients usually with malignant diseases. We report here a Japanese female with follicular lymphoma who subsequently developed PML. In addition to JCV, human herpesvirus 6 (HHV-6) was detected in the affected brain lesions of the patient by polymerase chain reaction and by in situ hybridization. HHV-6, recognized as a neurotropic virus, is known to be reactivated during immunosuppression and can cause fatal complications such as encephalitis/encephalopathy. It is likely that impaired immunity associated with lymphoma and the additional immunosuppression following cytopenia-inducing chemotherapies predisposed the patient to reactivated HHV-6 infection. Although it remains to be clarified whether HHV-6 plays an important role as a co-agent with JCV in causing demyelination of the brain, our observation alerts physicians to the possible association of HHV-6 with the pathogenesis of PML.

Adult↗
PubMed2001

Genomic organization, tissue expression, and cellular localization of AF3p21, a fusion partner of MLL in therapy-related leukemia.

We previously identified the AF3p21 gene, a novel fusion partner of the MLL gene, in a patient who had developed therapy-related leukemia with t(3;11)(p21;q23). The AF3p21 gene encodes a protein consisting of 722 amino acids, which has an SH3 (Src homology 3) domain, a proline-rich domain, and a bipartite nuclear localization signal. The protein's SH3 domain has high homology with that of FYN. Analysis of the DNA from the patient's leukemic cells revealed that intron 6 of the MLL gene was fused at a point upstream of exon 1 in the AF3p21 gene, and that the der(11) chromosome formed an MLL-AF3p21 fusion transcript in leukemic cells, whereas the der(3) chromosome did not form any fusion transcript. The AF3p21 gene on chromosome band 3p21 is 19 kb long and consists of 13 exons. The size of the mRNA of the AF3p21 gene is approximately 3.5 kb. The AF3p21 gene is widely expressed in normal human tissues including the bone marrow, brain, liver, thymus, lung, and skeletal muscle. Western blot and immunocytochemical analyses showed that AF3p21 protein has an apparent molecular weight of 80 kDa and is localized exclusively in the cell nucleus. These results suggest the possibility that AF3p21 protein plays a role in signal transduction in the nucleus.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Co-infection of HHV-6 and HHV-8 is rare in primary effusion lymphoma.

The presence and distribution of Epstein-Barr virus (EBV), as well as human herpesvirus-6 and-8 (HHV-6 and HHV-8) was investigated by polymerase chain reaction in 191 samples from a variety of lymphoproliferative disorders. HHV-6 DNA was detected in 18% (30 of 169) of non-HHV-8 related lymphoproliferative disorders, with the highest frequency in AIDS-related lymphomas (8 of 25, 32%). In contrast, HHV-6 DNA was present in less than 5% (1 of 22) of HHV-8 related lymphoproliferative disorders [21 primary effusion lymphomas (PEL), and 1 cases of Castleman disease]. As compared to HHV-6, EBV DNA was frequently detected in PEL (11 of 19 samples, 58%). This study suggests that transformation to PEL is not enhanced by HHV-6, furthermore HHV-6 and -8 may interfere with each other.

Castleman Disease↗
PubMed2000

Constitutional t(3;11)(p21;q23) in a family, including one member with lymphoma: establishment of novel cell lines with this translocation.

We describe a family with an inherited constitutional chromosome translocation (3;11) (p21;q23). Of three proven translocation carriers, one had duodenal malignant lymphoma (B-cell diffuse lymphoma, medium-sized cell type). The t(3;11)(p21;q23) was detected not only in hematopoietic cells including the patient's lymphoma cells, non-pathological bone marrow, and phytohemagglutinin-stimulated peripheral blood, but also in fibroblasts of the skin. We have successfully established an Epstein-Barr virus-transformed B-cell line and a Herpesvirus saimiri-transformed T-cell line from the patient, and found that both cell lines also carried this translocation. The patient's asymptomatic mother and sister had the same chromosomal abnormality. Chromosomal abnormalities of the 11q23 band occur frequently in various hematopoietic malignant disorders, and 3q21 has been linked to the pathogenesis of several solid tumors including carcinomas of the kidney, lung, and breast. Although 11q23 is known to recombine with many different chromosomal segments, t(3;11)(p21;q23) has not been reported to our knowledge. Further assessment is warranted to clarify if this constitutional translocation predisposes to certain malignancies. Our cell lines carrying the novel chromosome translocation would be useful for the molecular analysis of the rearranged genes involving both 3p21 and 11q23.

Adult↗
PubMed2000

Human herpesviruses in primary ocular lymphoma.

Several human lymphotropic herpesviruses have been found in certain lymphoproliferative disorders and implicated as possible etiologic factors or as modulating elements of the diseases. To assess a possible association of the human herpesviruses with lymphomas arising from mucosa-associated lymphoid tissue (MALT), we evaluated the presence of four human herpesviruses, Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), HHV-7, and HHV-8, in the biopsied specimens from 14 patients with primary ocular MALT lymphomas. EBV DNA sequences were detected in four specimens by polymerase chain reaction (PCR), and four cases were positive for HHV-6 DNA. In situ hybridization showed that three and two of 14 cases were positive for EBV mRNA and HHV-6 DNA, respectively. Neither HHV-7 nor HHV-8 sequences could be detected by PCR. These findings would stimulate further investigation as to the involvement of these lymphotropic viruses in the pathogenesis of a subset of low-grade primary ocular lymphomas.

Adult↗
PubMed2000

[Human herpesvirus 6(HHV-6) and HHV-8 in malignant lymphoma].

Over the past 14 years three new human herpesviruses(HHV-6, -7 and -8) have been recognized and implicated as etiological agents of several human diseases. HHV-6 has been cited as a possible cause or as a modulating element of certain human lymphoproliferative disorders, particularly malignant lymphomas including Hodgkin's disease and Burkitt's lymphoma. Despite the genomic homology and serological cross-reactivity between HHV-6 and HHV-7, evidence for the association of HHV-7 with lymphoproliferative diseases has been scarce. HHV-8 was originally found in patients with Kaposi's sarcoma, and subsequently shown to be implicated in primary effusion lymphoma(PEL), a novel lymphoma entity. We found that HHV-6 genome is integrated into host DNA of lymphoma cells. Further studies are warranted to determine whether chromosomally integrated HHV-6 has any role in the pathogenesis of viral genome-positive lymphoproliferative diseases.

DNA↗
PubMed1999

Inheritance of chromosomally integrated human herpesvirus 6 DNA.

Human herpesvirus 6 (HHV-6) genome has been detected in several human lymphoproliferative disorders with no signs of active viral infection, and found to be integrated into chromosomes in some cases. We previously reported a woman with HHV-6-infected Burkitt's lymphoma. Fluorescence in situ hybridization showed that the viral genome was integrated into the long arm of chromosome 22 (22q13). The patient's asymptomatic husband also carried HHV-6 DNA integrated at chromosome locus 1q44. To assess the possibility of chromosomal transmission of HHV-6 DNA, we looked for HHV-6 DNA in the peripheral blood of their daughter. She had HHV-6 DNA on both chromosomes 22q13 and 1q44, identical to the site of viral integration of her mother and father, respectively. The findings suggested that her viral genomes were inherited chromosomally from both parents. The 3 family members were all seropositive for HHV-6, but showed no serological signs of active infection. To confirm the presence of HHV-6 DNA sequences, we performed polymerase chain reaction (PCR) with 7 distinct primer pairs that target different regions of HHV-6. The viral sequences were consistently detected by single-step PCR in all 3 family members. We propose a novel latent form for HHV-6, in which integrated viral genome can be chromosomally transmitted. The possible role of the chromosomally integrated HHV-6 in the pathogenesis of lymphoproliferative diseases remains to be explained.

Burkitt Lymphoma↗
PubMed1998

Analysis of the Smad2 gene in hematological malignancies.

A total of 34 leukemia and lymphoma samples (17 clinical samples and 17 cell lines) were analyzed for mutations of the Smad2 gene by reverse transcriptase-polymerase chain reaction single strand conformation polymorphism (RT-PCR-SSCP) analysis. Nine of the 34 samples had 18q chromosomal abnormalities. No shifted bands were detected in any of the hematological malignancies. Our results suggest that resistance to cell growth inhibitory effects of TGF-beta in hematological malignancies is not due to alterations of the Smad2 gene.

Adolescent↗