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Whole-heart coronary magnetic resonance angiography (WH-MRA) is useful noninvasive examination. Its signal acquisition is performed during very short still timing in each cardiac motion cycle, and therefore the adequate still timing selection is important to obtain the better image quality. However, since the current available selection method is only manual one using visual comparison of cine MRI images with different phases, the selected timings are often incorrect and their reproducibility is not sufficient. We developed an automated selection method to detect the best still timing for the WH-MRA and compared the automated method with conventional manual one. Cine MRI images were used for the analysis. In order to extract the high-speed cardiac cine image, each phase directional pixel set at each pixel position in all cine images were processed by a high-pass filtering using the Fourie transform. After this process, the cine images with low speed timing became dark, and the optimal timing could be determined by a threshold processing. We took ten volunteers' WH-MRA with the manually and automatically selected timings, and visually assessed image quality of each image on a 5-point scale (1=excellent, 2=very good, 3=good, 4=fair, 5=poor). The mean scores of the manual and automatic methods for right coronary arteries (RCA), LDA left anterior descending arteries (LAD) and LCX left circumflex arteries (LCX) were 4.2±0.38, 4.1±0.44, 3.9±0.52 and 4.1±0.42, 4.1±0.24, 3.2±0.35 respectively. The score were increased by our method in the RCA and LCX, and the LCX was significant (p<0.05). As the results, it was indicated that our automated method could determine the optimal cardiac phase more accurately than or equally to the conventional manual method.

The p73gene, a member of the p53family, is a new candidate tumor suppressor gene. To investigate the possibility of genetic alteration of p73in leukemia and lymphoma, we examined 55 cell lines and 39 patient samples together with 17 nonhematopoietic cancer cell lines. Gene expression of p73was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) in cell lines (5 of 7 pre B/B-acute lymphoblastic leukemia [ALL], 13 of 21 T-ALL/lymphoblastic lymphomas [LBL], 9 of 10 B–non-Hodgkin's lymphomas [B-NHL], 8 of 9 acute myelogenous leukemias [AML], 2 of 2 T-NHL, 3 of 3 multiple myeloma), and in patient samples (16 of 23 pre B-ALL, 5 of 8 T-ALL/LBL, 5 of 8 B-NHL). PCR–single-strand conformation polymorphism (SSCP) of cDNAs showed no mutation in 43p73-expressing cell lines within the regions that corresponded to the 5 mutational hotspots of the p53gene. Neither homologous deletion nor rearrangement of the p73gene were found by Southern blot analysis in any of the cell lines that lack expression of p73.In contrast to prior published data, analysis of a polymorphic site showed that the p73gene was expressed biallelically in cell lines and normal peripheral blood. Notably, the p73-negative cell lines were hypermethylated at a CpG island in the 5′ untranslated region of the p73mRNA, and treatment of these cell lines with 5-azacytidine (5-AC), a demethylation reagent, induced p73expression. Taken together, we found that a sizable proportion (32%) of ALL/B-NHL cell lines and primary tumors had negligible or limited expression of the p73gene associated with hypermethylation of the gene. These findings suggest that silencing of the p73gene by hypermethylation may contribute to development and/or progression of lymphoid neoplasms.

The chromosomal translocation, t(8;21), is found frequently in acute myeloid leukemia (AML) with maturation (FAB-M2). We have previously mapped the translocation breakpoints of t(8;21) in a specific intron of the AML1gene on chromosome 21. In this study, we cloned cDNAs synthesized from a cell line carrying t(8;21) by reverse transcription polymerase chain reaction (RT-PCR) using an AML1-specific primer. The analysis of the cDNAs structure has led to the identification of the fusion of AML1with a gene named MTG8on chromosome 8, which seems to be identical to ETO. Northern analysis using MTG8 (ETO)probes detected 7.8-kb and 6.2-kb RNAs and several minor RNAs in the cell line with t(8;21), but failed to detect any transcripts in a cell line without t(8;21). A set of primers were designed to detect the AML1/MTG8(ETO)fusion by PCR. The PCR amplified identical products in all 6 patients and one cell line with t(8;21), suggesting that the AML1/MTG8(ETO)fusion is a constant feature associated with t(8;21) and the junctions of the AML1/MTG8(ETO)fusion are restricted in a unique site. Because the PCR detection of the AML1/MTG8(ETO)fusion at the RNA level is highly sensitive, it can be used as a sensitive method for diagnosis and detection of minimal residual disease in t(8;21) leukemia.

A novel leukemic cell line with an 8;21 chromosome translocation, designated as Kasumi-1, was established from the peripheral blood of a 7-year-old boy suffering from acute myeloid leukemia (AML). The Kasumi-1 cells were positive for myeloperoxidase showing a morphology of myeloid maturation. The response in proliferation assay was observed in the culture with interleukin-3 (IL-3), IL-6, granulocyte colony-stimulating factor (G-CSF), and granulocyte-macrophage CSF (GM-CSF), but not with IL-1 or IL-5. Neither granulocytic nor eosinophilic maturation was observed in the liquid culture by the addition of dimethyl sulfoxide, G-CSF, or IL-5, respectively. In contrast, induction of macrophagelike cells was seen by the addition of phorbol ester. This is the first report of a human AML cell line with t(8;21) that has characteristics of myeloid and macrophage lineages. The cell line could be a useful tool for elucidating the pathophysiology of AML with t(8;21).

Recant molecular evidence suggests an association with a new herpes virus, Kaposi's sarcoma-associated herpes virus (KSHV/HHV-8), and primary effusion lymphomas (PEL). PELs have a characteristic morphology, phenotype, and clinical presentation with malignant effusions in the absence of a contiguous solid tumor mass. Most cases of PEL have occurred in human immunodeficiency virus (HlV)-positive male patients who are coinfected with Epstein-Barr virus (EBV). This report describes two cases of PEL in HIV- and EBV-negative women. In one patient, a pleural cavity PEL was preceded by classic Kaposi's Sarcoma (KS) of the lower extremities. In the second patient, PEL developed in an artificial cavity related to the capsule of a breast implant. Both cases had the characteristic morphologic appearance of high-grade anaplastic/B-cell immunoblastic lymphomas, with loss of B-cell differentiation antigens, clonal immunoglobulin heavy chain gene rearrangements, and expression of activation antigen CD30. Both cases were negative for EBV, herpes virus simplex, and cytomegalovirus (CMV). DNA extracted from both lymphomas and skin KS specimen showed KSHV sequences by molecular analysis. This report expands the spectrum of KSHV-associated disease to include PEL in HIV-negative women.

Recent molecular evidence suggests an association with a new herpesvirus, Kaposi’s sarcoma-associated herpesvirus (KSHV/HHV - 8), and primary effusion lymphomas (PELs). PELs have a characteristic morphology, phenotype, and clinical presentation, with malignant effusions in the absence of a contiguous solid tumor mass. We have established a cell line (KS - 1) from a KSHV-positive human immunodeficiency virus (HlV)-negative patient with pleural cavity-based lymphoma that was passaged into triple-immunodeficient BNX mice. In contrast to cell lines from body cavity-based lymphomas derived from HIV-positive individuals that contain both KSHV and Epstein Barr viral genome, these cells contain only KSHV, allowing for uncontaminated virologic studies. Ultrastructural examination identified malignant cells with features of late differentiating B cells (immunoblasts). Cells with viral cytopathic effect contained typical 110-nm intranuclear herpesvirus nucleocapsids and complete cytoplasmic virions, confirming the association of PEL with KSHV.

Abstract 2963