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M Musashi

Publications and source records attributed to M Musashi.

At least 19 recordsLinked to original sources
PubMed2004

Monitoring of T-cell repertoire was useful for predicting graft-versus-host disease prognosis in a patient with chronic myelogeneous leukemia after allogeneic bone marrow transplantation.

We analyzed 24 T-cell receptor (TCR)beta chain subfamilies (Vbeta) and the chimerism of a patient with chronic myelogeneous leukemia who underwent allogeneic bone marrow transplantation (allo-BMT). The patient developed liver dysfunction at day 19 leading to worsening of his condition. He died on day 91 of hepatic failure. Complete donor chimerism was observed after day 19. The average complexity score of TCR-Vbeta, which was low on day 19 (5.50), because much lower on day 82 (3.77). The average value of normal volunteers is 7.69. Neither immunosuppressive therapy nor antiviral therapy was effective to treat his hepatic dysfunction. A liver specimen at autopsy showed necrotic tissue with invasion of lymphocytes under the endothelial cells of the bile ducts. These findings suggest that the liver dysfunction was due to graft-versus-host disease (GVHD). Careful monitoring of chimerism and TCR-Vbeta complexity may help to predict the prognosis of GVHD after allogeneic BMT.

Adult↗
PubMed2002

del11(p11-13) with overexpression of Wilms' tumor gene during leukemic transformation of myelodysplastic syndrome.

We report a case of leukemic transformation from myelodysplastic syndrome (MDS) with a sole chromosome abnormality of del11(p11-13). The patient had been diagnosed as having MDS (refractory anemia with excess of blast cells, RAEB) in May 1998. At that time, cytogenetic analysis of bone marrow cells showed a normal karyotype. The patient received sequential chemotherapy with low-dose cytosine arabinoside (AraC) and macrophage colony-stimulating factor (M-CSF). Complete remission was obtained with this treatment, but the disease gradually progressed after June 1999. Cytogenetical analysis showed del11(p11-13) in 6 of 40 cells analyzed at that time, and the disease had evoluted to overt leukemia in December 1999 with a gradual increase in the abnormal clone. Furthermore, mRNA of the WT1 gene located at chromosome 11p13 was overexpressed during leukemic transformation, whereas it was not detected at the time of the initial diagnosis of MDS (RAEB) in May 1998. It was thought that this chromosome deletion and overexpression of WT1 resulted in the leukemic transformation in this patient. This is the first case report of del11(p11-13) being considered to be the primary cause of leukemic transformation from MDS.

Blast Crisis↗
PubMed2001

Exfoliative esophagitis early after autologous peripheral blood stem cell transplantation.

Two patients with non-Hodgkin's lymphoma (NHL) suffered from hematemesis due to exfoliative esophagitis early after autologous peripheral blood stem cell transplantation (PBSCT). The chemotherapy regimens used for these 2 patients were the same and consisted of high-dose ranimustine, carboplatin, etoposide, and cyclophosphamide (MCVC regimen), which have been widely used in autologous PBSCT for NHL in Japan. Esophageal bleeding in both patients was stopped by conservative treatment without any special endoscopic manipulations. Gastrointestinal bleeding after hematopoietic stem cell transplantation is usually caused by viral infections, graft-versus-host disease, or conditioning chemo-radiotherapy. Although severe esophagitis is common in patients receiving stem cell transplantation, the exfoliative form detected by endoscopic examination has not been reported. We conclude that high-dose chemotherapy and frequent vomiting during treatment are risk factors for lower-esophageal bleeding in these cases.

Adult↗
PubMed2001

Peripheral T-cell lymphoma in a patient with osteopetrosis.

Osteopetrosis is a rare genetic disorder in which the function of osteoclasts is defective, resulting in impaired bone resorption. This disease is usually accompanied by myelosuppression due to decreased marrow space and by osteomyelitis, especially in the submandibular bone. We report the case of a 72-year-old woman with an autosomal dominant form of osteopetrosis who suffered from peripheral T-cell lymphoma. Accurate clinical and pathological diagnoses and staging were difficult due to nonspecific reactive hyperplasia of the lymph nodes, even though we used several scintigraphic techniques and [18F]fluorodeoxyglucose positron emission tomography. We also paid special attention to myelosuppression and exacerbation of osteomyelitis after combination chemotherapy. Severe infectious complications were avoided by early administration of G-CSF for leukocytopenia and by continuous oral administration of antibiotics. The patient achieved complete remission after four courses of chemotherapy and this status has been maintained for 6 months.

Aged↗
PubMed2001

Chronic eosinophilic leukemia with t(6;11)(q27;q23) translocation.

We report a rare case of chronic eosinophilic leukemia (CEL) with a chromosomal abnormality of t(6;11)(q27;q23). The patient was diagnosed as having thyroid cancer with metastases to the lung and cervical lymph nodes in 1993. Percutaneous ethanol injection therapy (PEIT), total thyroidectomy, and radiotherapy were performed. The patient was also diagnosed as having prostatic cancer with bone metastasis in July 1999, and hormonal therapy was performed. At the time of the diagnosis of prostatic cancer, leukocytosis with eosinophilia was also revealed. Thereafter, cytogenetical analysis and reverse transcriptase polymerase chain reaction (RT-PCR) analysis of bone marrow showed t(6;11)(q27;q23) translocation and MLL/AF6 fusion products, respectively. No transcripts of the BCR/ABL chimeric gene were found by RT-PCR in bone marrow. Analysis of serum cytokines revealed a slight elevation of GM-CSF but no elevation of IL-3 or IL-5. Tissue damage due to infiltration of eosinophils was not observed throughout the clinical course. On the basis of the cytogenetic and molecular abnormality, the patient was diagnosed as having CEL, rather than reactive eosinophilia due to thyroid or prostatic cancer or other reactive inflammation. This is the first case report of CEL with t(6;11)(q27;q23) translocation.

Aged↗
PubMed2001

Involvement of protein kinase C-epsilon in signal transduction of thrombopoietin in enhancement of interleukin-3-dependent proliferation of primitive hematopoietic progenitors.

We studied the effect of thrombopoietin (TPO) on interleukin-3 (IL-3)-dependent bone marrow cell colony formation of mice to clarify the role of protein kinase C (PKC) in the signal transduction of TPO for the proliferation of primitive hematopoietic progenitors. TPO alone hardly yielded colonies. However, TPO in combination with IL-3 increased colony numbers synergistically from 2- to 4-fold, compared with those supported by IL-3 alone. Serial observation of colony development showed that TPO may hasten the appearance of colonies by shortening the dormant period (G(0)) of primitive progenitors. Immunocytochemical studies on PKC isoforms in progenitor cells stimulated with TPO have revealed that the expression pattern of PKC-epsilon is changed, but not that of PKC-alpha, -beta, -gamma, -delta, or -zeta. Selective PKC inhibitors, such as calphostin C and GF 109203X, and PKC-epsilon-specific translocation inhibitor peptide abrogated the enhancing effect of TPO on IL-3-dependent colony formation and the changes in the intracellular expression pattern of PKC-epsilon. These data taken together suggest that TPO has a direct effect on primitive progenitors and enhances IL-3-dependent colony formation, at least partly through the activation of PKC-epsilon.

Animals↗
PubMed2000

Evolution to acute myeloblastic leukemia from chronic neutrophilic leukemia with dysplastic features in granulocytic lineage.

We experienced the case of an 82-year-old man with chronic neutrophilic leukemia (CNL) with dysplastic features in the granulocytic lineage which subsequently progressed to acute myeloblastic leukemia (AML) with myelofibrosis. The patient had hepatosplenomegaly, but there was no evident cause of neutrophilic leukocytosis. The cytogenetic study showed that he had a normal karyotype. Concentrations of the serum granulocyte colony-stimulating factor (G-CSF) were not detectable. Two years after the diagnosis of CNL, blastic transformation to AML occurred with myelofibrosis and significant morphological abnormalities in neutrophils. The blasts were positive for myeloperoxidase, CD33, CD34, and HLA-DR, and the presence of dysplasia within the granulocytic lineage suggested that he had an abnormality at the level of the granulocyte-committed progenitors. Heterogeneous origins of CNL might lead to various clinicopathological features in each case.

Aged↗
PubMed2000

[beta-thalassemia minor diagnosed in a patient with chronic myelogenous leukemia during hydroxyurea therapy].

A 55-year-old man was admitted to our hospital because of leukocytosis and microcytic anemia with hypochromia, target cells, and increased levels of hemoglobin A2 and hemoglobin F. The results of a gene analysis yielded a diagnosis of chronic myelogenous leukemia and beta-thalassemia minor. A gradual increase in hemoglobin was observed during hydroxyurea therapy, which was performed over a 12-week period. This increment appeared to be due to suppressed production of myeloid cells. It was been reported that hydroxyurea increases total hemoglobin due to increased hemoglobin F synthesis in patients with beta-thalassemia. However, hydroxyurea had no clear influence on hemoglobin concentration in this case.

Antineoplastic Agents↗
PubMed2000

Proliferation of CD4+ lymphocytes in a patient with chronic graft-versus-host disease after allogeneic bone marrow transplantation.

Expansion of donor-derived lymphocytes after allogeneic stem cell transplantation is a serious and sometimes fatal complication. Lymphoproliferative disorders are reportedly caused mainly by reactivation of Epstein-Barr virus (EBV) and non-EBV-associated secondary lymphoma or leukemia. In this paper, we report massive proliferation of CD4+ lymphocytes in peripheral blood of a patient with chronic graft-versus-host disease (GVHD) following allogeneic bone marrow transplantation (alloBMT) from an HLA-identical sibling donor. The abnormal lymphocytes showed CD3low, CD4+, CD8-, CD2+, CD5+, CD7+, CD25-, CD19-, CD20-, CD21-, CD16-, CD56low, T-cell receptor (TCR)-alpha/beta- and TCR-gamma/delta- phenotypes, and no rearrangement of either TCR-C beta 1 or IG(H)JH was detected from the lymphocytes by Southern blot analysis. EBV was not found in the nuclei of lymphocytes by an immunofluorescence antibody. The lymphoproliferation was resistant against immunosuppressive drugs, administered for the treatment of chronic GVHD, and it effectively inhibited aggravation of the chronic GVHD. Although antithymocyte globulin and cytosine arabinoside were administered later, the patient died of respiratory failure with bilateral pleural effusion and interstitial pneumonia. Because we found no evidence of monoclonality of the abnormal lymphocytes, we could not conclude that this patient had suffered from malignant lymphoproliferation. To our knowledge, this is the first case report of proliferation of CD4+ lymphocytes in a patient with chronic GVHD following alloBMT. In this paper, we discuss the possible pathophysiology of the patient.

Adult↗
PubMed2000

The role of protein kinase C isoforms in cell proliferation and apoptosis.

Protein kinase C (PKC) was first described as a calcium-activated, phospholipid-dependent serine/threonine protein kinase 22 years ago, and it has since been studied extensively as a second messenger transducing diverse signals regarding cell proliferation, activation of cellular function, differentiation, and even apoptosis. Because PKC consists of at least 11 isoforms, with possibly different biological properties, it is necessary to reevaluate its known functions as functions of each isoform. Recent studies have revealed that several other lipid metabolites generated by signal-induced hydrolysis of membrane phospholipids, such as ceramide and phosphatidylinositol-3,4,5-triphosphate, may also have the potential to mediate external signals. Here we describe the roles of PKC isoforms in cell proliferation and apoptosis, particularly in relation to other lipid metabolites.

Apoptosis↗
PubMed1999

Selective transendothelial migration of hematopoietic progenitor cells: a role in homing of progenitor cells.

To elucidate the mechanisms by which hematopoietic progenitor cells transmigrate via the bone marrow (BM) endothelial cells, we first established endothelial cell lines from BM and lung, and BM fibroblast cell lines; then we established an in vitro model of transendothelial migration of hematopoietic progenitor cells in the presence of chemoattractants secreted by BM fibroblast cells. The BM endothelial cells expressed vascular cell adhesion molecule-1 (VCAM-1), but the lung endothelial cells did not. The BM fibroblast cells secreted chemoattractants including stroma cell-derived factor (SDF)-1, which could attract hematopoietic progenitor cells to BM and activate the adhesion molecules expressed on hematopoietic progenitor cells after rolling along the endothelial cells. Anti-SDF-1 antibody inhibited the transendothelial migration of a hematopoietic progenitor cell line, FDCP-2. FDCP-2 that expressed very late activation antigen-4 (VLA-4) and normal progenitor cells transmigrated through BM endothelial cells but not lung endothelial cells, even if in the presence of chemoattractants produced by BM fibroblasts. Both anti-VLA-4 and anti-VCAM-1 antibodies inhibited the transendothelial migration of FDCP-2 cells and normal hematopoietic progenitor cells. These findings suggest that the transendothelial migration of hematopoietic progenitor cells is characteristic of BM endothelial cells, and that VLA-4/VCAM-1 and SDF-1 play important roles in the transendothelial migration and, consequently, homing of hematopoietic progenitor cells to BM.

Animals↗
PubMed1999

[Iron].

Explore the source record for details and available documents.

Female↗
PubMed1998

Monoclonal origin of an esophageal carcinosarcoma producing granulocyte-colony stimulating factor: a case report.

BACKGROUND: Carcinosarcomas are comprised of carcinomatous and sarcomatous elements, and their histogenesis remains unclear. The authors examined the serum concentrations of hematopoietic growth factors and performed immunohistochemical studies on an esophageal carcinosarcoma from a patient with marked granulocytosis to determine its histopathogenesis and clonality. METHODS: The authors examined the case of a 63-year-old man with a polypoid tumor of the esophagus associated with marked leukocytosis (131 x 10(9) per liter). Immunohistochemical staining of the esophageal tumor was performed using monoclonal antibodies against granulocyte-colony stimulating factor (G-CSF), keratin, epithelial membrane antigen (EMA), and vimentin. RESULTS: The patient's leukocyte count was increased (124 x 10(9) per liter) on admission. Because mature granulocytes predominantly were increased despite the absence of apparent infection, the patient's serum G-CSF concentration was examined and found to be 286.0 pg/mL and to increase with time. After thoracic esophagectomy was performed, granulocyte count and serum G-CSF concentration rapidly normalized. G-CSF concentration was 50-fold higher in the tumor tissue extract than in the extract from normal esophageal tissue. Microscopic examination of the resected specimens revealed that the tumor was comprised of squamous cell carcinoma (SCC) and spindle-shaped sarcomatous elements, and transitional features were observed within these two components. Immunohistochemical examination disclosed cells that were positive for keratin and EMA in the carcinomatous element and vimentin positive cells in the sarcomatous element. However, both types of tumor cells were positive for G-CSF. CONCLUSIONS: The presence of G-CSF in both SCC cells and spindle-shaped sarcomatous cells indicated that these two components originated from a single clone.

Carcinosarcoma↗
PubMed1998

Modulation of platelet activating factor-induced glycogenolysis in the perfused rat liver after administration of endotoxin in vivo.

The effect of endotoxin treatment in vivo on platelet activating factor (PAF)-induced glycogenolysis was studied in the perfused rat liver. The addition of PAF (20 nM) to the perfusate increased glucose production concomitant with suppression of oxygen consumption in control rats without endotoxin treatment. At 6 h after endotoxin administration, PAF caused severe suppression of oxygen consumption, but glucose production was greatly inhibited. At 24 h after endotoxin treatment, PAF caused less suppression of oxygen consumption than the control, and glucose production was partially restored. The metabolic responses in the control rat were abolished by the simultaneous presence of cyclooxygenase- and lipoxygenase-inhibitors. Combined use of leukotriene (LT) D4- and thromboxane (Tx) A2-receptor antagonists inhibited the metabolic responses in the rat given endotoxin 6 h before. The efflux of Tx B2 during PAF-infusion decreased 24 h after endotoxin treatment, and Tx A2 receptor antagonist, but not LT D4 receptor antagonist, prevented the suppression of oxygen consumption. These results suggest that different eicosanoids are involved in PAF-induced glycogenolysis in different stages of endotoxemia, and that LT D1 may also play a role in PAF-induced glycogenolysis.

Animals↗
PubMed1998

Bone marrow dysplasia with basophilic cells in a patient with angiocentric lymphoma.

We report a 46-year-old man suffering from angiocentric lymphoma of the skin. On admission, he had atypical cells rich in basophilic granules in the bone marrow and peripheral blood, in addition to skin eruptions and bone marrow dysplasia. Immediately after diagnosis, the patient was treated with multidrug combination chemotherapy. At first, the chemotherapy markedly relieved the skin eruption and bone marrow dysplasia, and atypical cells in the bone marrow and peripheral blood disappeared rapidly. However, the disease gradually became resistant to chemotherapy, resulting in a gradual deterioration of the skin eruption and bone marrow dysplasia, and reappearance of atypical cells. The levels of serum cytokines such as interleukin-4 and interleukin-6, and of soluble interleukin-2 receptor correlated well with the disease states. These results suggest that the lymphoma cells directly or indirectly induce the production of these cytokines and that a dysregulated cytokine network, which might be caused by lymphoma cells, induces an increase in atypical cells.

Bone Marrow↗
PubMed1997

Phorbol ester enhancement of IL-3-dependent proliferation of primitive hematopoietic progenitors of mice in culture.

Protein kinase C (PKC) is a Ca++- and phospholipid-dependent protein kinase activated by diacylglycerol that is either released from cell membranes in response to certain growth factors or mimicked by 12-O-tetradecanoyl phorbol-13-acetate (TPA). We studied the effects of TPA on interleukin-3 (IL-3)-dependent colony formation of mouse bone marrow cells from mice injected with 5-fluorouracil 2 days before examination in order to clarify the significance of PKC in the proliferation of primitive hematopoietic progenitors. Although TPA alone did not support colony formation, TPA in combination with IL-3 increased colony numbers from 1.5 to 2 times that formed with IL-3 and vehicle. TPA increased not only the granulocyte/macrophage colonies, but also the multilineage colonies. A sequential colony count showed that TPA, unlike IL-6, did not hasten the appearance of colonies. Because TPA enhanced IL-3-dependent colony formation derived from lineage-negative marrow cells obtained from mice that received 5-FU 2 days before, it is possible that it might act directly on primitive progenitors. Prolonged pretreatment of marrow cells with TPA prevented TPA-augmented colony growth. Calphostin C, a specific PKC inhibitor, and certain specific tyrosine kinase inhibitors, such as genistein and herbimycin A, abrogated the enhancing effects of TPA on IL-3-dependent colony formation. These data suggest that TPA had a direct effect on the primitive progenitors and enhanced IL-3-dependent colony formation via activation of PKC and certain tyrosine kinases.

Animals↗