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Yuko Mishima

Publications and source records attributed to Yuko Mishima.

10 recordsLinked to original sources
PubMed2006

A Japanese case of eosinophilic esophagitis.

Eosinophilic esophagitis (EE) is a rarely diagnosed condition involving eosinophilic infiltration of the esophageal mucosa. Here we present a case of EE in a 69-year-old Japanese man, who presented with abdominal pain, appetite loss, and a history of bronchial asthma. Laboratory findings included peripheral eosinophilia and an increased serum immunoglobulin E level. Computed tomography showed diffuse severe thickening of the esophageal wall, and a barium esophagogram revealed a small caliber of the middle and lower portion of the esophagus, without normal peristaltic contractions. Endoscopy of the esophagus showed a pale mucosa, with adherent whitish exudates resembling fungal infection, and prominent ring-like contractions. Histologic examination of a biopsy specimen revealed marked eosinophil infiltration into the esophageal mucosa. Endoscopic ultrasonography (EUS) demonstrated marked circumferential thickening of the esophageal submucosal layer, and an esophageal manometry study showed a high percentage of ineffective esophageal peristalsis and high-amplitude esophageal body contractions. EUS findings showed no change even after oral corticosteroid therapy, although the histological findings were improved. This is thought to be the first documented Japanese case of EE. EE should be considered in the differential diagnosis in cases of esophageal motility disturbance, even if the patients do not complain of dysphagia.

Aged↗
PubMed2006

Blockade of bulky lymphoma-associated CD55 expression by RNA interference overcomes resistance to complement-dependent cytotoxicity with rituximab.

Recently, anti-CD20 (rituximab) and anti-Her2/neu (trastuzumab) antibodies have been developed and applied to the treatment of malignant lymphoma and breast cancer, respectively. However, bulky lymphoma is known to be resistant to rituximab therapy, and this needs to be overcome. Fresh lymphoma cells were collected from 30 patients with non-Hodgkin's lymphoma, the expression of CD20 and CD55 was examined by flow cytometry, and complement-dependent cytotoxicity (CDC) assays were carried out. Susceptibility to CDC with rituximab was decreased in a tumor size-dependent manner (r=-0.895, P<0.0001), but not in a CD20-dependent manner (r=-0.076, P=0.6807) using clinical samples. One complement-inhibitory protein, CD55, contributed to bulky lymphoma-related resistance to CDC with rituximab. A decrease in susceptibility to CDC with rituximab was statistically dependent on CD55 expression (r=-0.927, P<0.0001) and the relationship between tumor size and CD55 expression showed a significant positive correlation (r=0.921, P<0.0001) using clinical samples. To overcome the resistance to rituximab by high expression of CD55 in bulky lymphoma masses, small interfering RNA (siRNA) was designed from the DNA sequence corresponding to nucleic acids 1-380 of the CD55 cDNA. Introduction of this siRNA decreased CD55 expression in the breast cancer cell line SK-BR3 and in CD20-positive cells of patients with recurrent lymphoma; resistance to CDC was also inhibited. This observation gives us a novel strategy to suppress bulky disease-related resistance to monoclonal antibody treatment.

Antibodies, Monoclonal↗
PubMed2006

Differential regulation of eotaxin-1/CCL11 and eotaxin-3/CCL26 production by the TNF-alpha and IL-4 stimulated human lung fibroblast.

Allergic asthma and allergic dermatitis are chronic inflammatory diseases and are characterized by an accumulation of eosinophils at sites of inflammation. Eotaxin-1/CCL11 and eotaxin-3/CCL26 are members of the CC chemokine family, which are known to be potent chemoattractants for eosinophils. We observed that a human lung fibroblast, HFL-1 produces eotaxin-1 and -3 in response to TNF-alpha plus IL-4 stimulation, accompanied with NF-kappaB and STAT6 activation. We explored which signaling pathways are operative in the production of eotaxin-1 and -3 using several inhibitors. Eotaxin-1/CCL11 production was inhibited by a p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, but not by the MEK (MAPK/ERK kinase) inhibitors, PD98059 and U0126. In contrast, eotaxin-3/CCL26 production was inhibited similarly by PD98059 as well as U0126 and SB203580. In addition, two proteasome inhibitors, N-acetyl-leucyl-leucyl-norleucinal (ALLN) and bortezomib with significant inhibitory activity on NF-kappaB activation, inhibited eotaxin-1/CCL11 production with IC50 8 microM for ALLN and IC50 16 nM for bortezomib. In contrast, eotaxin-3/CCL26 production was not inhibited significantly up to 10 microM of ALLN (IC50 16 microM) and up to 10 nM of bortezomib (IC50 11 nM), giving inhibition of eotaxin-3/CCL26 less sensitive than eotaxin-1/CCL11 production by the proteasome inhibitors. Synergistic inhibition was observed among lower doses of SB203580 and proteasome inhibitors, particularly in the eotaxin-1/CCL11 production. No such prominent synergism was found on the eotaxin-3/CCL26 production. The suppression of eotaxin family production by these inhibitors may be efficacious against allergic diseases.

Asthma↗
PubMed2005

[An autopsied case of metastatic endocrine carcinoma of the pancreas with primary site difficult to identify].

A 40-year-old man suffering from right cheek swelling was first diagnosed with ameloblastoma or anaplastic poorly-differentiated carcinoma of the head and neck region. He received 2 courses of CDDP/TXT chemotherapy (cisplatin 75 mg/m2, docetaxel 80 mg/m2) and achieved a partial response, but his carcinoma of the pancreas recurred. He also achieved a partial response with 2 courses of CBDCA/TXL regimen (carboplatin AUC=6, paclitaxel 200 mg/m2), but later died from his progressive disease. The autopsy revealed a pathological diagnosis of metastatic endocrine carcinoma of the pancreas. This case was close to a cancer with an unknown primary (CUP) site, and several favorable sub-sets of CUP have been identified, which are responsive to systemic chemotherapy. Poorly-differentiated neuroendocrine carcinomas like this case are highly sensitive to chemotherapy, and a careful pathological diagnosis may clarify its sensitivity to chemotherapy and the prognosis.

Adult↗
PubMed2004

Combination chemotherapy (cyclophosphamide, doxorubicin, and vincristine with continuous-infusion cisplatin and etoposide) and radiotherapy with stem cell support can be beneficial for adolescents and adults with estheisoneuroblastoma.

BACKGROUND: Adolescent-onset and adult-onset esthesioneuroblastoma is a rare disease and is considered incurable. In many patients, local resection and radiation are chosen as clinical therapy with or without chemotherapy. It was reported previously that local resection and radiotherapy led to temporary remission and, in many patients, recurrent disease. Although combination with chemotherapy has been regarded as promising, an effective regimen has not been established. In the current study, the authors investigated the effect and tolerability of the combination of chemotherapy, radiotherapy, and peripheral blood stem cell transplantation (PBSCT). METHODS: The study population included 12 patients with adolescent-onset and adult-onset esthesioneuroblastoma classified as Kadish Stage A-D. The patients received two cycles of combination chemotherapy, which consisted of cyclophosphamide, doxorubicin, and vincristine (CAD) with continuous-infusion cisplatin and etoposide (CVP). This was combined with radiotherapy with or without PBSCT. RESULTS: Nine of 12 patients (75%) obtained more than a partial response after only 2 cycles of chemotherapy. After radiation with or without PBSCT, six patients obtained a complete remission (CR). The longest survival was > 3 years. All patients who underwent PBSCT obtained a CR. The most severe side effects were loss of sodium and potassium induced by cisplatin-related renal tubular distress. Those abnormalities were temporary, and all patients recovered. CONCLUSIONS: The chemotherapy regimen with CADO and CVP does not require continuation for a long time and is very effective and tolerable for patients with adolescent-onset and adult-onset esthesioneuroblastoma. The combination with radiotherapy and PBSCT may lead to a CR without facial disfigurement. In this report, the authors discuss the feasibility and efficacy of this multidisciplinary approach.

Adolescent↗
PubMed2004

[Proteasome inhibitors].

Bortezomib, one of the proteasome inhibitors, has been approved in the United States for multiple myeloma as a second-line chemotherapy. In Japan, bortezomib has been used for for phase I clinical trials for multiple myeloma. As the action mechanism, it has been proposed that bortezomib inhibits NF-kappaB via IkappaB alpha. It also demonstrated positive results for non-Hodgkin's lymphoma and non-small cell lung cancer, but not for colorectal cancer or chronic lymphocytic leukemia. The mechanism of drug resistance has been well analized. Bortezomib is very effective but still induces adverse effects including hypotension especially when there is an overdose. Medical oncologists or hematology/oncologists must exert due caution.

Boronic Acids↗
PubMed2004

[Rituximab and hematological malignancy].

After genetic recombination with murine and human cDNA, monoclonal antibody has been produced in chimeric form. CD20 is a B cell antigen, which can be a target molecule for antibody therapy. Rituximab is an anti-CD20 monoclonal antibody that has an efficacy against B cell lymphomas. Combination therapy with CHOP regimen as well as single therapy will give rise to new treatment strategy for CD20+B cell lymphomas. Mechanism is not clarified, but induction of apoptosis, complement-mediated cell toxicity, and antibody-dependent cell toxicity are considered. Synergy with chemotherapy agents such as CHOP, ICE, DHAP and stem cell transplantation will help the patients who suffer lymphomas, CLL and Waldenstrom's macroglobulinemia. Treatment with rituximab is well tolerated and we must be careful about infusion reaction after administration.

Antibodies, Monoclonal↗
PubMed2003

[Simultaneous detection of both non-Hodgkin's lymphoma cells and breast cancer cells in pleural effusion--a case report].

A 55-year-old woman underwent breast-conserving surgery with irradiation for Stage IIB (T2 N1 M0) breast cancer of her right breast. Thereafter, she was treated orally with oral UFT and tamoxifen. Three years following surgery, she was diagnosed as having a non-Hodgkin's lymphoma. She underwent 6 cycles of EPOCH-G (etoposide, vincristine, adriamycin, cyclophosphamide, prednisolone, G-CSF) therapy, and obtained complete remission. Two years later, her neck and inguinal lymph nodes were swollen. Biopsy confirmed the relapse of NHL. She underwent salvage chemotherapies of MST-16, carboplatin, IVAC, and CPT-11, but the disease was refractory. In May 2000, bilateral pleural effusion was detected. Cytomorphologically, the pleural fluid specimen showed both atypical lymphoid cells and adenocarcinoma cells simultaneously. Existence of double cancer in the pleural effusion has not been reported, suggesting that this case is rare.

Adenocarcinoma↗
PubMed2002

New human myelodysplastic cell line, TER-3: G-CSF specific downregulation of Ca2+/calmodulin-dependent protein kinase IV.

We have established a new hematopoietic cell line from a patient with myelodysplastic syndrome (MDS), which was refractory anemia with excess blasts (RAEB). This cell line, designated TER-3, depends on several cytokines for long-term survival and growth, and requires interleukin-3 (IL-3) for continuous growth. Cytochemical analysis revealed that TER-3 cells are weakly dianisidine positive and nonspecific esterase positive, but peroxidase negative. The surface marker profile shows that the TER-3 cells are strongly positive for myeloid, lymphoid, and megakaryocytic antigens such as CD15, CD19, and CD61, and negative for some common multilineage antigens such as CD13, CD33, and CD34. Thus, this cell line has a multilineage phenotype, suggesting that the transformation event occurred in multipotent stem cells. Dianisidine- and nonspecific esterase-positive TER-3 cells increase with granulocyte-colony stimulating factor (G-CSF) rather than with IL-3. These results suggest that the cell line is useful for understanding the mechanism underlying G-CSF-associated hematopoietic cell differentiation and activation in the patient with MDS.

Antigens, Surface↗