Publications by authors named "Satoko Osanai"

The patient, a 56-year-old lady, also exhibited numerous lymphadenopathy, hepatosplenomegaly, hyperleukocytosis (167,200/µl, aberrant lymphocytes 91.5%), and fever. A lymph node biopsy revealed follicular lymphoma (FL), grade 1.

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  • A 79-year-old man with primary plasma cell leukemia experienced multiple extramedullary plasmacytomas and developed thrombotic microangiopathy (TMA) after starting treatment with carfilzomib, lenalidomide, and dexamethasone (KLd).
  • After the diagnosis of TMA on day 7 of treatment, KLd therapy was stopped, leading to improvement in TMA symptoms, indicating a strong link between the drug and the condition.
  • After reducing the dose of KLd and achieving a very good partial response (VGPR), the patient has remained in remission, suggesting that dose adjustment for patients experiencing TMA might be a viable option in effective treatments.
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  • The study focused on the role of PRAME (preferentially expressed antigen in melanoma) in bone marrow cells from 116 patients with myelodysplastic syndromes (MDS).
  • High levels of PRAME expression were linked to worse survival rates in MDS patients, particularly those with low bone marrow blast percentages and lower IPSS-R risk categories.
  • The findings indicate that PRAME could serve as a potential prognostic factor for assessing disease progression and outcomes in MDS patients.
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We herein report two cases of thrombotic thrombocytopenic purpura (TTP) complicated by other autoimmune disorders, autoimmune hepatitis and immune thrombocytopenia, respectively. In both cases, corticosteroids were continuously administered for the treatment of preceding autoimmune disorders. However, a sufficient objective response for TTP was not obtained by plasma exchange and corticosteroid treatment.

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The PLCG1 gene, which encodes the phospholipase C γ1 isoform, is located within the commonly deleted region of the long arm of chromosome 20 (del(20q)) observed in myelodysplastic syndromes (MDS). Phospholipase C is involved in diverse physiological and pathological cellular processes through inositide signaling. We hypothesized that reduced PLCG1 expression because of haploinsufficiency by del(20q) plays a role in the molecular pathogenesis of MDS.

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Deletion of the long arm of chromosome 20 (del(20q)) is observed in 5-10% of patients with myelodysplastic syndromes (MDS). We examined the expression of 28 genes within the common deleted region (CDR) of del(20q), which we previously determined by a CGH array using clinical samples, in 48 MDS patients with (n = 28) or without (n = 20) chromosome 20 abnormalities and control subjects (n = 10). The expression level of 8 of 28 genes was significantly reduced in MDS patients with chromosome 20 abnormalities compared to that of control subjects.

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The efficacy of 30 platelet concentrate (PC) products transfused to a patient with myelodysplastic syndrome (MDS) was evaluated by calculating the 1-hour post-transfusion corrected count increment (1h-CCI). Of the 30 transfusions, all HLA-A/B-matched, the cross-match (CM) test was negative in 23 (CM(-)-PC) and weakly positive (CM(+)-PC) in 2, and the CM test was not conducted in 5 (non-CM-PC). The effective rate was higher with CM(-)-PC compared to non-CM-PC (82.

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