Glioblastoma is one of the most malignant brain tumors, causing death within two years despite maximal tumor resection and concurrent radio-chemotherapy. Tumor stem cells are thought to be closely related to tumor progression and recurrence and are attractive therapeutic targets. It is common to culture cell lines in serum-free medium with growth factors to stimulate spheres of enriched tumor stem cells. To avoid spontaneous differentiation and cell death in the sphere environment, Pollard et al. formulated an adherent culture method using laminin-coated plates. We here evaluated collagen-1-coated plates, which are superior to laminin-coated plates in handling and cost, as an alternative adherent culture method of CD133 expressing glioblastoma cells.

A 68-year-old female with palmoplantar pustulosis was referred to our hospital in July, 2009 because of liver dysfunction, a positive test for HTLV-1, and circulating abnormal lymphocytes with irregularly shaped nuclei. A diagnosis of acute type adult T cell leukemia/lymphoma (ATLL) was made based on generalized lymph node swelling and high levels of serum LDH, in addition to the findings described above. The associated palmoplantar pustulosis responded to some extent to antibiotics, steroid ointment, and narrow band UBV light irradiation. For ATLL, she was serially treated with CHOP chemotherapy, an LSG 15 protocol, and CytaBOM protocol with consequent partial remission. These chemotherapies did not affect the palmoplantar pustulosis. For ATLL in partial remission, we performed allogeneic peripheral blood stem cell transplantation (allo-PBSCT) from a related donor (HTLV-1-negative) with a conditioning regimen consisting of fludarabine, melphalan, and total body irradiation with 3 Gy in February, 2010. After the engraftment of donor hematopoietic cells, ATLL cells disappeared and the patient currently (as of April, 2012) remains in complete remission (CR). The residual palmoplantar pustulosis was further improved soon after allo-PBSCT and disappeared on Day 84 after transplantation. This refractory skin disease has also been in CR to date.

We studied immunophenotypic analysis of hematogones by flow cytometry. A total of 102 specimens from 93 patients with acute leukemia (52 specimens), myelodysplastic syndromes (4), or malignant lymphoma (46) were analyzed between April and August, 2011. Hematogones were detected in 55 specimens and highly identified in patients with acute myeloid leukemia in remission and B cell lymphoma. Stage 1 (CD34(+)CD20(-)) and stage 2/3 (CD34(-)CD20(+)) were detected in 9.9% and 52.7%, respectively. In addition, the intermediate type (CD34(+)CD20(+)) was identified in 37.4%. All specimens of stage 3 in bright CD45 expression were positive for CD5 and included CD5(+)CD23(-)CD11c(-), 11.1%, CD5(+)CD23(+)CD11c(-), 85.2%, and CD5(+)CD23(+)CD11c(+), 3.7%. These findings suggest that hematogones with unreported immunophenotypes may exist and the appearance of hematogones in hematologic malignancies may be relatively frequent.

A 34-year-old man with paroxysmal nocturnal hemoglobinuria (PNH) was scheduled for emergency laparotomy. PNH is an acquired disorder of stem cells, and the common manifestations are complement mediated hemolytic anemia and deep venous thrombosis. Perioperative hemolysis occurs under the activation of complement induced by stress such as acidosis, infection, and insufficient pain control. Activation of complement secondary leads to platelet aggregation and hypercoagulability. We administrated remifentanil for the pain control during the operation and fentanyl after the operation. We avoided hypoventilation and dehydration to prevent acidosis. Washed red blood cells were given to reduce the chance of complement activation and we administrated low molecular weight heparin up to the seventh postoperative day to prevent deep venous thrombosis. The perioperative course was uneventful without complication.

A 63-year-old female with BJP-multiple myeloma (Durie-Salmon stage III B, International Staging System III) showed an increased level of KL-6, a sialylated carbohydrate antigen that is a MUC1 molecule expressed in type II pneumocytes and reflects activity of interstitial pneumonia. At the time of diagnosis, KL-6 was as high as 22,030 U/ml; however, surfactant protein D (SP-D) was normal, and stroma-related pneumonia was not indicated on CT images. Expression of KL-6 in multiple myeloma cells was detected by immunostaining and the patient was diagnosed with KL-6-positive multiple myeloma. Usually, MUC1 is encoded by chromosome 1q21, but the karyotypic analysis of the patient's bone marrow cells lacked chromosome 1. KL-6 increased as the disease progressed. The patient did not respond to chemotherapy, including bortezomib, showed an increase of pleural effusion, and died. For this patient, multiple myeloma with high KL-6 was refractory to chemotherapy, suggesting that new treatment strategies, including transplantation of hematopoietic stem cells, are required.