Research Topics
Species | Naohi SaharaSummaryAffiliation: Hamamatsu University School of Medicine Country: Japan Publications
| Collaborators
|
Detail Information
Publications
Clinicopathological and prognostic characteristics of CD56-negative multiple myelomaNaohi Sahara
Internal Medicine III, Hamamatsu University School of Medicine, 1 20 1 Handayama, Hamamatsu shi, 431 3192 Japan
Br J Haematol 117:882-5. 2002..0002). We conclude that CD56- MM is a discrete entity associated with more aggressive disease. The higher incidence of plasmablastic cases suggested that CD56- MM may develop from a less mature plasma cell than CD56+ MM...
Prognostic significance of surface markers expressed in multiple myeloma: CD56 and other antigensNaohi Sahara
Internal Medicine III, Hamamatsu University School of Medicine, 1 20 1 Handayama, Hamamatsu shi, 431 3192, Japan
Leuk Lymphoma 45:61-5. 2004..We also report that CD56-negative MM is the unique entity characterized by poor prognosis with high incidence of extramedullary disease, Bence Jones protein, renal insufficiency, thrombocytopenia and plasmablastic morphology...
Clinicopathological and prognostic characteristics of CD33-positive multiple myelomaNaohi Sahara
Internal Medicine III, Hamamatsu University School of Medicine, Hamamatsu shi, Japan
Eur J Haematol 77:14-8. 2006..These results suggest that the CD33 expression might be associated with drug resistance to these conventional agents, and CD33 might be a useful target for the development of new therapeutic agents in MM...
Phenylarsine oxide (PAO) more intensely induces apoptosis in acute promyelocytic leukemia and As2O3-resistant APL cell lines than As2O3 by activating the mitochondrial pathwayNaohi Sahara
Internal Medicine III, Hamamatsu University School of Medicine, Hamamatsu, Japan
Leuk Lymphoma 45:987-95. 2004..PAO is a considerable agent for relapsed/refractory APL and for purging APL cells following stem cell transplantation...
Role for interleukin-6 and insulin-like growth factor-I via PI3-K/Akt pathway in the proliferation of CD56- and CD56+ multiple myeloma cellsNaohi Sahara
Internal Medicine III, Hamamatsu University School of Medicine, Hamamatsu, Japan
Exp Hematol 34:736-44. 2006..Interleukin-6 (IL-6) or insulin-like growth factor I (IGF-I) induce proliferation of MM cells. In this study, we report about the relationship between CD56 expression and responsiveness to these cytokines...
Etodolac inhibits EBER expression and induces Bcl-2-regulated apoptosis in Burkitt's lymphoma cellsMiki Kobayashi
Department of Internal Medicine III, Hamamatsu University School of Medicine, Hamamatsu, Japan
Eur J Haematol 75:212-20. 2005..Moreover, racemate of etodolac more effectively induced apoptosis than R- and/or S-etodolac. Therefore, these activities of etodolac potentially extend to the treatment of patients with Burkitt's lymphoma resistant to chemotherapy...
Two patients with all-trans retinoic acid-resistant acute promyelocytic leukemia treated successfully with gemtuzumab ozogamicin as a single agentAkihiro Takeshita
Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan
Int J Hematol 82:445-8. 2005..After GO treatment, both patients achieved complete hematologic and molecular remission. GO may be another promising agent for the treatment of ATRA-resistant relapsed APL when given as salvage chemotherapy...
Etodolac induces apoptosis and inhibits cell adhesion to bone marrow stromal cells in human myeloma cellsSatoki Nakamura
Department of Internal Medicine III, Hamamatsu University School of Medicine, 1 20 1 Handayama, Hamamatsu, Shizuoka 431 3192, Japan
Leuk Res 30:123-35. 2006..Cyclooxygenase-2 (COX-2) is reported to regulate apoptosis and to be an important cellular target for therapy...
Two cases of acute promyelocytic leukemia complicated by torsade de pointes during arsenic trioxide therapyKensuke Naito
Division of Hematology, Department of Medicine III, Hamamatsu University School of Medicine, Hamamatsu, Japan
Int J Hematol 83:318-23. 2006..Patient 2 had cardiomyopathy and hypokalemia. Careful management is needed during arsenic trioxide therapy because this treatment prolongs the QT interval, possibly inducing episodes of TdP...
Arsenic trioxide therapy in relapsed or refractory Japanese patients with acute promyelocytic leukemia: updated outcomes of the phase II study and postremission therapiesKazuyuki Shigeno
Department of Medicine III, Hamamatsu University School of Medicine, 1 20 1 Handayama, Hamamatsu, Japan
Int J Hematol 82:224-9. 2005..ATO therapy was remarkably effective for relapsed APL; however, postremission therapies were necessary to maintain a durable remission...
Delayed recovery of normal hematopoiesis in arsenic trioxide treatment of acute promyelocytic leukemia: a comparison to all-trans retinoic acid treatmentKaori Shinjo
Department of Internal Medicine III, Hamamatsu University School of Medicine, Japan
Intern Med 44:818-24. 2005..CONCLUSION: In comparison with ATRA treatment, the recovery of several components in the peripheral blood cells was delayed in As2O3 treatment. Therefore we should pay more and longer attention in As2O3 treatment...
Pharmacokinetics of arsenic species in Japanese patients with relapsed or refractory acute promyelocytic leukemia treated with arsenic trioxideShinya Fujisawa
Department of Medicine III, Hamamatsu University School of Medicine, Hamamatsu, Japan
Cancer Chemother Pharmacol 59:485-93. 2007..To investigate the pharmacokinetics of arsenic species in Japanese patients with relapsed or refractory acute promyelocytic leukemia (APL) treated with arsenic trioxide (ATO) at a daily dose of 0.15 mg/kg...
Development of packaging cell lines for generation of adeno-associated virus vectors by lentiviral gene transfer of trans-complementary componentsSatoki Nakamura
Department of Internal Medicine III, Hamamatsu University School of Medicine, Handayama, Japan
Eur J Haematol 73:285-94. 2004..VA.E2A.E4. cells, the AAV vectors can be generated by the transfection of one AAV vector plasmid, and large-scale AAV production can be easily achieved. It is important that cumbersome, variable, and costly transfection is avoided...
Deletion 6p23 and add(11)(p15) leading to NUP98 translocation in a case of therapy-related atypical chronic myelocytic leukemia transforming to acute myelocytic leukemiaAkihiro Takeshita
Department of Internal Medicine, Hamamatsu University School of Medicine, 1 20 1 Handayama, Hamamatsu shi, 431 3192, Japan
Cancer Genet Cytogenet 152:56-60. 2004..Further investigation of molecular characterization of this NUP98 translocation and interaction with 6p23 abnormalities might be worthwhile for understanding leukemogenesis...
