研究者総覧

畑野 かおる (ハタノ カオル)

  • 内科学講座(血液学部門) 講師
Last Updated :2021/11/23

研究者情報

学位

  • 医学博士(自治医科大学(JMU))

ホームページURL

J-Global ID

研究キーワード

  • 多発性骨髄腫   multiple myeloma   

研究分野

  • ライフサイエンス / 血液、腫瘍内科学

学歴

  •         - 2008年   自治医科大学(JMU)   医学研究科
  •         - 1998年   宮崎医科大学   医学部
  •         - 1998年   Miyazaki medical University   Faculty of Medicine

所属学協会

  • 日本臨床血液学会   日本血液学会   日本内科学会   

研究活動情報

MISC

  • K. Noborio-Hatano, J. Kikuchi, M. Takatoku, R. Shimizu, T. Wada, M. Ueda, M. Nobuyoshi, I. Oh, K. Sato, T. Suzuki, K. Ozaki, M. Mori, T. Nagai, K. Muroi, Y. Kano, Y. Furukawa, K. Ozawa ONCOGENE 28 (2) 231 -242 2009年01月 [査読無し][通常論文]
     
    Multiple myeloma ( MM) is incurable, mainly because of cell adhesion-mediated drug resistance (CAM-DR). In this study, we performed functional screening using short hairpin RNA (shRNA) to de. ne the molecule(s) responsible for CAM-DR of MM. Using four bona. de myeloma cell lines (KHM-1B, KMS12-BM, RPMI8226 and U266) and primary myeloma cells, we identified CD29 (beta 1-integrin), CD44, CD49d (alpha 4-integrin, a subunit of VLA-4), CD54 ( intercellular adhesion molecule-1 (ICAM-1)), CD138 (syndecan-1) and CD184 (CXC chemokine receptor-4 (CXCR4)) as major adhesion molecules expressed on MM. shRNA-mediated knockdown of CD49d but not CD44, CD54, CD138 and CD184 significantly reversed CAM-DR of myeloma cells to bortezomib, vincristine, doxorubicin and dexamethasone. Experiments using blocking antibodies yielded almost identical results. Bortezomib was relatively resistant to CAM-DR because of its ability to specifically down-regulate CD49d expression. This property was unique to bortezomib and was not observed in other anti-myeloma drugs. Pretreatment with bortezomib was able to ameliorate CAM-DR of myeloma cells to vincristine and dexamethasone. These results suggest that VLA-4 plays a critical role in CAM-DR of MM cells. The combination of bortezomib with conventional anti-myeloma drugs may be effective in overcoming CAM-DR of MM.
  • K Noborio, K Muroi, T Izumi, M Toshima, C Kawano-Yamamoto, T Otsuki, T Nagai, N Komatsu, K Ozawa LEUKEMIA & LYMPHOMA 44 (2) 357 -359 2003年 [査読無し][通常論文]
     
    A 35-year-old male, blood group B, Rh(D)+ type, received an allogeneic peripheral blood stem cell (PBSC) transplant after a non-myeloablative regimen of fludarabine and cyclophosphamide for resistant gammadelta cutaneous T-cell lymphoma (CTCL). The donor was his HLA-identical brother, blood group O, Rh(D)+ type. Graft-versus-host disease (GVHD) prophylaxis was performed with cyclosporine alone. On day +8, massive immune hemolysis occurred, followed by acute renal failure. Hemodialysis was performed eight times until recovery of renal function on day +24. The risk of delayed immune hemolysis after non-myeloablative allogeneic PBSC transplantation with minor ABO-incompatibility must be considered.
  • K Noborio, K Muroi, T Izumi, M Toshima, C Kawano-Yamamoto, T Otsuki, T Nagai, N Komatsu, K Ozawa LEUKEMIA & LYMPHOMA 44 (2) 357 -359 2003年 [査読無し][通常論文]
     
    A 35-year-old male, blood group B, Rh(D)+ type, received an allogeneic peripheral blood stem cell (PBSC) transplant after a non-myeloablative regimen of fludarabine and cyclophosphamide for resistant gammadelta cutaneous T-cell lymphoma (CTCL). The donor was his HLA-identical brother, blood group O, Rh(D)+ type. Graft-versus-host disease (GVHD) prophylaxis was performed with cyclosporine alone. On day +8, massive immune hemolysis occurred, followed by acute renal failure. Hemodialysis was performed eight times until recovery of renal function on day +24. The risk of delayed immune hemolysis after non-myeloablative allogeneic PBSC transplantation with minor ABO-incompatibility must be considered.

共同研究・競争的資金等の研究課題

  • biology of multiple myeloma
    The Other Research Programs
    研究期間 : 2003年 -2007年
  • 多発性骨髄腫の細胞生物学的検討
    その他の研究制度
    研究期間 : 2003年


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