Kyoto University · 의학
모모코 히시코리 교수의 연구실은 B-cell 림프종, 특히 알라프티크 라지셀 림프종(ALK+ ALCL)과 호지킨 림프종의 분자 기전을 중심으로 연구를 진행하고 있습니다. 주로 CD30, BCL3, NF-κB 및 ERK 신호 경로와 같은 면역조절 및 세포 사멸 관련 분자들이 림프종의 발병과 진행에 미치는 영향을 규명하고 있으며, 특히 조혈모세포의 신호전달 이상이 림프종 발생에 기여하는 메커니즘을 탐구하고 있습니다. 또한, 히스톤 메틸트랜스퍼라제 억제제(tazemetostat)와 같은 신약의 작용 기전을 분석함으로써 표적 치료의 새로운 가능성을 모색하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
B7-H1 is a member of the B7 family that inhibits the function of T-cells through its receptor programmed death-1 (PD-1). We examined B7-H1 expression in anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) and found that it was constitutively expressed in both clinical samples and cell lines. In anaplastic lymphoma kinase-positive (ALK(+)) ALCL cells, B7-H1 expression was suppressed by the blocking of extracellular signal-regulated kinase (ERK) signaling and upregulated by the augment
Nuclear factor-κB (NF-κB) is a family of highly regulated dimeric transcription factors that play pivotal roles in inflammatory responses and immunological reactions. Although they are often activated concurrently, classical and alternative NF-κB activation pathways have distinct regulatory functions, producing secondary inflammatory responses and regulating lymphoid organ development, respectively. As NF-κB functions in the proliferation, differentiation, and survival of lymphocytes, increased
Anaplastic large cell lymphoma (ALCL) with t(2;5)(p23;q35) and Hodgkin disease (HD) share many cellular features, including expression of CD30. We compared gene expression profiles of 4 ALCL (Karpas 299, SU-DHL-1, DEL, SR-786) and 3 HD cell lines and found that BCL3, which encodes a nuclear protein belonging to the I kappa B family of inhibitors of nuclear factor-kappa B (NF-kappa B) transcriptional factors, was expressed at higher levels in ALCL than HD. Northern and Western blotting analyses c
Anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) express CD30 at high levels, but stimulation of this molecule has been reported to induce contradictory effects. To elucidate the molecular mechanism of CD30-mediated apoptosis of ALCL, we compared the gene expression profiles of t(2;5)(p23;q35)-positive ALCL with those of HL altered by CD30 agonistic stimulation. The results showed that BCL3, the high-level expression of which in ALCL was previously reported, was further upregulate
An inhibitor of the histone methyltransferase enhancer of zeste homologue 2 (EZH2), tazemetostat, has been developed for the treatment of B-cell lymphoma, but its mechanisms of action are not fully elucidated. We screened for genes targeted by tazemetostat in eleven B-cell lymphoma cell lines and found that tazemetostat significantly increased the expression of chemokine (C-C motif) ligand 17 (CCL17)/thymus- and activation-regulated chemokine (TARC) in all, which codes for a chemokine that is a
Primary central nervous system lymphoma (PCNSL) is a distinct subtype of extranodal lymphoma with aggressive clinical course and poor outcome. As increased IL-10/IL-6 ratio is recognized in the cerebrospinal fluid (CSF) of PCNSL patients, we hypothesized that PCNSL might originate from a population of B cells with high IL-10-producing capacity, an equivalent of "regulatory B cells" in mice. We intended in this study to clarify whether Tim-1, a molecule known as a marker for regulatory B cells in
