The molecular and cellular origins of Hodgkin's disease.
about
Analysis of interleukin-27 (EBI3/p28) expression in Epstein-Barr virus- and human T-cell leukemia virus type 1-associated lymphomas: heterogeneous expression of EBI3 subunit by tumoral cellsRole of immune escape mechanisms in Hodgkin's lymphoma development and progression: a whole new world with therapeutic implicationsNuclear factor kappaB-dependent gene expression profiling of Hodgkin's disease tumor cells, pathogenetic significance, and link to constitutive signal transducer and activator of transcription 5a activityA senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19(ARF)-p53 signaling.Single agent bortezomib in the treatment of relapsed and refractory Hodgkin lymphoma: cancer and leukemia Group B protocol 50206.Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-kappaB signaling and depleting Bcr-Abl.Expression of CCL28 by Reed-Sternberg cells defines a major subtype of classical Hodgkin's disease with frequent infiltration of eosinophils and/or plasma cells.Nuclear transcription factor-kappaB in Hodgkin's disease.The putative tumor suppressor Zc3h12d modulates toll-like receptor signaling in macrophagesConstitutive nuclear factor kappaB activity is required for survival of activated B cell-like diffuse large B cell lymphoma cellsHodgkin's lymphoma: molecular targets and novel treatment strategies.Augmented efficacy of brentuximab vedotin combined with ruxolitinib and/or Navitoclax in a murine model of human Hodgkin's lymphomaMicroRNA-mediated down-regulation of PRDM1/Blimp-1 in Hodgkin/Reed-Sternberg cells: a potential pathogenetic lesion in Hodgkin lymphomas.Nuclear factor-κB2 represses Sp1-mediated transcription at the CD99 promoter.Triptolide inhibits the proliferation of cells from lymphocytic leukemic cell lines in association with downregulation of NF-κB activity and miR-16-1*.Novel treatment strategies for patients with relapsed classical Hodgkin lymphoma.Hodgkin disease and the role of the immune system.Mechanisms underlying the association between obesity and Hodgkin lymphoma.Ubiquitination and translocation of TRAF2 is required for activation of JNK but not of p38 or NF-kappaB.Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B.Hodgkin's lymphoma cells are efficiently engrafted and tumor marker CD30 is expressed with constitutive nuclear factor-kappaB activity in unconditioned NOD/SCID/gammac(null) mice.Microarray analysis of gene expression mirrors the biology of an ovarian cancer model.The intersection of Epstein-Barr virus with the germinal center.Gene expression profiling defines molecular subtypes of classical Hodgkin's disease.NF-κB Activation in Lymphoid Malignancies: Genetics, Signaling, and Targeted Therapy.
P2860
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P2860
The molecular and cellular origins of Hodgkin's disease.
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2000 nî lūn-bûn
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2000年の論文
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2000年論文
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2000年論文
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name
The molecular and cellular origins of Hodgkin's disease.
@ast
The molecular and cellular origins of Hodgkin's disease.
@en
type
label
The molecular and cellular origins of Hodgkin's disease.
@ast
The molecular and cellular origins of Hodgkin's disease.
@en
prefLabel
The molecular and cellular origins of Hodgkin's disease.
@ast
The molecular and cellular origins of Hodgkin's disease.
@en
P2860
P356
P1476
The molecular and cellular origins of Hodgkin's disease.
@en
P2093
L M Staudt
P2860
P304
P356
10.1084/JEM.191.2.207
P407
P577
2000-01-01T00:00:00Z
2000-01-17T00:00:00Z