Novel targeted deregulation of c-Myc cooperates with Bcl-X(L) to cause plasma cell neoplasms in mice.
about
The diabetes-linked transcription factor PAX4 promotes {beta}-cell proliferation and survival in rat and human isletsPreclinical validation of interleukin 6 as a therapeutic target in multiple myelomaA novel mouse model for multiple myeloma (MOPC315.BM) that allows noninvasive spatiotemporal detection of osteolytic diseaseThe IgH 3' regulatory region and c-myc-induced B-cell lymphomagenesisOsteolytica: An automated image analysis software package that rapidly measures cancer-induced osteolytic lesions in in vivo models with greater reproducibility compared to other commonly used methodsBortezomib resistance can be reversed by induced expression of plasma cell maturation markers in a mouse in vitro model of multiple myelomaKSHV Latency Locus Cooperates with Myc to Drive Lymphoma in MiceDeregulation of c-Myc Confers distinct survival requirements for memory B cells, plasma cells, and their progenitorsGene expression profiling reveals different pathways related to Abl and other genes that cooperate with c-Myc in a model of plasma cell neoplasia.IL-6 and MYC collaborate in plasma cell tumor formation in mice.Tracking human multiple myeloma xenografts in NOD-Rag-1/IL-2 receptor gamma chain-null mice with the novel biomarker AKAP-4Plasmacytomagenesis in Eμ-v-abl transgenic mice is accelerated when apoptosis is restrained.B-cell activating factor and v-Myc myelocytomatosis viral oncogene homolog (c-Myc) influence progression of chronic lymphocytic leukemia.Kaposi sarcoma-associated herpesvirus-encoded viral FLICE inhibitory protein (vFLIP) K13 cooperates with Myc to promote lymphoma in mice.CDDO-Imidazolide inhibits growth and survival of c-Myc-induced mouse B cell and plasma cell neoplasms.GP130 activation induces myeloma and collaborates with MYC.A therapeutic role for targeting c-Myc/Hif-1-dependent signaling pathways.The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.Targeting signalling pathways for the treatment of multiple myeloma.Anaplastic plasmacytomas: relationships to normal memory B cells and plasma cell neoplasms of immunodeficient and autoimmune mice.AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements.Regulation of AID expression in the immune responseAntitumor activity of the investigational proteasome inhibitor MLN9708 in mouse models of B-cell and plasma cell malignancies.Growth factors and antiapoptotic signaling pathways in multiple myeloma.Myeloid-derived suppressor cells regulate growth of multiple myeloma by inhibiting T cells in bone marrow.Bone marrow PMN-MDSCs and neutrophils are functionally similar in protection of multiple myeloma from chemotherapyBCL-B (BCL2L10) is overexpressed in patients suffering from multiple myeloma (MM) and drives an MM-like disease in transgenic miceIn a model of immunoglobulin heavy-chain (IGH)/MYC translocation, the Igh 3' regulatory region induces MYC expression at the immature stage of B cell development.Restricting activation-induced cytidine deaminase tumorigenic activity in B lymphocytes.A novel rapid-onset high-penetrance plasmacytoma mouse model driven by deregulation of cMYC cooperating with KRAS12V in BALB/c mice.c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis.The role of Bcl-2 and its pro-survival relatives in tumourigenesis and cancer therapy.Deciphering the rules of programmed cell death to improve therapy of cancer and other diseasesNew frontiers in promoting tumour cell death: targeting apoptosis, necroptosis and autophagy.Mouse models as a translational platform for the development of new therapeutic agents in multiple myeloma.The investigational proteasome inhibitor ixazomib for the treatment of multiple myeloma.Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.Generation of precursor, immature, and mature murine B1-cell lines from c-myc/bcl-xL-overexpressing pre-BI cells.Reduced CXCR4 expression is associated with extramedullary disease in a mouse model of myeloma and predicts poor survival in multiple myeloma patients treated with bortezomibTargeted overexpression of an activated N-ras gene results in B-cell and plasma cell lymphoproliferation and cooperates with c-myc to induce fatal B-cell neoplasia.
P2860
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P2860
Novel targeted deregulation of c-Myc cooperates with Bcl-X(L) to cause plasma cell neoplasms in mice.
description
2004 nî lūn-bûn
@nan
2004 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
name
Novel targeted deregulation of c-Myc cooperates with Bcl-X
@nl
Novel targeted deregulation of ...... plasma cell neoplasms in mice.
@ast
Novel targeted deregulation of ...... plasma cell neoplasms in mice.
@en
type
label
Novel targeted deregulation of c-Myc cooperates with Bcl-X
@nl
Novel targeted deregulation of ...... plasma cell neoplasms in mice.
@ast
Novel targeted deregulation of ...... plasma cell neoplasms in mice.
@en
prefLabel
Novel targeted deregulation of c-Myc cooperates with Bcl-X
@nl
Novel targeted deregulation of ...... plasma cell neoplasms in mice.
@ast
Novel targeted deregulation of ...... plasma cell neoplasms in mice.
@en
P2093
P2860
P356
P1476
Novel targeted deregulation of ...... plasma cell neoplasms in mice.
@en
P2093
Brian Van Ness
Joong Su Kim
Liangping Peng
Michael Linden
Roberto D Polakiewicz
Siegfried Janz
Wan Cheung Cheung
P2860
P304
P356
10.1172/JCI200420369
P407
P577
2004-06-01T00:00:00Z