Lymphoma and the control of B cell growth and differentiation
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Rui, Lixin; Goodnow, Christopher
Description
It is now widely accepted that lymphomagenesis is a multistep transformation process. A number of genetic changes and environmental and infectious factors contributing to the development and malignant progression of B-cell lymphoproliferative disorders are well documented. Reciprocal chromosomal translocations involving the immunoglobulin loci are a hallmark of most mature B cell lymphomas and lead to dysregulated expression of proto-oncogenes (c-myc) important for cell proliferation or genes...[Show more]
dc.contributor.author | Rui, Lixin | |
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dc.contributor.author | Goodnow, Christopher | |
dc.date.accessioned | 2015-12-13T23:05:42Z | |
dc.date.available | 2015-12-13T23:05:42Z | |
dc.identifier.issn | 1566-5240 | |
dc.identifier.uri | http://hdl.handle.net/1885/85660 | |
dc.description.abstract | It is now widely accepted that lymphomagenesis is a multistep transformation process. A number of genetic changes and environmental and infectious factors contributing to the development and malignant progression of B-cell lymphoproliferative disorders are well documented. Reciprocal chromosomal translocations involving the immunoglobulin loci are a hallmark of most mature B cell lymphomas and lead to dysregulated expression of proto-oncogenes (c-myc) important for cell proliferation or genes involved in cell cycle progression (cyclin D1), differentiation block (bcl-6, PAX5) and cell survival (bcl-2 NF-κB). In addition, genetic alterations that inactivate tumor suppressor genes (p53, p16) have been frequently detected in some lymphoma tissues. Many of these genes are normally regulated by signals from the B cell antigen receptor. The high prevalence of bacterial and viral infection in lymphoma patients supports the hypothesis that infectious agents may play a contributory role in the development and evolution of B cell lymphoproliferative disorders by either directly inducing polyclonal B cell hyperactivation (EBV, HCV), or providing a chronic antigenic stimulus (EBV, HCV, HBV, H. pylori), or mimicking B cell antigen receptor signaling (EBV, HCV, HHV8), although whether these are causative factors or they are secondary to genetic changes in lymphomagenesis remains to be defined. Stimulatory signals from reactive T cells, local cytokines and growth factors can also contribute, to some extent, to the progression of transformation. Modulation of B cell antigen receptor signaling therefore emerges as a potentially powerful strategy for controlling the growth of certain B cell lymphomas. | |
dc.publisher | Bentham Science Publishers Ltd | |
dc.source | Current Molecular Medicine | |
dc.subject | Keywords: antisense oligonucleotide; B lymphocyte antibody; B lymphocyte antigen; B7 antigen; cancer vaccine; CD28 antigen; CD40 antigen; CD40 ligand; CD5 antigen; cyclin D1; Fas antigen; FAS ligand; immunoglobulin D; immunoglobulin enhancer binding protein; immuno Anti-B cell antibody; B cell antigen receptor signaling; B lymphocyte; Bacterial and viral infection; Lymphoma; Proto-oncogene; Transformation; Tumor suppressor gene | |
dc.title | Lymphoma and the control of B cell growth and differentiation | |
dc.type | Journal article | |
local.description.notes | Imported from ARIES | |
local.description.refereed | Yes | |
local.identifier.citationvolume | 6 | |
dc.date.issued | 2006 | |
local.identifier.absfor | 111299 - Oncology and Carcinogenesis not elsewhere classified | |
local.identifier.ariespublication | MigratedxPub14214 | |
local.type.status | Published Version | |
local.contributor.affiliation | Rui, Lixin, College of Medicine, Biology and Environment, ANU | |
local.contributor.affiliation | Goodnow, Christopher, College of Medicine, Biology and Environment, ANU | |
local.bibliographicCitation.issue | 3 | |
local.bibliographicCitation.startpage | 291 | |
local.bibliographicCitation.lastpage | 308 | |
local.identifier.doi | 10.2174/156652406776894563 | |
dc.date.updated | 2015-12-12T08:01:55Z | |
local.identifier.scopusID | 2-s2.0-33646591853 | |
Collections | ANU Research Publications |
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