|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0015923,
umls-concept:C0021469,
umls-concept:C0033684,
umls-concept:C0079744,
umls-concept:C0178539,
umls-concept:C0205101,
umls-concept:C0441712,
umls-concept:C0449560,
umls-concept:C0534519,
umls-concept:C1442161,
umls-concept:C1511738,
umls-concept:C1514559,
umls-concept:C1516044,
umls-concept:C1523987,
umls-concept:C1539477,
umls-concept:C1704259,
umls-concept:C1705987
|
|
pubmed:issue |
11 Pt 1
|
|
pubmed:dateCreated |
2006-6-2
|
|
pubmed:abstractText |
Large B-cell lymphomas (LBCL) arise from normal antigen-exposed B cells at germinal center (GC) or post-GC stages of differentiation. Negative selection of normal low-affinity or self-reactive GC B-cells depends on CD95 (FAS)-mediated apoptosis. FAS mutations that result in deletion of the cytoplasmic death domain destabilize the trimeric receptor and inhibit FAS-mediated apoptosis. This apoptotic pathway is also inhibited when the nuclear factor kappaB (NFkappaB) target, cellular FADD-like interleukin 1beta converting enzyme inhibitory protein (cFLIP), interacts with the death-inducing signaling complex, assembled around the FAS death domain. Herein, we ask whether FAS death domain mutations and NFkappaB-mediated overexpression of cFLIP represent alternative mechanisms for deregulating the extrinsic apoptotic pathway in LBCL subtypes defined by gene expression profiling [oxidative phosphorylation, B-cell receptor/proliferation, and host response diffuse LBCLs and primary mediastinal LBCLs].
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jun
|
|
pubmed:issn |
1078-0432
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
1
|
|
pubmed:volume |
12
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
3265-71
|
|
pubmed:dateRevised |
2007-11-15
|
|
pubmed:meshHeading |
pubmed-meshheading:16740746-Antigens, CD95,
pubmed-meshheading:16740746-Apoptosis,
pubmed-meshheading:16740746-CASP8 and FADD-Like Apoptosis Regulating Protein,
pubmed-meshheading:16740746-Chromosome Aberrations,
pubmed-meshheading:16740746-Chromosomes, Human, Pair 14,
pubmed-meshheading:16740746-Chromosomes, Human, Pair 18,
pubmed-meshheading:16740746-DNA Mutational Analysis,
pubmed-meshheading:16740746-Down-Regulation,
pubmed-meshheading:16740746-Gene Deletion,
pubmed-meshheading:16740746-Gene Expression Profiling,
pubmed-meshheading:16740746-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16740746-Humans,
pubmed-meshheading:16740746-Lymphoma, B-Cell,
pubmed-meshheading:16740746-Lymphoma, Large B-Cell, Diffuse,
pubmed-meshheading:16740746-NF-kappa B,
pubmed-meshheading:16740746-Point Mutation,
pubmed-meshheading:16740746-Protein Structure, Tertiary,
pubmed-meshheading:16740746-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:16740746-Proto-Oncogene Proteins c-bcl-6,
pubmed-meshheading:16740746-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16740746-Translocation, Genetic
|
|
pubmed:year |
2006
|
|
pubmed:articleTitle |
FAS death domain deletions and cellular FADD-like interleukin 1beta converting enzyme inhibitory protein (long) overexpression: alternative mechanisms for deregulating the extrinsic apoptotic pathway in diffuse large B-cell lymphoma subtypes.
|
|
pubmed:affiliation |
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
|
|
pubmed:publicationType |
Journal Article
|
