Linked Life Data

1625486

Source:http://linkedlifedata.com/resource/pubmed/id/1625486

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1992-8-10
pubmed:abstractText
B-cell chronic lymphocytic leukemia (B-CLL) is a hematologic malignancy characterized by the proliferation and accumulation of mature-looking B lymphocytes. Patients with B-CLL exhibit a number of immune defects including: auto-antibodies, depressed cell-mediated immunity and hypogammaglobulinemia (HG). We investigated the control of Ig production in the malignant CLL B-cell at a transcriptional and translation level. We isolated fresh leukemic B-cells from CLL patients and analyzed for the presence of nuclear factors OCT-1, OCT-2, and NF-KB. Malignant B-cells were purified to greater than 90% B-cells, and total cellular RNA and nuclear proteins were isolated from these cells. Mobility shift assays were probed with 32P-labeled oligonucleotides specific to the immunoglobulin (Ig) enhancer and promotor regions. We detected endogenous OCT-1, OCT-2, and NF-KB in all patients tested (n = 5). We then evaluated whether activation of CLL B cells could augment kappa-mRNA levels. CLL cells (n = 3) exposed to phorbol ester and A23187 were harvested at 0, 2, 4, 8, and 48 min and examined for kappa-mRNA by Northern blot. All CLL patients (n = 3) had easily detectable levels of endogenous kappa-mRNA. However, only one patient had an obvious increase in kappa-mRNA post-induction with TPA/A23187. There was no concomitant increase in this patient's OCT-1, OCT-2, or NF-KB level. This finding prompted us to survey other B-CLL patients (n = 6) for Ig nuclear transcriptional factors pre- and post-induction. In summary, CLL B cells express Ig transcriptional factor OCT-1, OCT-2, and NF-KB constitutively. The endogenous level of NF-KB may account for the basal kappa-mRNA detected in B-CLL cells. However, the inability to augment NF-KB levels may, in part, explain the low levels of Ig synthesis in CLL B-cells.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0887-6924
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
675-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:1625486-Base Sequence, pubmed-meshheading:1625486-Calcimycin, pubmed-meshheading:1625486-Cell Nucleus, pubmed-meshheading:1625486-DNA-Binding Proteins, pubmed-meshheading:1625486-Gene Expression Regulation, Neoplastic, pubmed-meshheading:1625486-Genes, Immunoglobulin, pubmed-meshheading:1625486-Humans, pubmed-meshheading:1625486-Immunoglobulin kappa-Chains, pubmed-meshheading:1625486-Leukemia, Lymphocytic, Chronic, B-Cell, pubmed-meshheading:1625486-Molecular Sequence Data, pubmed-meshheading:1625486-NF-kappa B, pubmed-meshheading:1625486-Octamer Transcription Factor-2, pubmed-meshheading:1625486-Oligodeoxyribonucleotides, pubmed-meshheading:1625486-RNA, Messenger, pubmed-meshheading:1625486-RNA, Neoplasm, pubmed-meshheading:1625486-Transcription Factors, pubmed-meshheading:1625486-Transcriptional Activation, pubmed-meshheading:1625486-Tumor Cells, Cultured
pubmed:year
1992
pubmed:articleTitle
B-chronic lymphocytic leukemia cells contain both endogenous kappa immunoglobulin mRNA and critical immunoglobulin gene activation transcription factors.
pubmed:affiliation
Department of Medicine, Veterans Affairs Medical Center, Minneapolis, Minnesota.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.