Linked Life Data

16532038

Source:http://linkedlifedata.com/resource/pubmed/id/16532038

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2006-4-27
pubmed:abstractText
The suppressors of cytokine signaling (SOCS) are critically involved in the regulation of cellular proliferation, survival, and apoptosis via cytokine-induced JAK/STAT signaling. SOCS-1 silencing by aberrant DNA methylation contributes to oncogenesis in various B-cell neoplasias and carcinomas. Recently, we showed an alternative loss of SOCS-1 function due to deleterious SOCS-1 mutations in a major subset of primary mediastinal B-cell lymphoma (PMBL) and in the PMBL line MedB-1, and a biallelic SOCS-1 deletion in PMBL line Karpas1106P. For both cell lines our previous data demonstrated retarded JAK2 degradation and sustained phospho-JAK2 action leading to enhanced DNA binding of phospho-STAT5. Here, we analysed SOCS-1 in laser-microdissected Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL). We detected SOCS-1 mutations in HRS cells of eight of 19 cHL samples and in three of five Hodgkin lymphoma (HL)-derived cell lines by sequencing analysis. Moreover, we found a significant association between mutated SOCS-1 of isolated HRS cells and nuclear phospho-STAT5 accumulation in HRS cells of cHL tumor tissue (P < 0.01). Collectively, these findings support the concept that PMBL and cHL share many overlapping features, and that defective tumor suppressor gene SOCS-1 triggers an oncogenic pathway operative in both lymphomas.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2679-84
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16532038-Amino Acid Sequence, pubmed-meshheading:16532038-Base Sequence, pubmed-meshheading:16532038-Cell Nucleus, pubmed-meshheading:16532038-Gene Expression Regulation, Neoplastic, pubmed-meshheading:16532038-Genes, Tumor Suppressor, pubmed-meshheading:16532038-Hodgkin Disease, pubmed-meshheading:16532038-Humans, pubmed-meshheading:16532038-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:16532038-Lasers, pubmed-meshheading:16532038-Molecular Sequence Data, pubmed-meshheading:16532038-Mutation, pubmed-meshheading:16532038-Phosphorylation, pubmed-meshheading:16532038-Reed-Sternberg Cells, pubmed-meshheading:16532038-Repressor Proteins, pubmed-meshheading:16532038-STAT5 Transcription Factor, pubmed-meshheading:16532038-Sequence Homology, Amino Acid, pubmed-meshheading:16532038-Suppressor of Cytokine Signaling Proteins
pubmed:year
2006
pubmed:articleTitle
Mutations of the tumor suppressor gene SOCS-1 in classical Hodgkin lymphoma are frequent and associated with nuclear phospho-STAT5 accumulation.
pubmed:affiliation
Department of Pathology, University of Ulm, Ulm, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't