Linked Life Data

18035322

Source:http://linkedlifedata.com/resource/pubmed/id/18035322

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-11-23
pubmed:abstractText
Chronic lymphocytic leukemia (CLL) is a B-cell malignancy endowed with a number of features that recall autoimmune disorders, including the CD5 expression and the development of autoimmune manifestations restricted to self antigens expressed by hematopoietic cells. Several evidences strongly support the possibility that an antigenic stimulation through the B-cell receptor (BCR) is involved in the selection and possibly also the expansion of the malignant clone. Though all evidences suggest specific Ag recognition and possibly stimulation at different time-points, the nature of the Ag(s) is still unknown. It appears likely that CLL cells derive from a pool of auto/polyreactive CD5(+) B cells. Hence CLL appears to be a B-cell malignancy triggered or facilitated in its development and evolution by an auto-Ag. The crucial issues have become to what extent this deleterious binding capacity is central to the natural history of the disease and how it relates to the malignant transformation of the cell.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1568-9972
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-31
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
From normal to clonal B cells: Chronic lymphocytic leukemia (CLL) at the crossroad between neoplasia and autoimmunity.
pubmed:affiliation
Unit of Lymphoid Malignancies, Department of Oncology, Università Vita-Salute San Raffaele and Istituto Scientifico San Raffaele, Milano, Italy. ghia.paolo@hsr.it
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't