Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-4-6
pubmed:abstractText
Multiple myeloma (MM) comprises B and plasma cell compartments that originate from the same parent B cell and share as a cancer signature the same clonotypic IgH VDJ gene rearrangement. Here, we hypothesize that functional interactions between MM plasma cells (MM-PC) and their sister population of MM monocytoid B cells lead to the generation of microvessel endothelium of malignant origin from the monocytoid B cell progenitors. Published reports confirm that endothelial cells can harbor a molecular cancer signature characteristic of a given malignancy. We predict that MM monocytoid B cells-in response to both paracrine and autocrine pathways-contribute to tumor neovascularization in the bone marrow of MM patients. Our hypothesis further predicts that in MM, endothelial cells of malignant origin coexist with those of normal origin. We speculate that malignant development of MM incorporates functionally distinct sister lineages arising from the same MM progenitor that-by working together-ensure survival of the MM clone. We hypothesize that these two arms of the malignant MM clone are functionally interlinked to promote growth of the MM-PC compartment; by providing its own microenvironment, MM clonal evolution may ensure neovascularization to support an expanding malignancy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1029-2403
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
592-7
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Multiple myeloma may include microvessel endothelial cells of malignant origin.
pubmed:affiliation
Department of Oncology, University of Alberta, Edmonton, Canada T6G1Z2. lpilarsk@ualberta.ca
pubmed:publicationType
Journal Article, Review