Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1988-9-7
pubmed:abstractText
Transgenic mice harboring a c-myc gene subjugated to the immunoglobulin heavy chain enhancer offer a unique opportunity to investigate whether deregulated myc expression potentiates the transformation of B lymphoid cells by other oncogenes. By assessing colony formation in semi-solid medium, we have compared the potential of bone marrow cells from E mu-myc mice and their normal littermates for transformation by Harvey murine sarcoma virus and Abelson murine leukemia virus. E mu-myc bone marrow yielded more lymphoid colonies than normal marrow after infection with Harvey virus. The increased transformation frequency may reflect increased clonogenicity due to complementation between myc and ras and/or the increased number of pre-B cells in E mu-myc marrow. Surprisingly, however, the number of lymphoid colonies induced by Abelson virus was not enhanced. Our interpretation of these results is that the primary Abelson target is more primitive than the pre-B cells expressing the E mu-myc transgene and is therefore not present at increased frequency in the E mu-myc marrow. The cells from most virus-infected E mu-myc colonies failed to grow indefinitely when placed in liquid culture in the absence of a feeder layer. Thus expression of a deregulated c-myc gene together with either v-Ha-ras or v-abl does not ensure fully autonomous growth of early B lymphoid cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0890-6467
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
403-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Transformation of bone marrow cells from E mu-myc transgenic mice by Abelson murine leukemia virus and Harvey murine sarcoma virus.
pubmed:affiliation
Ludwig Institute for Cancer Research, Victoria, Australia.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't