| pubmed-article:16571819 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16571819 | lifeskim:mentions | umls-concept:C0682459 | lld:lifeskim |
| pubmed-article:16571819 | lifeskim:mentions | umls-concept:C0233820 | lld:lifeskim |
| pubmed-article:16571819 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:16571819 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:16571819 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:16571819 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:16571819 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:16571819 | pubmed:dateCreated | 2006-3-30 | lld:pubmed |
| pubmed-article:16571819 | pubmed:abstractText | The Graffi murine leukemia virus (MuLV) was isolated in 1954 by Arnold Graffi, who characterized it as a myeloid leukemia-inducing retrovirus. He and his team, however, soon observed the intriguing phenomenon of hematological diversification, which corresponded to a decrease of myeloid leukemias and an increase of other types of leukemias. Recently, we derived two different molecular clones corresponding to ecotropic nondefective genomes that were named GV-1.2 and GV-1.4. The induced leukemias were classified as myeloid based on morphological analysis of blood smears. In this study, we further characterized the two variants of the Graffi murine retrovirus, GV-1.2 and GV-1.4, in three different strains of mice. We show that the Graffi MuLV is a multipotent retrovirus capable of inducing both lymphoid (T- and B-cell) and nonlymphoid (myeloid, erythroid, megakaryocytic) leukemia. Many of these are very complex with concomitant expression of different hematopoietic lineages. Interestingly, a high percentage of megakaryocytic leukemias, a type of leukemia rarely observed with MuLVs, arise in the FVB/n strain of mice. The genetic backgrounds of the different strains of mice influence greatly the results. Furthermore, the enhancer region, different for GV-1.2 and GV-1.4, plays a pivotal role in the disease specificity: GV-1.2 induces more lymphoid leukemias, and GV-1.4 induces more nonlymphoid ones. | lld:pubmed |
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| pubmed-article:16571819 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16571819 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16571819 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16571819 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16571819 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:16571819 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:16571819 | pubmed:author | pubmed-author:RassartEricE | lld:pubmed |
| pubmed-article:16571819 | pubmed:author | pubmed-author:HoangTrangT | lld:pubmed |
| pubmed-article:16571819 | pubmed:author | pubmed-author:BaratCorinneC | lld:pubmed |
| pubmed-article:16571819 | pubmed:author | pubmed-author:VoisinVéroniq... | lld:pubmed |
| pubmed-article:16571819 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16571819 | pubmed:volume | 80 | lld:pubmed |
| pubmed-article:16571819 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16571819 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16571819 | pubmed:pagination | 4026-37 | lld:pubmed |
| pubmed-article:16571819 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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