Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1990-12-27
pubmed:abstractText
E mu-myc transgenic mice were back-crossed to BALB/c mice up to back-cross generation 3. The offspring that included transgene-carrying and -negative mice in approximately equal proportions were randomly divided into 2 groups. Thirty-four mice (group I) were treated with pristane, followed by A-MuLV, and 40 (group II) were injected with A-MuLV alone. Altogether, 16 lymphoid tumors developed in group I and 17 in group II. Nine of the tumors in group I and 4 in group II appeared as ascitic tumors. The ascites contained lymphoblasts and 10 to 45% plasmacytoid cells. These tumors were designated as plasmablastic lymphomas (PLs). All tumors except one were transgene-positive and did not carry translocations. An exceptional tumor in group I carried a variant 6;15 translocation but not the transgene. It obviously corresponds to the regular Abelson + pristane-induced plasmacytoma. Among 11 tested PLs, 10 had a single retroviral insertion site, while one tumor showed 3. Among 18 untreated transgenic descendants (group III), chosen randomly during serial back-crosses, 15 (83%) developed lymphomas, with no sign of plasmacytoid differentiation. The incidence was comparable in all 3 groups, assuming 50% of the mice in groups I and II to be transgenic. The time distribution of tumor development was also similar. Spleen cells from transgene-carrying mice with no clinical sign of lymphoma were infected in vitro with A-MuLV and transplanted i.p. into BALB/c recipients. PLs developed in 26 of 31 pristane-treated recipients, but in only one of 18 untreated recipients. One of 6 PLs tested was monoclonal, whereas the remaining 5 were oligoclonal. They all expressed v-abl. These results show that some of the preneoplastic B-cells that expressed constitutively active myc transgene turned into plasmablasts after infection with A-MuLV. Full development of their neoplastic potential was facilitated by the presence of pristane-granuloma.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
46
pubmed:geneSymbol
E&mgr;-myc
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
845-52
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2228313-Animals, pubmed-meshheading:2228313-B-Lymphocytes, pubmed-meshheading:2228313-Carcinogens, pubmed-meshheading:2228313-Cell Transformation, Neoplastic, pubmed-meshheading:2228313-Cell Transformation, Viral, pubmed-meshheading:2228313-Female, pubmed-meshheading:2228313-Gene Expression Regulation, Neoplastic, pubmed-meshheading:2228313-Genes, myc, pubmed-meshheading:2228313-Lymphocyte Activation, pubmed-meshheading:2228313-Lymphoma, pubmed-meshheading:2228313-Male, pubmed-meshheading:2228313-Mice, pubmed-meshheading:2228313-Mice, Inbred BALB C, pubmed-meshheading:2228313-Mice, Transgenic, pubmed-meshheading:2228313-Neoplasm Transplantation, pubmed-meshheading:2228313-Plasmacytoma, pubmed-meshheading:2228313-Retroviridae, pubmed-meshheading:2228313-Spleen, pubmed-meshheading:2228313-Terpenes, pubmed-meshheading:2228313-Tumor Virus Infections
pubmed:year
1990
pubmed:articleTitle
Abelson murine leukemia virus transforms preneoplastic Emu-myc transgene-carrying cells of the B-lymphocyte lineage into plasmablastic tumors.
pubmed:affiliation
Department of Tumor Biology, Karolinska Institutet, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't