Linked Life Data

3084503

Source:http://linkedlifedata.com/resource/pubmed/id/3084503

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1986-6-18
pubmed:abstractText
3611 MSV, a raf-oncogene-transducing murine retrovirus, induces fibrosarcomas and erythroid hyperplasia in newborn mice after a latency of 4-8 wk. In contrast, new recombinant murine retroviruses carrying the myc oncogene (J-3, J-5 construct viruses) do not induce tumors before greater than 9 wk. A combination of both oncogenes in an infectious murine retrovirus (J-2) induces hematopoietic neoplasms in addition to less prominent fibrosarcomas and pancreatic adenocarcinoma 1-3 wk after inoculation. The hematologic neoplasms consist of immunoblastic lymphomas of T and B cell lineage and erythroblastosis. If animals were inoculated with a variant of the J-3 virus, which induces altered foci in cultures of NIH 3T3 cells, carcinoma developed in the pancreas with a 2-6 mo latency. In parallel to the synergistic action of both oncogenes on hematopoietic cells in vivo, we find that raf-oncogene-induced transformation of bone marrow cells in culture is enhanced by the addition of myc, which by itself does not transform these cells when grown in standard media. We conclude that concomitant expression of raf and myc oncogenes in hematopoietic and epithelial cells alters their respective transforming activities. The contribution of v-myc in this synergism was examined by use of a series of recombinant murine retroviruses capable of expressing the avian v-myc to study the effect of altered myc expression on hematopoietic/lymphoid cells. With either interleukin 3- or interleukin 2-dependent cell lines, introduction of the recombinant viruses abrogated the requirement for IL 3 or IL 2 for growth, and associated with this was the suppression of c-myc expression. The findings suggest that myc is a component in the signal transduction pathway for IL 3 and IL 2 and support an autoregulatory mechanism of c-myc expression. In contrast to v-myc, expression of v-raf in primary lymphoid/hematopoietic cells has an immortalizing function without abrogating the requirement for IL 3 for growth. This suggests that v-raf and v-myc affect different components of growth regulation, as, for example, commitment (v-myc) and cell cycle progression (v-raf).
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0730-2312
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
195-218
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:3084503-Animals, pubmed-meshheading:3084503-Animals, Newborn, pubmed-meshheading:3084503-Base Sequence, pubmed-meshheading:3084503-Cell Division, pubmed-meshheading:3084503-Cell Line, pubmed-meshheading:3084503-Cell Transformation, Viral, pubmed-meshheading:3084503-Cells, Cultured, pubmed-meshheading:3084503-DNA, Recombinant, pubmed-meshheading:3084503-Electrophoresis, Polyacrylamide Gel, pubmed-meshheading:3084503-Fibrosarcoma, pubmed-meshheading:3084503-Gene Expression Regulation, pubmed-meshheading:3084503-Interleukin-2, pubmed-meshheading:3084503-Interleukin-3, pubmed-meshheading:3084503-Lymphokines, pubmed-meshheading:3084503-Lymphoma, pubmed-meshheading:3084503-Mice, pubmed-meshheading:3084503-Mice, Inbred Strains, pubmed-meshheading:3084503-Neoplasm Proteins, pubmed-meshheading:3084503-Neoplasms, Experimental, pubmed-meshheading:3084503-Oncogenes, pubmed-meshheading:3084503-Proto-Oncogene Proteins, pubmed-meshheading:3084503-Proto-Oncogene Proteins c-myc, pubmed-meshheading:3084503-Retroviridae, pubmed-meshheading:3084503-Sarcoma, Experimental, pubmed-meshheading:3084503-Time Factors
pubmed:year
1986
pubmed:articleTitle
Interaction between Raf and Myc oncogenes in transformation in vivo and in vitro.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.