Search PubMed⌕ Search

Biomedical subjects

G Levan

Publications and source records attributed to G Levan.

194 records · Page 11Linked to original sources
PubMed1972

Tumor etiology and chromosome pattern.

Fibrosarcomas induced in Chinese hamsters and rats by Rous sarcomla virus and 7,12-dimethylbenz(a)anthracene are associated with nonrandom chromosome variation. Although histologically indistinguishable, the tumors induced by the virus or chemical in each host species are characterized by completely different karyotypic patterns.

Animals↗
PubMedDate not supplied

Rat c-myc oncogene is located on chromosome 7 and rearranges in immunocytomas with t(6:7) chromosomal translocation.

Two B-cell-derived tumours, human Burkitt's lymphoma (BL) and murine plasmacytoma (MPC), are regularly associated with a distinctive form of chromosomal translocation (for reviews see refs 1, 2). In BL, the distal portion of chromosome 8 breaks off and is transposed, in most cases, to chromosome 14, known to carry the immunoglobulin heavy-chain locus. In about 5% of the cases the same distal part of the chromosome 8 has moved to either chromosome 2 or 22, to the neighbourhood of the kappa or the lambda locus, respectively. In MPC the distal region of chromosome 15 is transposed to the chromosome 12, known to carry the immunoglobulin heavy-chain locus, or enters into reciprocal exchange with the kappa locus-carrying chromosome 6 (ref. 7). Several laboratories have located c-myc, the cellular homologue of the MC29 retroviral oncogene v-myc, to human chromosome 8 (refs 8-10) and mouse chromosome 15 (refs 11-13). It has also been shown that the BL- and MPC-associated translocations remove the c-myc gene from its original site and transpose it into or close to one of the immunoglobulin gene clusters. In view of the above findings we also looked for possible involvement of the c-myc gene in a B-cell-derived tumour of a third species, the rat. Rat immunocytomas of spontaneous origin carry a reciprocal translocation between chromosomes 6 and 7 (ref. 17). Here we have localized the c-myc locus to chromosome 7 of the rat. Moreover, we have found that the c-myc gene was rearranged in four of five immunocytomas carrying the characteristic chromosomal translocation.

Animals↗
PubMedDate not supplied

Amplification and enhanced expression of the c-myc oncogene in mouse SEWA tumour cells.

SEWA tumour cells are derived from an osteosarcoma induced in an A.SW mouse by infection with polyoma virus. Cytogenetic analyses have revealed three different characteristic chromosomal abnormalities diagnostic for the presence of amplified genes: 'double minutes' (DMs), homogeneously staining chromosomal regions (HSRs) and C-bandless chromosomes (CMs; for review see ref. 2). DMs may undergo fluctuation in number depending on the conditions in which the cells grow. Their number usually increases after injection of cells into a mouse and often is reduced to undetectable levels when the cells are explanted back into tissue culture; when the cells are re-introduced into the mouse, they again acquire multiple DMs. We show here that cells of SEWA lines carrying DMs, HSRs or CMs contain amplified copies of the proto-oncogene c-myc and enhanced levels of c-myc messenger RNA and c-myc protein. DMs or CMs are the sites of c-myc amplification in two different SEWA lines.

Animals↗
PubMedDate not supplied

Characterization of multidrug resistance in SEWA mouse tumor cells: increased glutathione transferase activity and reversal of resistance with verapamil.

The glutathione transferase (EC 2.5.1.18) activity of multidrug-resistant and drug-sensitive SEWA mouse tumor cells was determined. Increase in activity was found in all multidrug-resistant sublines. Electrophoretic separation of cytosolic proteins and immunodetection, using antisera against Class Alpha, Class Mu and Class Pi glutathione transferase, revealed a two-fold increase of the Class Pi transferase in the resistant cells. The role of glutathione transferase of Class Pi in the multidrug resistance and its distinction from the over-produced 21,000 dalton protein p21 is discussed. Reversal of the resistance, using the calcium antagonist verapamil, and different sensitivity to verapamil between different sublines are also reported.

Animals↗
PubMedDate not supplied

Pleiotropic drug resistance, protein overexpression, and cytogenetic signs of gene amplification in mouse tumor cells.

We have isolated pleiotropic drug resistant mouse tumor cell lines with resistance-associated double minute chromosomes (DM) or homogeneously staining regions (HSR). In resistant cells, two-dimensional protein electrophoresis revealed elevated levels of a 21,000 dalton protein. Two resistant lines, with cytogenetically unstable (DM) and stable (HSR) gene amplification, were grown in the absence of drug for several weeks. The resistance and the protein overexpression was correlated to the presence of either HSR or DM. This suggests that the 21,000 dalton protein is a gene amplification product, and its importance for the resistance is discussed.

Animals↗