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G I Evan

Publications and source records attributed to G I Evan.

97 records · Page 6Linked to original sources
PubMed1984

The protein encoded by the human proto-oncogene c-myc.

The proto-oncogene c-myc may play a role in controlling the growth and division of normal cells, and abnormalities of the gene have been implicated in the genesis of a substantial variety of human tumors. To facilitate further study of these issues, we developed antisera that permit the identification and isolation of the protein encoded by the human and other mammalian versions of c-myc. We found that c-myc(human) gives rise to at least two phosphoproteins with apparent molecular weights of 62,000 [pp62c-myc(human), the major product] and 66,000 [pp66c-myc(human), produced in smaller quantities and possibly a modified version of the Mr 62,000 protein]. Both proteins have relatively short half-lives of approximately equal to 30 min. Mouse c-myc encodes similar proteins with molecular weights of 64,000 and 66,000. The use of cells transformed by DNA-mediated gene transfer sustained previous deductions that the entire coding domain of c-myc(human) is contained in the second and third exons of the gene and resolved previous ambiguities by showing that analogous exons specify the entire protein product of c-myc(chicken). Tumor cells containing amplification of c-myc(human) produce relatively large amounts of pp62/pp66c-myc(human). By contrast, translocations of c-myc found in cells derived from Burkitt lymphoma appear merely to sustain expression of c-myc(human) at levels found also in nontumorigenic lymphoblastoid cells, rather than to increase expression of the gene to manifestly abnormal levels.

Animals↗
PubMed1984

Induced differentiation of avian myeloblastosis virus-transformed myeloblasts: phenotypic alteration without altered expression of the viral oncogene.

Cells of a clone of avian myeloblastosis virus-transformed myeloblasts were induced to differentiate to adherent myelomonocytic cells by treatment with lipopolysaccharide. These adherent cells were subcultured and maintained as a line for more than 6 months with lipopolysaccharide present. Cells of this line were induced to differentiate to nondividing macrophage-like cells by the addition of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate. In this way, the following homogeneous cell populations representing three distinct stages of myeloid differentiation were obtained: I, actively dividing myeloblasts that grew in suspension: II, actively dividing adherent cells; and III, fully differentiated nondividing cells resembling macrophages. When the expression of v-myb (the oncogene of avian myeloblastosis virus) was examined in cells of these three differentiation stages, it was found that the protein encoded by v-myb (p45v-myb) continued to be synthesized in similar quantities and showed no obvious alteration (assessed by partial proteolytic digestion and two-dimensional gel electrophoresis) during differentiation. These results show that cells transformed by v-myb can be induced to differentiate without affecting the expression of v-myb and imply that, during differentiation, the effect of v-myb is suppressed by a mechanism other than altered expression of the oncogene.

Animals↗
PubMed1984

Isolation of monoclonal antibodies specific for products of avian oncogene myb.

We isolated a series of monoclonal antibodies which were raised against a bacterially expressed protein, bp37v-myb, and coded for by part of the avian v-myb gene. These monoclonal antibodies recognized a range of antigenic specificities on bp37v-myb, and this was reflected in their differing specificities for the gene products of the v-myb, c-myb, and E26 viral oncogenes. One monoclonal antibody recognized, in addition to the v-myb and c-myb gene products, a conserved nuclear protein found in all tested cells. We describe the characterization of these monoclonal antibodies.

Animals↗
PubMed1983

A monoclonal anti-HLA antibody recognizes a mouse tumor-associated antigen.

The monoclonal antibody W6/32.1 recognizes a public determinant on the HLA-A, B and C antigens of all tested human haplotypes. Though the antibody does not bind to normal mouse cells of any H-2 haplotype, it does show an unexpected specificity for the T cell leukemia line MBL-2 from a C57BL/6 mouse. It is shown that the murine antigen recognized by W6/32.1 is on an H-2-like molecule which also carries the determinant recognized by the monoclonal antibody B22-249 R1, specific for the H-2Db antigen. Unlike B22-249 R1, however, W6/32.1 does not bind to normal H-2b lymphocytes, nor to a variety of tumor cell lines of the H-2b haplotype. This cross-reaction is specific to W6/32.1, and is not shared by other monoclonal antibodies of similar anti-HLA specificities. Moreover, the affinity of W6/32.1 for its human antigen is substantially higher than for its mouse antigen. We conclude that W6/32.1 fortuitously recognizes a novel determinant on the H-2Db antigen of MBL-2, rather than an extensive region of structural homology shared between HLA and H-2. Thus for cells of the H-2b allotype this determinant is detected only on MBL-2, and by definition is thus an example of a tumor-associated antigen.

Animals↗
PubMedDate not supplied

High levels of c-myc protein in human breast tumours determined by a sensitive ELISA technique.

We have previously examined the expression of (H-ras) oncogene related transcripts (Spandidos and Agnantis: Anticancer Res 4: 269-272, 1984) and also the activation of the H-ras oncogene (Spandidos: Anticancer Res 7: 991-996, 1987) in human malignant breast cancers. Our results revealed overexpression of the H-ras transcripts in malignant compared to normal tissues, while in the same tumour specimens certain point mutations and other genetic changes have been found in the H-ras gene. In this paper we have investigated c-myc oncoprotein expression in the same tumour samples using an ELISA technique (Moore et al: Oncogene Res 2: 65-80, 1989). Elevated c-myc oncoprotein expression was found in all of the tumour specimens compared with normal breast tissues from a patient with no evidence of the disease. A correlation was found between T stage and c-myc expression in both the normal tissue from the resection margin and in the breast tumour specimens. However, no correlation was found between survival and elevated c-myc expression.

Adult↗