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Biomedical subjects

G Levan

Publications and source records attributed to G Levan.

At least 163 records · Page 9Linked to original sources
PubMed1985

The thyroglobulin gene resides on chromosome 8 in man and on chromosome 7 in the rat.

Human chromosomes were separated by a dual laser FACS sorter and their DNA hybridized with a thyroglobulin gene probe. A strong hybridization signal was obtained with DNA from chromosome 8. A panel of mouse-rat cell hybrids was used to determine the chromosomal localization of the rat thyroglobulin gene by the Southern blotting method. Comparison of the cytogenetic data with the hybridization signals obtained with the rat thyroglobulin probe allowed assignment of this gene to rat chromosome 7. It is concluded that the synteny relationship between the thyroglobulin gene and the c-myc oncogene has been conserved in rat and man.

Animals↗
PubMed1984

Resistance to actinomycin D and to vincristine induced in a SEWA mouse tumor cell line with concomitant appearance of double minutes and a low molecular weight protein.

By increasing stepwise the drug concentration of the medium, we have induced, in a cell line of the murine SEWA tumor, resistance to actinomycin D (AMD) and vincristine (VCR) 30-50 times above the normal. In both types of resistant cells, we have revealed, by two-dimensional gel electrophoresis, a protein (MW 21K , pI 5) not found in control cells. Large fractions of the resistant cells contained double minutes (DM). In AMD-resistant cells, correlation was demonstrated between number of DM and degree of resistance. Back in AMD-free medium, resistant cells lost both the DM and the 21K protein. Cross-resistance prevailed between AMD and VCR. Cells resistant to AMD and VCR showed erratic resistance to methotrexate (MTX), but no significant resistance existed in the reverse direction.

Animals↗
PubMed1984

Gene mapping in the rat by mouse-rat somatic cell hybridization: synteny of the albumin and alpha-fetoprotein genes and assignment to chromosome 14.

The methods of somatic cell genetics and molecular hybridization were applied to a panel of mouse X rat hepatocyte hybrids segregating rat chromosomes to assign the rat genes coding for two serum proteins, albumin and alpha-fetoprotein (Alb and Afp). The molecular hybridization of DNAs from different hybrids with cloned DNA probes showed that all the hybrid clones possessing the rat Alb gene and expressing it also retained the rat Afp locus, which is not expressed in these hybrids. So the Alb and Afp genes are syntenic in the rat, as in the mouse. Furthermore, the cytogenetic analysis allowed the assignment of these two loci to rat chromosome 14.

Animals↗
PubMed1983

Epstein-Barr virus (EBV)-induced lymphoproliferative disease in cotton-topped marmosets.

Six cotton-topped marmoset monkeys (Sangiunus oedipus) were inoculated with 10(5) transforming units of B95-8 virus, and two of them developed fatal lymphoproliferative disease. The EBV-carrying tumor cells from these marmosets had the following characteristics: (1) they were polyclonal by surface immunoglobulin and immunoglobulin production in vitro; (2) they had no specific chromosome abnormalities, and (3) they failed to form colonies in large percentages in agarose. It is proposed that a spectrum of phenotypes of EBV-induced lymphoproliferative diseases in the cotton-topped marmosets may be identified and are more akin to fatal infectious mononucleosis or X-linked lymphoproliferative syndrome than to Burkitt's lymphoma.

Animals↗
PubMed1981

The different origin of primary and secondary chromosome aberrations in cancer.

We have proposed a hypothetical model to explain the role of chromosomal aberrations in malignant development. In this model we postulate two kinds of chromosomal changes: (1) primary, active changes caused by direct interaction between the oncogenic agent and the hereditary material of the host cell. These changes are mainly somatic mutations, but may also be associated with directed structural changes visible in the microscope; and (2) secondary, passive changes arising randomly by nondisjunction and structural rearrangements. They are followed by selection of cells with changes that amplify the primary change and thus appear as nonrandom chromosome patterns. This hypothesis is discussed in the light of 1827 cases of human malignancy in which we have recently surveyed and systematized chromosomal aberrations. Special support for the idea of somatic mutations as the initiator of malignant development comes from work of Knudson and collaborators in human retinoblastoma. The Ph1 chromosome, predominant during the chronic phase of chronic myeloid leukemia (CML), is proposed as an instance of a primary change, whereas the chromosome changes during the blastic crisis of CML will illustrate the secondary changes. The most common of these secondary changes is actually the doubling of the Ph1 and thus an amplification of the primary change. The increase in number of copies of a specific chromosome reported by Green and collaborators demonstrates that this kind of amplification can result in direct response to the need for a specific gene located in that chromosome.

Chromosome Aberrations↗
PubMed1981

Chromosomes and cell surface markers of marmoset lymphocytes and Epstein-Barr virus-transformed marmoset cell lines.

The G-banded karyotypes of both normal lymphocytes and Epstein-Barr virus (EBV)-transformed lymphocytes of cotton-topped marmosets (Saguinus oedipus) were examined. The marmoset lymphocytes and EBV-transformed lymphoblastoid cells had normal diploid chromosomes (2n = 46) with no specific cytogenic change associated with transformation in vitro. EBV-transformed marmoset lymphocytes expressed the cell surface markers of B lymphocytes and EB viral antigens.

Animals↗
PubMed1980

The induction of host cell mitoses in a transplantable ascites tumor.

The implantation intraperitoneally of in vitro cell lines of the SEWA mouse ascites tumor into syngeneic mice and into allogeneic thymus-less nude mice stimulated mitotic activity in the host component of the ascites cell population. The mitoses were found almost exclusively during the first month after the change in environment, while the tumor cells gradually readapted to in vivo growth. Normal mitoses appeared immediately after the transfer in vivo, reached a maximum at days 10 to 20, then decreased in frequency and disappeared completely after day 33. At that time, the tumor cells had recovered viability and started growing with full vigor. The ascites samples in which normal cells were undergoing mitotic division often contained a low proportion of tumor cells and a high proportion of small inflammatory cells. The chromosomes of the normal mitoses differed from those of the tumor mitoses by being smaller and more crowded. Their relative uniformity in type was also accentuated by the fact that they were all characterized by a low but ubiquitous incidence of chromatid breaks. These features suggested that the normal mitoses belonged to the lymphocytic population and represented a defense mechanism of the host towards the tumor. Since normal mitoses were especially frequent in the ascites cell population of the thymus-less mice, it may be speculated that T-lymphocytes were not the main target cells for the mitotic induction.

Animals↗
PubMed1979

Absence of late-replicating X-chromosome in a female patient with acute myeloid leukemia and the 8;21 translocation.

Autoradiography was used to demonstrate that the x-chromosome of the 45,X,-X,t(8;21) stemline of a female patient with acute myeloid leukemia (AML) was the active X-chromosome. This suggested that in patients housing AML with the 8;21 translocation, the loss of the inactive X-chromosome in females and of the Y in males (which is known to occur in nearly half of the patients) entails selective advantage to the stemline.

Adult↗
PubMed1978

A new chromosome type replacing the double minutes in a mouse tumor.

For several years the SEWA mouse ascites tumor has been a carrier of double minute chromosomes (DMs), some 90% of its cells containing from one to several hundred DMs. In one specific subline of this tumor, the cells with DMs had decreased in frequency to less than 5% of the cells. At the same time, the stemline chromosome number had increased from 43 to around 50. This was due to the presence, in addition to the ordinary telocentric chromosomes, of a varying number of medium-sized metacentrics. The fact that these chromosomes deviated from ordinary mouse chromosomes in special features, such as median centromeric position, early DNA replication, and complete lack of centromeric heterochromatin, indicates that they represent a new type of chromosome. Their striking agreement with the DMs in many properties makes it tempting to associate their origin with the disappearance of the DMs.

Animals↗