A study was undertaken to determine whether cytogenetic abnormalities can be identified in an invasive melanoma cell population that has been selected in vitro out of a larger cell population of low invasive potential. The selecting agent was a denuded human amniotic membrane situated within Mega-Membrane Invasion Culture System chambers. Invasive cells were collected, grown, and harvested for cytogenetic analysis. Metaphases of these cells were examined for chromosomal abnormalities and for evidence of gene amplification in the form of double minute chromosomes. Invasive cell lines evinced changes in their degree of aneuploidy which were not seen in parental control lines of the same passage number. Significant karyotypic abnormalities identified in invasive cell lines were an increased dosage of chromosome 7 and multiple 1q translocation marker chromosomes. Double minute chromosomes were found in up to 18% of invasive cell metaphases examined and in 3% of parental controls. The incidence of double minutes was found to decrease as a function of passage number.

No description available.

No description available.

At least some areas of the embryonic blastoderm in Drosophila melanogaster appear to be determined by substances produced under control of the maternal genome without involvement of the embryonic genome. Study of mutant genes controlling the production of such morphogenic substances would provide valuable information about these substances and the nature of determination itself. In this thesis, the adult ovaries in offspring of females containing sex chromosomes originating from a wild-type strain of Drosophila melanogaster collected on Margarita Island, Venezuela have been examined. After selection on such chromosomes, over 50% of the offspring produced by homozygous females contained either one or two agametic gonads. The delayed expression is due to temperature-sensitive gene expression duringoogenesis. Two micron sections of normal and abnormal ovaries of this strain indicate the mesodermal components of the abnormal ovaries including the ovarian sheaths and the ovariole epithelial sheaths, were normal. In addition, attachment of the ovaries to the oviducts are normal. The abnormal ovarioles contain cells which appear to be mesodermally-derived follicle cells, but no normal egg chambers are seen. The germaria also contain follicle cells but no cells resembling stem cells or cystocytes are seen. It is concluded: (1) the development of ovarian germinal and mesodermal components are completely independent and (2) the mutant gene(s) prevent normal differentiation of pole cells into germ cells.

Thesis submitted for the degree of Doctor of Philosophy in the University of the Witwatersrand, Johannesburg. / Biology, having outgrown its purely descriptive phase, has, for nearly a century, been in an era of causal analysis. It has been a period of extreme compartmentalisation of the general field into many disciplines, each endowed with a defined range of problems, with peculiar materials of study and with special approaches and techniques.From the nature of things, it is inevitable that each biologist should have been a specialist. The field of living things ramified so vastly that the species of scientist known as the biologist or naturalist became largely extinct: instead, there were geneticists, systematists, physiologists, embryologists, biochemists, cytologlsts and others. Specialisation did not stop even at that point for the systematists split into mammalogists, ornithologists, helminthologists, etc.; the geneticists into experimental geneticists, cytogeneticists, phenogenetlclsts, and so on. Good and bad consequences flowed from this tendency. The advantage of specialisation was a great increase in the store of factual information; the disadvantage lay in the isolation between representatives of the various disciplines and in the absence of cross-pollination in the development and evaluation of concepts. / WHSLYP2017

Thesis (Ph.D.)--University of Hong Kong, 2003. / Also available in print.

Thesis (Ph. D.)--University of Hong Kong, 2007. / Title proper from title frame. Also available in printed format.

Thesis (Ph.D.)--University of Hong Kong, 2003. / Also available in print.

Murine plasmacytoma is induced by plastic implants, injection of paraffin oil or pristane, or through viral infection, and Myc is invariably overexpressed in the tumour cells. Although translocation and juxtaposition of the Myc locus to an immunoglobulin locus is the prominent nonrandom cytogenetic aberration observed, the significance of other karyotypic instabilities in murine plasmacytoma is not clear, including the previously observed occurrence of trisomy 11. As well as identifying new cytogenetic mutations in murine plasmacytomagenesis, this study provides evidence for their combined and sequential accumulation that may offer new parallels to human B-cell malignancies. Plasmacytomas were induced in Balb/c Rb6.15 mice by intraperitoneal (i.p.) pristane injection prior to infection with the ABL-MYC retrovirus, and confirmed by histological examination. Spectral karyotype analysis of tumour samples identified frequent aneuploidy, tetraploidy, and amplification of chromosomes 11, 12 and 16. In contrast, control mice treated by i.p. pristane injection did not develop plasmacytoma, and lipopolysaccharide-stimulated splenocytes from control mice had mainly normal diploid karyotypes. However, karyotypic instability in a minority of splenocytes indicated that control mice showing no signs of plasmacytoma development nevertheless are prone to numerical and structural cytogenetic mutations that may possibly result in plasmacytoma initiation and progression under favourable conditions, such as infection with ABL-MYC virus with the resulting high expression of v-abl and Myc in target cells. These results indicate the possible existence of proto-oncogenes present on murine chromosomes 11, 12, and 16 that are important for plasmacytoma initiation and/or progression. There are also indications that T(1;6) and monosomy of the X chromosome may also play roles in plasmacytomagenesis, and that trisomy 12 may only occur in cells with pre-existing nonrandom mutations, thereby acting as a late mutation event. As other experimental models of murine plasmacytoma have not shown a similar karyotypic etiology, there appears to be several possible redundant cytogenetic mutation events that lead to plasmacytoma. Also, as tumours in this study present various combinations of the aforementioned amplified chromosomes, their combined amplification may serve redundant purposes as well. / May 2008

published_or_final_version / abstract / toc / Clinical Oncology / Doctoral / Doctor of Philosophy