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Biomedical subjects

W Campbell

Publications and source records attributed to W Campbell.

100 records · Page 6Linked to original sources
PubMedDate not supplied

[Intra-arterial chemotherapy, using the hepatic artery, in metastases of colorectal carcinoma].

Hepatic metastasis is the major cause of death in advanced cancer of the colon and rectum. Various modes of therapy have been attempted with only partial success. Infusion of cytotoxic agents into the hepatic artery has allowed a higher concentration of drug into the tumor capillary bed than is achievable with intravenous administration. We review the data on therapeutic outcome, administration techniques and toxicity of hepatic arterial chemotherapy for colorectal cancer metastatic to the liver.

Antineoplastic Agents↗
PubMedDate not supplied

Combined strategy of conventional cytogenetics, fluorescent in situ hybridization and chromosome morphometry for analysis of parotid gland tumor.

The limiting factors in conventional cytogenetic analysis of cell culture, especially of solid tumors, include insufficient metaphases, overgrowth of abnormal mitotic cells by normal cells, and suboptimal quality of harvesting and banding. Despite the availability of numerous protocols to induce G-banding, as well as Q-, R-, and C-banding, occasions still arise in which the analysis is severely limited by these factors and incomplete conclusions are often drawn as to the precise nature of the chromosomal abnormality, if indeed any can be detected. By adopting a rational approach of (1) close monitoring of cultures and rapid harvesting as soon as it is feasible, and (2) analysis of available metaphases by a combination of the GTG technique, fluorescent in situ hybridization (FISH), and chromosome morphometry using a graphic arts tool, a significant improvement in success rate may be more readily achieved. Here pathological and cytogenetic data are presented of a case of parotid gland carcinoma ex mixed tumor with the karyotype of 46, XX, del(5)(q12), dir ins(8;5)(q12;q12qter), add(12)(p13)/46, XX. This case is utilized to illustrate the importance of application of our combined strategy.

Chromosomes, Human, Pair 12↗
PubMedDate not supplied

Integration of human papillomavirus sequences in cervical tumor cell lines.

The establishment of three cell lines from keratinizing and nonkeratinizing cervical carcinomas was previously reported. These cell lines were analyzed for growth properties in vitro and in vivo. Metaphases prepared from tissue culture of these cell lines were cytogenetically characterized using GTG-banding and fluorescent in situ hybridization (FISH) using chromosome-specific alpha-satellite probes. Although the karyotypes of most cells were extremely complex, nonrandom karyotypic abnormalities could be identified. Molecular data had suggested that TC140, derived from a keratinizing cervical tumor, may contain HPV 16 in the episomal state, while TC146, derived from a nonkeratinizing large-cell cervical carcinoma, contained HPV 16 in the integrated state. Therefore, a fluorescent in situ hybridization study was undertaken using biotinylated HPV 16 DNA as a probe on order to confirm and to corroborate the original molecular study, as FISH is the most direct approach for mapping cellular and viral sequences in mammalian chromosomes. The results previously reported in abstract demonstrated the presence of positive hybridization signals on the long arms of the apparent homologs of a human D-group chromosome in cell line TC146. The results of recently completed experiments clearly indicated that while the predominant state of viral existence in the TC140 cell line was apparently episomal, consistent viral integration was found in the TC146 cell line. Furthermore, where viral sequences of HPV 16 integration were observed in cells of TC146, integration was apparently nonrandom. Fluorescent in situ hybridization using various chromosome-specific alpha-satellite and HPV 16 probes clearly indicated that viral integration occurred nonrandomly and at a specific site on chromosome 13. By chromosome morphometry, the viral integration site was localized to 13q14, also the mapped locus of the retinoblastoma (Rb) tumor suppressor gene.

Chromosome Banding↗