Directable cannula for gastrojejunal catheterization.
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Catheterization↗
Biomedical subjects
M I Pedersen
Publications and source records attributed to M I Pedersen.
Chromosomal evolution in the progression and metastasis of human malignant melanoma. A multiple lesion study.
In order to distinguish those chromosomal aberrations associated with tumorigenesis from those associated with tumor progression of malignant melanoma, chromosome analysis was performed on eight tumors derived from one patient. Three common marker chromosomes, a deletion of chromosome 1, a deletion of chromosome 9, and a translocation involving chromosomes 7 and 12, were identified in each tumor. The presence of common markers in these intrapatient tumors indicates the monoclonal origin of these tumors. Furthermore, the consistent and specific involvement of chromosome 9 in both interpatient and intrapatient studies suggests the crucial role that chromosome 9 plays during the development of human malignant melanoma. In addition to common markers, different overlapping markers including those involving chromosomes 2, 3, and 6, were also identified, suggesting that chromosomes 2, 3, and 6 are most likely associated with the progression, instead of the genesis, of the tumor. Finally, lesion-specific marker chromosomes were identified in each tumor indicating the nonrandom selection and modification of the metastatic process. The nature of chromosomal evolution among the eight tumors was clearly demonstrated by the retention and amplification of specific marker chromosomes, with the latter tumors containing more overlapping markers than the early tumors and the recurrence of identical markers in the different branches of evolution. One of the last three tumors obtained immediately before the death of the patient contained all the overlapping markers identified in other tumors, which may indicate that a plateau of chromosomal evolution of these tumors has been reached. These observations demonstrate a nonrandom or programmed chromosome evolution of human neoplasia that could be intrinsic to the aneuploid nature of neoplasia.
Chromosome Aberrations↗
Nonrandom chromosome structural aberrations and oncogene loci in human malignant melanoma.
Short-term cultures of 10 malignant melanomas derived from 8 patients were analyzed cytogenetically. The chromosome composition of the tumors was found to be similar in terms of modal number and structural and numerical aberrations, especially the nonrandom nature of breakpoints. Six chromosomes were consistently involved in marker formation. Aberrations of chromosomes #1 and #9 were identified in every tumor, whereas structural alterations of chromosome #2 were found in 9 tumors. In contrast, aberrations of chromosomes #6, #3, and #7 were identified in 7, 7, and 8 of the tumors, respectively. The nonrandom breakpoints on these chromosomes frequently coincided with known oncogenic loci and resulted in morphologically identical marker chromosomes. Consecutive lesions were obtained for two patients. Common markers were identified in both cases, indicating the clonal origin of the tumors. In addition, many marker chromosomes characteristic of the individual lesions were also identified. The presence of these lesion-specific markers indicates the nonrandom selective nature of the metastatic process and suggests the possible heterogeneity of the original tumor cell population.
Adult↗