A physician decries managed care ethics.
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Attitude of Health Personnel↗
Biomedical subjects
T L Holloway
Publications and source records attributed to T L Holloway.
Detection of chromosome 20q deletions in bone marrow metaphases but not peripheral blood granulocytes in patients with myeloproliferative disorders or myelodysplastic syndromes.
Myeloproliferative disorders and myelodysplastic syndromes arise in multipotent progenitors and may be associated with chromosomal deletions that can be detected in peripheral blood granulocytes. We present here seven patients with myeloproliferative disorders or myelodysplastic syndromes in whom a deletion of the long arm of chromosome 20 was detectable by G-banding and/or fluorescence in situ hybridization in most or all bone marrow metaphases. However, in each case, microsatellite polymerase chain reaction (PCR) using 15 primer pairs spanning the common deleted region on 20q showed that the deletion was absent from most peripheral blood granulocytes. The human androgen receptor clonality assay was used to show that the vast majority of peripheral blood granulocytes were clonal in all four female patients. This represents the first demonstration that the 20q deletion can arise as a second event in patients with pre-existing clonal granulopoiesis. Microsatellite PCR analysis of whole bone marrow from two patients was consistent with cytogenetic studies, a result that suggests that cytogenetic analysis was not merely selecting for a minor subclone of cells carrying the deletion. Furthermore, in one patient, the deletion was present in both erythroid and granulocyte/monocyte colonies. This implies that the absence of the deletion in most peripheral blood granulocytes did not reflect lineage restriction of the progenitors carrying the deletion but may instead result from other selective influences such as preferential retention/destruction within the bone marrow of granulocytes carrying the deletion.
Aged↗
Comparative genomic hybridization in acute myeloid leukemia. A comparison with G-banding and chromosome painting.
Comparative genomic hybridization (CGH) represents a new technique for global analysis of a whole genome for net loss or gain of chromosome regions. It offers several advantages over alternative techniques. It permits analysis of a whole genome in a single hybridization reaction, it does not require the generation of metaphases from tumor cells, and it only requires very small numbers of tumor cells. Most previous studies have concentrated on the application of CGH to the analysis of chromosome defects associated with solid tumors. In this paper we report the use of CGH to study bone marrow samples from a patient with acute myeloid leukemia and complex karyotypic abnormalities. The results obtained using CGH were compared with G-banding analysis. Both G-banding and CGH detected a 5q deletion, a 7q deletion, additional material derived from 8q, and an HSR on 11q. However, several apparently discrepant results were also obtained. Paints for chromosomes 3, 5, 7, 8, 11, 12, 14, 17, 22, and X were therefore used to resolve these differences. Our results demonstrate that CGH detected chromosome abnormalities associated with acute myeloid leukemia and that CGH provided information that was not obtained by G-banding analysis alone. These data suggest that CGH may prove a useful adjunct to conventional cytogenetic and molecular analysis of hematologic malignancies.
Acute Disease↗
A recombination event that redefines the Huntington disease region.
We report both a recombination event that places the Huntington disease gene proximal to the marker D4S98 and an extended linkage-disequilibrium study that uses this marker and confirms the existence of disequilibrium between it and the HD locus. We also report the cloning of other sequences in the region around D4S98, including a new polymorphic marker R10 and conserved sequences that identify a gene in the region of interest.
Chromosomes, Human, Pair 4↗