A common cytogenetic abnormality and DNA content alterations in dedifferentiated chondrosarcoma

Article Abstract:

While flow cytometry is useful in screening human cancers for chromosome abnormalities, only karyotyping is the definitive test. Karyotyping requires the growth of living cells from a biopsy or blood sample. The test demands skill and patience, and is generally not suitable for mass screening. Nevertheless, the cases of two patients with dedifferentiated chondrosarcoma illustrate that the karyotype provides information that is not available by other techniques. Chondrosarcomas are the second most common form of bone cancer. They usually affect older patients and generally occur as slow-growing low-grade cartilaginous growths. However, about 10 percent of chondrosarcomas lose their differentiated state (dedifferentiation) and become poorly differentiated aggressive high-grade cancers with a poor prognosis. Fresh chondrosarcoma tissue was obtained from two patients at surgery. Flow cytometric analysis was performed on both specimens; one was found to have the normal diploid chromosome complement, while the other was found to have a pathological aneuploid complement. Karyotyping was performed on cells and revealed abnormalities within the cells of both specimens. While numerous abnormalities were observed in both specimens, the aneuploid specimen was cytogenetically more complex, as would be expected. However, one defect was common to the chondrosarcoma cells from both patients. This common feature consisted of breaks in the short arm of chromosome 1. These breaks revealed themselves as a deletion in one chromosome homolog and recombination in the other. In both patients, the deletion and recombination occurred at the same chromosome band, in the region of 1p36. This same region is lost in neuroblastoma (a malignant cancer that usually affects infants and children) and has been shown to be involved in myxoid chondrosarcoma. It is not yet known if the 1p36 break will prove to be a consistent finding in these tumors. However, the same break occurring in both patients cannot be attributed only to coincidence; investigation of the genes near the 1p36 point is likely to reveal interesting mechanisms of the malignant transformation of cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Usage, Genetic aspects, Flow cytometry, Chromosome deletion, Human chromosome abnormalities, Chondrosarcoma

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The Philadelphia chromosome translocation: a paradigm for understanding leukemia

Article Abstract:

The author, along with Dr. Peter C. Nowell, received the 1989 Charles S. Mott Prize given by the General Motors Cancer Research Foundation. At the prizewinner's lecture series, she reviewed the research on the Philadelphia chromosome, which has provided important insights into the cause of chronic myeloid leukemia, and discussed how this chromosomal abnormality can be considered a paradigm for the understanding of other cancers as well. The Philadelphia chromosome was first observed in 1960 as simply one chromosome which was a bit too small. It was not until the 1970s that improved cytogenetic techniques made more detailed examination of chromosomes possible. Dr. Rowley applied these techniques to the Philadelphia chromosome, and found that it involved a translocation between chromosomes 9 and 22. A small piece from chromosome 9 was translocated to 22, and a piece of 22 was translocated to 9. The effect was most notable on the smaller chromosome 22, which was now noticeably reduced in size. The translocation takes place in a region of chromosome 22 called the breakpoint cluster region, or BCR, simply because no better name is known; the function of this region remains a mystery. It is clear, however, that the translocated piece of chromosome 9 contains a gene for the Abelson protein, or ABL. ABL plays a key role in the regulation of cellular replication, and is an example of what the molecular biologists have termed a proto-oncogene. ABL has been shown to play a role in the development of leukemia in mice. In most people, ABL protein is much smaller than in the cells of patients with chronic myeloid leukemia. The extra length of ABL in these patients seems to be due to BCR genes getting ''tacked on'' to the ABL gene. The net result is an abnormal protein, which apparently functions abnormally as well, ultimately causing leukemia. Although the Philadelphia chromosome is the most widely studied, over 50 chromosome abnormalities have now been associated with leukemia, and further research will no doubt provide new insights into the development of this disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Translocation (Genetics), Chromosomes, Philadelphia chromosome, Myeloid leukemia, Philadelphia-positive, Philadelphia-positive myeloid leukemia

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Favorable cytogenetic abnormalities in secondary leukemia

Article Abstract:

Secondary leukemia occurs in some patients after radiotherapy or chemotherapy for another tumor. In general, secondary leukemia responds poorly to treatment and survival is short. The cells involved in secondary leukemia often show chromosomal abnormalities, frequently involving chromosomes 5 and 7. However, some secondary leukemias have chromosomal abnormalities which may predispose them to a better response to chemotherapy and longer remission periods. These chromosome abnormalities are the same as those which have been observed in a primary leukemia called acute nonlymphoblastic leukemia (ANLL). Five patients were identified who had one of the following chromosome abnormalities that are similar to those observed in ANLL: an inversion of chromosome 16; or translocations of chromosomes 8 and 21, chromosomes 15 and 17, or chromosomes 9 and 11. Four of these five patients previously had solid tumors, and all responded to aggressive chemotherapy; relapses have been observed in two subjects. Unfortunately, follow-up data is limited for three patients, so few conclusions can be drawn from this study alone. However, it appears that cytogenetic analysis is important in cases of secondary leukemia, and that a subset of patients who will respond well to aggressive chemotherapy can be identified. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Cytodiagnosis

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