A search for double minute chromosomes in cultured lymphocytes from different types of tumors (original) (raw)
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Double-minute chromosomes (DMs) were observed in repeated samples in the leukocytes of a patient with a previous history of cervical carcinoma. The most interesting cytogenetic finding was the coexistence of DMs and a dicentric chromosome along with chromosome- and ehromatid-type breaks and gaps. This observation suggests that DMs might originate through the breakage of existing chromosomes. The presence of DMs in leukocytes may also indicate the possibility that certain common agents cause DMs in tumor cells as well as in normal cells.
Incidence of double minutes, cytogenetic equivalents of gene amplification, in human carcinoma cells
International Journal of Cancer, 1984
Screening of the occurrence of double minutes (DM) was performed in more than I ,OW metaphases obtained from a total of 22 solid human breast tumors and more than 3,600 metaphases from a total of 55 malignant effusions (45 patients with different types of carcinomas). D M were observed in I 5 of these breast tumor cases and in 34 of the effusions (obtained from 29 cancer patients). The percentage of cells exhibiting DM as well as the number of DM per respective cell vaned widely. It could be seen that metastatic cells from malignant effusions exhibited on the average more DM per cell than did cells of primary breast carcinomas. Differences in the incidence of DM could be observed between different carcinomas as well as between different age groups. In addition, it did not appear that D M could be induced by mutagenic tumor therapy. D M are thus not a rare finding in human solid tumors but, as cytogenetic equivalents of gene amplification, they rather represent a fundamental biological characteristic of tumor development.
Double minute chromosomes in an invasive adenocarcinoma of the prostate
Cancer Genetics and Cytogenetics, 1994
Cytogenetic analysis of an uncultured, primary and invasive adenocarcinoma of the prostote showed several clonal abnormalities in a hyperdiploid koryotype, including double minute (drain/ chromosomes. The latter, although sporadic in this type of tumor, were previously reported in two cases ofinvasive prostatic cancer. This anomaly may there~re be associated w/th increased malignant properties.
Cancer Genetics and Cytogenetics, 1991
A consistent degree of chromosome instability was found in cultured lymphocytes and in fibroblasts derived from skin biopsies of three patients with multiple endocrine neoplasia type 1 (MEN1). In both tissues, there was a significant increase in chromasamal breakage. Dicentrics and tricentries, rings, translacations, deletions, acentrie fragments, and presumptive double minutes were the most fl'equent abnormalities in lymphocytes. The fibrablusts of two patients had large clones consisting of trisamy 7 and trisumy 18 cells, respectively.
Double minutes (dmin) are small, paired chromatin bodies that lack a centromere and represent a form of extrachromosomal gene amplification. Although they have been found in a variety of solid tumors, their presence in hematological malignancies, especially acute myeloid leukemia (AML), is rare. In addition, the presence of dmin may be a mechanism for upregulated oncogene expression and is generally associated with a poor prognosis. We describe two patients who had dmin at initial presentation of AML, including the first case of M5a with C-MYC amplification on dmin, and another case with C-MYC amplification as the only cytogenetic finding. We review here a total of 33 cases with dmin in AML. C-MYC was amplified by the dmin in 25 cases, while other putative oncogenes were amplified in the other 8. Am.
Historical Studies in the Natural Sciences, 2014
In this paper I analyze the trajectory of research objects and experiments on tumor cells that led the Swedish geneticist, Albert Levan, through successive collaborations with Theodore Hauschka in Philadelphia (U.S.) and Joe Hin Tjio in Lund (Sweden), from plants to mice and from mice to human chromosomes. Tumor chromosomes were created and recreated in mice bodies by Eva Klein and Georg Klein as ascites—fluid—tumors, whereas human tumors were transplanted from the bodies of cancer patients into mice by Helene W. Toolan. The cultures of cytogenetics and microscopic observation were therefore opened up, from agricultural and botanical research to the clinical laboratory. I suggest it was research on tumors and cancer cells that led to a method for obtaining clear slides, thereby providing evidence of the new number of forty-six human chromosomes, as presented by Tjio and Levan in 1956. Along this research trajectory, the knowledge and practices of cytogenetics were medicalized—a medi...
Journal of Clinical Investigation, 1990
Amplification of oncogenes has been found to be an important prognostic factor in behavior of patients' malignancies. In this study we have used new gel electrophoresis techniques to follow the location of amplified c-myc oncogene sequences in HL-60 promyelocytic leukemia cells. In passages 46-62 of the cells, the cells contain amplified c-myc sequences on submicroscopic circular extrachromosomal DNA (episomes). With increased passages in culture (passages 63-72) the cells lose the episome c-myc sequences with a shift of those sequences to double minutes. With additional passage in culture, the c-myc shifts from the double minutes to a chromosomal site der(5)t(5; 17Xqll.2;q?11.2). Concomitant with the shift of the c-myc sequences into the chromosomal compartment is a phenotypic change of a shortened cell-doubling time. These studies provide the first molecular evidence of a progression from a submicroscopic location for amplified oncogene sequences to a chromosomal location for the amplified sequences. This molecularly documented model can now be used to test various strategies to prevent incorporation of extrachromosomally located oncogene sequences into chromosomal sites. Prevention of integration of the oncogene sequences into chromosomal sites could modulate progression of patients'
Chromosomes and causation of human cancer and leukemia. LIV. Near-tetraploidy in acute leukemia
Cancer genetics and cytogenetics, 1985
The chromosome constitution in marrow cells was determined in 219 cases of acute leukemia, 113 with the myeloblastic and 106 with the lymphoblastic forms. Aneuploidy was found in 50% of the cases; the remaining 50% were diploid. The karyotypes showed remarkable variability from case to case and, except for a small number of cases with group-C trisomy, no consistent or characteristic chromosomal changes were found in acute leukemia. Even though minor variations may appear with time, generally the karyotypes of the leukemic cells showed considerable stability during phases of remission and relapse. Hyperdiploidy characterized the aneuploid lymphoblastic leukemia, whereas the myeloblastic cases may be accompanied by either hypoor hyperidploidy. A statistical analysis revealed that no one chromosomal From the Roswell Park Mcmorial Institute, niiffalo, N.Y. 14203.