We report the sublocalization of the breakpoint in chromosome 22 in 33 patients with chronic myeloid leukemia (CML) who also had unusual marrow cytogenetics. In 23 patients, the leukemic clones were characterized by Philadelphia (Ph1) chromosomes that arose through complex translocations that involved three or more chromosomes. In the remaining ten patients, there were no detectable Ph1 chromosomes despite molecular evidence for the presence of rearrangements in the major breakpoint cluster region (bcr) of chromosome 22 in all cases. There was no significant difference between the two groups with respect to location of the breakpoints within the bcr. When these two groups of patients were combined, there was a significant excess of breakpoints in one segment of the bcr when compared to the distribution of breakpoints seen in 119 patients with simple 9;22 translocations. The difference in breakpoint distributions did not appear to be entirely attributable to differences between groups in disease duration at the time of study. These data support the notion that the unusual genetic recombinations that give rise to BCR/ABL fusion genes in CML involve specific DNA sequences of BCR (and possibly ABL) and additional, recombinogenic sequences, at least some of which are present in loci known to be nonrandomly involved in complex Ph1 translocations.
Summary. The sensitivity of the standardized partial thromboplastin time technique in detecting circulating heparin during low‐dose calcium heparin prophylaxis in gynaecological surgery has been evaluated and compared with an anti Xa assay and a chomogenic substrate method. The PTT test and anti Xa test were performed daily on plasmas from eight control and seven heparin treated patients. Both the PTT and anti Xa test showed significant prolongation in heparin‐treated patients receiving the 5000 units regime 12‐hourly. In control patients the PTT test showed a significant shortening, maximal on the fifth day after operation. This interferes with the detection of heparin by the PTT during this period. Nevertheless, the effect of small concentrations of heparin is observable during low‐dose prophylaxis by its prevention of the post‐operative acceleration of the PTT test. By contrast, the anti Xa test is relatively unaffected by the post‐operative acceleration and is more prolonged by the low‐dose heparin therapy.
The heparin levels in 17 plasmas from gynaecological surgical patients receiving low‐dose therapy were determined by PTT, anti‐Xa and chromogenic substrate. The chromogenic substrate and anti Xa assays showed reasonably good intra‐class correlation. Heparin levels determined by the PTT test were invalidated by the post‐operative acceleration of the test. If, however, this post‐operative acceleration is of clinical significance and relates to a prethrombotic state, its detection by the PTT may be important and may be a valuable indicator for the need for an increase of the heparin dosage. Unless it is shown that the anti Xa effect of heparin is of more importance in the prevention of thrombosis than the prolongation of the PTT, the standardized PTT appears to offer a simple method of control of low‐dose heparin administration.
A method of cold-shock synchronization of immature granulocytic cells from peripheral blood or bone marrow is described. It is shown that this method provides an increased yield of early metaphases and offers advantages over others currently employed. The peaks of mitotic activity following the cold-shock treatment differ for patients with acute nonlymphoblastic leukemia (ANLL) and patients with chronic myeloid leukemia (CML) by an interval of 2 h. This method is considered to be suitable for routine cytogenetic studies on hematological patients.
Recent suggestions of a correlation between the extent of acquired deletions of the long arm of chromosome 5 [del(5q)] in association with myelodysplastic syndromes and acute non-lymphoblastic leukemia, and the morphological features, prompted us to review 34 patients with these conditions and del(5q). We found no correlation between the morphological diagnosis with which the patient presented and the extent of the deletion of 5q. All cases showed involvement of band 5q31, in common with most previously reported series. The consistent involvement of 5q31 is in keeping with the concept that a single gene at band 5q31 may be involved in the pathogenesis of these myeloid clonal expansions and that the deletion of genes in the long arm of chromosome 5, known to be involved in hemopoietic growth regulation, is unlikely to be the principal determinant of the hematological disorder.
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