Leukaemia cytogenetics / H. Jackson Woodliff.

  • Woodliff, H. Jackson.
Date:
1971
Catalogue details

Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: Leukaemia cytogenetics / H. Jackson Woodliff. Source: Wellcome Collection.

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    78 leukaemia cytogenetics must be distinguished from those due to the disorder itself. The pseudodiploidy found by Goh (1967a) occurred in both untreated patients and treated patients and is therefore reasonably ascribed to the disorder. Radiation damage similar to that seen in polycy- thaemia vera is not uncommon in treated cases of chronic lympho¬ cytic leukaemia but the progression to acute leukaemia seen in the former and attributed by some to radiotherapy has not been seen in chronic lymphocytic leukaemia. However, patients v^ith chronic lymphocytic leukaemia usually survive for a shorter time after radiation than do those with polycythaemia vera. Aetiology and Pathogenesis The cause of chronic lymphocytic leukaemia is unknown and the chromosome studies have so far made little contribution to the understanding of the pathogenesis; however, changes that have been recorded may be significant and two of these need to be considered further, namely the relationship to the G group chromo¬ somes and the occurrence of pseudodiploidy. Since the visible deletions in the G group chromosomes seen in the families studied in Christchurch are uncommon, they are not of general signifi¬ cance but are of possible importance in the family in which they were described in initiating the leukaemic process. Smaller dele¬ tions or condensations of the G group chromosomes which are not ordinarily visible may, however, occur in chronic lympho¬ cytic leukaemia. Fitzgerald (1965a and b) found that the total length of the G group chromosomes was shorter in chronic lympho¬ cytic leukaemia when compared with controls and thought that this may have been due to the greater degree of spiralization and condensation of some small acrocentrics. We have been unable to confirm this important finding in a study using both measure¬ ments of length and area of the G group chromosomes (Woodliff, 1969¿>); this may have been because we were examining cells which were not leukaemic or the methods we used were too insen¬ sitive to pick up any small differences. If Fitzgerald's findings could be confirmed they would provide further evidence connecting the G group chromosomes with leukaemia. If pseudodiploidy is as common in chronic lymphocytic leukaemia cells as suggested by Goh, then this may be significant, in that any aberrations of the chromosomes may be associated with leukaemia. The possibility, however^ remains that all cytogenetic changes are secondary.