Abstract
The hypothesis is advanced that abnormalities of the chromosome group 17,18 play a special role in the genesis and/or evolution of some reticuloendothelial neoplasms. Aberrations of the group 17,18 chromosomes in tumour cells exceed in variety the reported anomaliesof any other chromosome. Both the frequency of these aberrations and their nature make them most unlikely to be due to chance. They appear to be non-random, often occurring in every cell of a tumour, and like the Ph1 anomaly in chronic granulocytic leukaemia, mightpossess aetiological significance. The Ep- and Eqchromosomal anomalies resemble the Ph1 in being fine structural modifications, which occur as acquired lesions only in neoplasms, often in tumour cells with otherwise normal karyotypes.
Aberration of the group 17,18 chromosomes may sometimes be secondary to neoplasia but nevertheless of evolutionary significance for the tumour cells. Changes leading to relative or absolute excess of long-arm material of chromosome 18 may confer survival advantage upon cells, particularly if a normal complement of short-arm material is simultaneously retained. However, specific deletion of the distal part of the long arms of No. 18 may also favour cell survival. The short arms of chromosome 18 may carry genes limiting cell reproduction, while the long arms carry material promoting proliferation. More distally on the long arms, there may be genes which also limit reproduction. Disturbances affecting the balance between these components of the genome may be important in inception of neoplasia or subsequent evolution of tumour cell lines.
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Selected References
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