On the topology of normal chromatids and on their translocations in myelogenous leukemia

After some comments on the topology of chromatids, restructuring of the interphase nucleus is conjectured to depend upon the nuclear vesicle apparatus. These vesicles change the intrinsic shape of chromatids to fit the different topology of the interphase nuclear spheroid. Reciprocal translocations between selected chromatids result whenever the nucleus of malignant cells organizes de novo certain exceptional or emergency differentiation paths. However, the almost unavoidable chimeric genes resulting from these translocations may be less ominous than hitherto suspected. This seems to be the case for chronic myelogenous leukemia, where the bcr-abl chimeric gene lessens the aggressiveness of the primary clone when functioning in the context of myelomonocitic differentiation. Finally, our model estimates the statistical incidences of the bcr-abl chimera. These estimates are found to agree with clinical data better than evaluations from the random mutation theory.