Viggo Jønsson¹, Geir E. Tjønnfjord², Tom B. Johannesen³, Sven Ove Samuelsen⁴ and Bernt Ly⁵

¹Department of Hematology, Aker University Hospital, University of Oslo, Norway. ²Department of Hematology, Rikshospital and Radium Hospital, University of Oslo, Norway. ^3,5The National Norwegian Cancer Registry, Oslo, Norway. ⁴Department of Biostatistics, Faculty of Mathematics, University of Oslo, Norway.

Abstract

Based on the concept that the tumorogenesis in chronic lymphocytic leukaemia comprises both an initial, inherited mutation and subsequent somatic mutations, the pleiotypic diversity of familial chronic lymphocytic leukaemia and related malignant lymphoproliferative disorders is generally explained by a repertoire of monoallelic polygenes in the initial mutation. Epigenetic genomic imprinting is a likely mechanism behind of the asynchroneous replicating monoallelic polygenes which is discussed in the light of pleiotrophy and birth order effect. Furthermore, it is discussed that one possible mechanism available for the epigenetic transfer of these genes could be the physiological pregnancy-related microchimerism between mother and fetus.