Summary The role of β‐catenin in epithelial neoplasms has been widely studied whereas current knowledge regarding β‐catenin gene and protein expression in bone marrow cells derived from normal haematopoiesis and clonal haematological disorders is lacking. β‐Catenin gene expression was quantitatively investigated in bone marrow cells derived from clonal haematological disorders [acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL), Philadelphia chromosome‐positive chronic myeloid leukaemia (Ph+ CML], Ph− myeloproliferative disorders, n = 96) compared with non‐neoplastic haematopoiesis (n = 33) by real‐time reverse transcription polymerase chain reaction. Cellular localization of β‐catenin protein was detected by immunocytochemistry. β‐Catenin gene expression was significantly increased in AML compared with ALL cases (P < 0·0001), Ph+ CML (P < 0·0001) and non‐neoplastic haematopoiesis (P = 0·019). Immunocytochemistry revealed that, in non‐neoplastic haematopoiesis, the granulopoietic lineage as well as megakaryocytes showed membranous and cytoplasmic staining to various degrees along with unlabelled nuclei. Besides haematopoiesis, β‐catenin prominently marked bone marrow vascularity and diverse stroma cells. β‐Catenin gene was inversely expressed in AML and ALL with a lack of protein expression in neoplastic cells in ALL. In contrast, the other haematological disorders under study, except for Ph+ CML, did not show significant alterations of overall β‐catenin gene expression compared with normal bone marrow. These data suggest different regulatory mechanisms in the expression and function of β‐catenin in haematopoietic cells.

Fli-1 is rather constitutively expressed by bone marrow cells in Ph(-) CMPD independent of the underlying JAK2 status. The overall stronger labelling for Fli-1 in megakaryocytes in Ph(-) CMPD most likely reflects the degree of polyploidisation but aberrant activation of nuclear target genes can not be excluded.

Summary.Little is known about the expression of the polycythaemia rubra vera-1 (PRV-1) gene in bone marrow cells. To determine the expression level of PRV-1 in the bone marrow, we analysed PRV-1 quantitatively in Polycythaemia vera, other chronic myeloproliferative disorders, and reactive states. We demonstrated that PRV-1 was constitutively expressed in both myeloproliferative and reactive states. We concluded that, rather than an upregulation of the PRV-1 gene in the clonal haematopoiesis of polycythaemia vera, a failure to downregulate PRV-1 in granulocytes emigrating from the bone marrow might be responsible for the increase of transcripts in peripheral cells.