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Ki‐S1 and PCNA expression in erythroid precursors and megakaryocytes—A comparative study on proliferative and endoreduplicative activity in reactive and neoplastic bone marrow lesions
Author(s) -
Thiele Juergen,
Bertsch Hans Peter,
Kracht Lutz Walter,
Anwander Thomas,
Zimmer Joerg Detlef,
Kreipe Hans,
Fischer Robert
Publication year - 1994
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711730103
Subject(s) - proliferating cell nuclear antigen , bone marrow , biology , pathology , myeloid , immunostaining , polycythemia vera , cell cycle , erythropoiesis , ki 67 , neoplastic transformation , staining , immunohistochemistry , cancer research , cell , immunology , medicine , carcinogenesis , cancer , biochemistry , anemia , genetics
The monoclonal antibody Ki‐S1 reacts with a cell proliferation‐associated nuclear antigen which is expressed in the G1 through G2/M phases of the cell cycle and is resistant to formalin fixation. We have studied Ki‐S1 and PCNA (PC10) immunostaining of erythroid precursors (proliferative activity) and megakaryocytes (endoreduplicative activity) in bone marrow trephine biopsies in a variety of reactive and neoplastic lesions using double immunohis‐tochemistry to identify both cell lineages. A significant increase in Ki‐S1 labelling compared with PCNA positivity was found in all conditions studied. In particular, specimens derived from secondary polycythaemia (SP), polycythaemia vera (P. vera), and primary osteomyelofibrosis (OMF), and from splenic tissue with myeloid metaplasia (MM), revealed a disproportionally high labelling index of erythropoiesis, which was not present in chronic myelogenous leukaemia (CML), AIDS, and autoimmune (idiopathic) thrombocytopenia (ITP). Enhancement of Ki‐S1 (PCNA) staining in SP and P. vera is in keeping with the relevant increase in erythroid precursor proliferation, but in OMF and MM there is overexpression of both proliferation markers, possibly due to secondary folic acid deficiency, which is known to cause a block in the S‐phase of the cell cycle. A significant correlation was observed between the sizes of megakaryocytes and their nuclei with Ki‐S1 (and also PCNA) staining. Ki‐S1 (and PCNA) labelling of predominantly smaller elements of this lineage supports a hypothesis that the phases of the cell cycle have different durations in the various steps of polyploidization, with a prolongation of G1/G2 at higher ploidy levels. A considerable number of large to giant (hyperpolyploid) megakaryocytes may have reached the end stage of endoreduplicative activity (Ki‐S1‐/PCNA‐negative GO phase). A comparative evaluation of these two proliferation markers adds significantly to our understanding of cell kinetics in erythro‐ and megakaryo‐poiesis, and sheds some light on the biological behaviour of these cell lineages in various disorders.