Landberg, G. & Roos, G. The cell cycle in breast cancer. APMIS 105: 575-589, 1997. Breast cancer is a heterogeneous disease regarding morphology, invasive behavior, metastatic capacity, hormone receptor expression and clinical outcome. For prediction of prognosis, tumor cell kinetics is an important feature, traditionally evaluated by estimation of cell growth-associated parameters such as mitotic index, S-phase fraction and expression of proliferation coupled proteins, for example proliferating cell nuclear antigen (PCNA) and Ki-67 antigen. Recent data indicate that deregulation of the cell cycle can occur at different levels in cancer and that the "deregulation pattern" can be of clinical significance. In the present overview we give a short description of approaches used for cell proliferation assessments, whereafter more recent data on cell cycle deregulation are discussed. Alterations of importance in breast cancer include overexpression of cyclins D1 and E, down-regulation of cyclindependent kinase inhibitors, such as p16, and inactivation of the retinoblastoma and p53 tumor suppressor proteins.

Homogenates of highly purified polymorphonuclear leucocytes and of a mixture of mononuclear leucocytes and platelets from human blood were separated by differential and isopyknic centrifugation. A heterogeneity in granules containing digesting enzymes was found in both cell preparations. Enzymes typical of lysosomes were found in the two cell preparations in a similar density range. Granules of low density were indicated in polymorphonuclear leucocytes by alkaline phosphatase. In both cell preparations a third granule, of lower density, seemed to exist enriched in amino acid naphthylamidase, acid hydrolases and in polymorphonuclear leucocytes also alkaline phosphatase and lysozyme. A remarkable difference between the two cell preparations was the occurrence of amino acid napthylamidase in denser granules of polymorphonuclear leucocytes only, although the nature of these granules could not be determined.