In order to study adhesion-molecule expression and its consequences for cellular recognition, the presence of adhesion molecules ICAM-1, VCAM-1, VLA-4, LFA-1, alpha, LFA-1 beta, LFA-3, b1-integrin and b3-integrin was studied on specimens from breast tissue by immunohistochemistry and on cells from breast cell lines propagated in vitro. Breastcancer tissue and the breast-cancer cell lines MCF-7, SK-BR-3 and ZR-75-1 showed expression of ICAM-1 and VLA-4 significantly lower than that of benign breast cells or normal breast epithelium. Of various cytokines tested, including recombinant human (rh) interleukin-6 (IL-6), rh tumor necrosis factor alpha (TNF-a), interleukin 2 (IL-2), granulocyte/macrophagecolony-stimulating-factor (GM-CSF), interferon-alpha (IFN-a) and interferon-gamma (IFN-g), only TNF was able to reinduce expression of ICAM-1 on cells from MCF-7, SK-BR-3 and ZR-75-1. Further, the ability of either unstimulated or lymphokine-stimulated killer ( Cellular adhesion has been shown to be mediated by membraneassociated adhesion molecules (Butcher, 1991) and is physiologically important for a series of mechanisms, including morphogenesis (Krotoski et al., 1986), cell migration (Albelda, 1993) and cellular interaction (Hynes, 1992). These are essential for the proper function of immunologic processes (Mackay and Imhof, 1993) and the development of tumor metastases (Behrens, 1993). In the last instance, variation in adhesion-molecule expression influences not only the metastatic cascade, including the destruction of normal cell-cell and cell-substrate cohesion, the penetration of tumor cells into the vascular system and the further spread into distant organs (Frenette and Wagner, 1996), but also the recognition of tumor cells by lytic effector cells (Kushner and Cheung, 1992). Thus, defective regulation of adhesion-molecule expression by tumor cells might play an important role in the evolution of tumors, their metastatic spread and their escape from immunologic surveillance.In the present study, therefore, we investigated the expression of various adhesion molecules, first, on pathohistologic specimens from benign and malignant breast tissue by immunohistochemistry and, later, on various benign and malignant breast cell lines propagated in vitro. Moreover, like Hutchins and Steel (1994), we studied the ability of various cytokines to modulate adhesionmolecule expression on cells derived from breast-cancer lines and the resulting consequences in the context of tumor-cell lysis by native and by interleukin-2-activated (lymphokine-activated killer, LAK*) effector cells. MATERIAL AND METHODS ImmunohistochemistryTissues were snap-frozen and stored in liquid nitrogen and cryostat sections (5-8 µm) were cut for immunohistochemistry and fixed with ethanol/methanol (1:1) for 10 min at room temperature. For immunohistochemistry, the Dako APAAP kit system 40 monoclonal antibodies (MAbs) (Dako, Glostrup, Denmark) was used. Tissue samples were pre-incubated with normal rabbit serum (Sigma, St. Louis, MO) for 20 min. After w...

Lymphedema of the arm is one of the most disabling and serious complications of breast cancer. Apart from tumor infiltration or fibrosis of lymphatic pathways, little is known about factors favoring the development of lymphedema. In the present study, we investigated the impact of rheologic parameters, e.g. red cell aggregation (EA) and plasma viscosity (PV), and of capillary morphology and capillary flow in patients with breast cancer with (n = 18) and without (n = 18) lymphedema. Patients with lymphedema showed a significant increase of red cell aggregation (p < 0.001) that indicates a systemic component of lymphedema and might offer a possibility of prevention and therapy of this condition. A hitherto unclassified protein factor favoring red cell aggregation and lymphedema might be postulated.

Background. Patients with testicular cancer can be cured by cisplatin‐based chemotherapy in many cases. Thus, concern about possible late toxicities of treatment is warranted. Methods. In this investigation, the absolute number of natural killer (NK) cells according to their CD56+ phenotype, NK cell activity, and antibody dependent cellular cytotoxicity (ADCC) were investigated in 29 patients with seminomas or nonseminomatous germ cell tumors (NSGCT) a median of 31 months (range, 5‐73 months) after termination of chemotherapeutic treatment. Results. No difference in the absolute number of NK cells, NK cell activity, and ADCC was found between patients with testicular cancer after either standard poly‐chemotherapy consisting of bleomycin, etoposide, and cisplatin (BEP) or monotherapy with carboplatin and healthy control subjects. When patients were analyzed further using multivariate analysis, a significant (P < 0.05) detrimental influence of BEP polychemotherapy versus carboplatin monotherapy on NK cell activity was found. Moreover, NK cell activity also depended significantly (P < 0.05) on the time elapsed after chemotherapy was administered, but normalized with time. Because the absolute number of NK cells was not affected, is was assumed that polychemotherapy induced a functional defect. In a subanalysis of patients with NSGCTs, metastases at diagnosis resulted in a significant (p < 0.05) and persistent stimulation of NK cell activity but not of ADCC. Conclusion. Cytostatic chemotherapy in patients with testicular cancer did not lead to compromised lytic effector cell function as assessed by NK cell activity and ADCC. However, a short, time‐dependent reduction was found that also depended on the intensity of chemotherapeutic treatment. This finding related to the observation of a long‐lasting stimulus of NK cell activity by initial metastases in patients with NSGCTs. Cancer 1995; 75:539–44.

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