In chronic inflammatory diseases, cells are recruited but may also derive from local proliferation. In normal bronchial epithelium, under 5% of cells are in cycle but in asthma and chronic bronchitis, proliferation may occur. Cycling cells can be identified by immunohistochemistry using PC10 monoclonal antibody (Proliferating Cell Nuclear Antigen, PCNA). We enumerated PCNA-positive cells (labeling index = LI) in bronchial biopsies of 11 healthy non-smokers (HNS), seven healthy smokers (HS), 30 non-smoking asthmatics (NSA), six smoking asthmatics (SA) and 18 chronic bronchitics (CB). Twenty non-small cell lung cancer patients were used as positive control subjects. Ciliated and secretory cells were PCNA-negative. Basal cells were PCNA-positive in one of the 11 HNS (LI = 0.18 +/- 0.60), none of the seven HS, two of the 30 NSA (LI = 0.05 +/- 0.20), two of the six SA (LI = 2.4 +/- 4.3) and 11 of the 18 CB (LI = 12 +/- 20). In smokers, PCNA positivity correlated with tobacco consumption (Rho = 0.62, p < 0.0008) and in patients with chronic bronchitis, with the degree of metaplasia (tau = 0.815, p < 0.0001). The submucosa of most subjects showed no PCNA immunoreactivity. These findings suggest that the bronchial mucosa of nonsmokers is not hyperproliferative, even in asthmatics. Tobacco smoking increases PCNA immunoreactivity, possibly leading to the metaplasia of chronic bronchitis.
Prostaglandin H synthases or cyclooxygenases 1 (PGHS-1) and 2 (PGHS-2) catalyze the conversion of arachidonic acid to prostaglandin endoperoxides, leading to the formation of prostaglandin and thromboxane mediators of inflammation. The expression of these enzymes in the respiratory epithelium has not been determined, although they may be relevant to the pathophysiology of inflammatory disorders such as asthma and chronic bronchitis (CB). We studied PGHS-1 and PGHS-2 immunoreactivity in bronchial biopsies obtained from 22 patients with chronic stable asthma, seven patients with CB, and 12 normal subjects. Both types of PGHS were mainly expressed in the epithelium (basal and ciliated cells), and PGHS-1 and PGHS-2 were found in 21 of 41 and 34 of 41 biopsies, respectively. We did not find any differences in PGHS expression between the patient populations. There were no correlations between any of the clinical parameters studied or the pathologic patterns and the presence and characteristics of the PGHS immunoreactivities. Thus, both PGHS enzymes are expressed in normal human respiratory epithelium and are not quantitatively upregulated in the main bronchi in stable asthma and CB.
Aims-Interleukin 6 (IL-6) is expressed in the majority of renal cell carcinomas and has an important role in the proliferation of some renal cell carcinoma cell lines. This action is mediated by two membrane proteins, gp8O (the IL-6 receptor; IL-6R), which binds IL-6, and gpl30, which transduces the signal. The soluble form of gp80 (sIL-6R) is able to activate gpl30 when complexed to the IL-6 molecule. These considerations prompted an investigation of IL-6R expression in this malignancy. IL-6, C reactive protein (CRP), and sIL-6R were also measured in serum and correlated to clinical and pathological features. Methods-Immunostaining was performed on cryostat sections from renal cell carcinoma tumours with M91, an anti-IL-6R monoclonal antibody, using the alkaline phosphatase antialkaline phosphatase technique. The proliferation index was measured using the KI-67 monoclonal antibody. CRP, IL-6, and sIL-6R were measured in serum before nephrectomy, using an immunoenzymatic or immunoradiometric assay. Results-There were significant differences in survival in patients with tumours larger than 8 cm, metastasis at diagnosis, high nuclear grade tumours, detectable serum concentrations of IL-6 (correlated to CRP serum concentration), more than 4% proliferating cells, and the presence of the IL-6R in situ. Furthermore, the serum IL-6 concentration correlated with tumour size and stage. The mean serum sIL-6R concentration was not significantly different from that observed in 40 normal subjects. Tumour IL-6R expression was present in 10 samples. There was a significant association between the presence of the IL-6 receptor in tumours and tumour stage, nuclear grade, proliferation index, and serum IL-6.Conclusions-This study revealed the importance of IL-6/CRP and IL-6R expression in situ as potential new prognostic factors and opens the way to new therapeutic strategies in renal cell carcinoma. (7 Clin Pathol 1997;50:835-840)
The purpose of this study was to immunocytochemically investigate two new markers, the sigma-1 receptor and the human sterol isomerase (hSI), in comparison with a series of clinicopathological and immunocytochemical prognostic factors in a trial including 95 patients with operable primary breast cancers. Our results showed no statistically significant relationship between these two markers and the age of the patients, their menopausal status, the tumour size and its histological grade, the nodal status and the expression of the Ki-67 proliferative marker. However, we evidenced a close correlation between the sigma-1 receptor expression and the hormonal receptor positivity ( P = 0.008), essentially due to a link with the progesterone receptor status ( P = 0.01). By contrast there was an inverse relationship between hSI expression and the oestrogen receptor and/or progesterone receptor positivity ( P = 0.098). A significant relationship was shown between both the sigma-1 receptor, hSI expressions and Bcl2 expression, with P = 0.017 and 0.035 respectively. We also assessed whether the expression of the sigma-1 receptor or hSI might be linked with disease-free survival (DFS) and found that the presence of hSI and the absence of sigma-1 receptor expression were associated with a poorer disease-free survival ( P = 0.007). Altogether these results suggest that in primary breast carcinomas in association with the evaluation of the steroid receptor status, the sigma-1 receptor and hSI may be interesting new markers useful to identify those patients who might be able to benefit from an adjuvant therapy. © 2000 Cancer Research Campaign
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