The role of E-cadherin expression in non-small cell lung cancer.

The purpose of this study is to evaluate the clinical significance of E-cadherin expression in lung cancer. E-cadherin expression was detected by immunohistochemistry using a monoclonal antibody (HECD-1). Strongly positive (++) E-cadherin tumors were classified as a type of preserved E-cadherin expression (Pr type), while the others (+, - tumors) were classified as a type of reduced E-cadherin expression (Rd type). The frequency of Pr type in squamous cell carcinomas (59.0%) was higher than Rd type. However, in adenocarcinomas, the frequency of Rd type was higher than Pr type. E-cadherin expression pattern was significantly correlated with differentiated state (Pearson correlation coefficient 0.394, p<0.001). E-cadherin expression of well-differentiated tumors was more frequently preserved than that of poorly differentiated tumors (60.0% vs. 25.9%). With regard to the correlation between E-cadherin expression and stages of lymph node metastasis in non-small cell lung cancers, the percentage of tumors with Pr type E-cadherin expression declined from 66.3% (< or = N1) to 38.6% (> or = N2), indicating that loss of E-cadherin expression is responsible for acquisition of invasive potential of lung cancer as well as the possible role of E-cadherin in the histological differentiation of lung cancer.

Clinical improvement and immunohistochemical findings in severe atopic dermatitis treated with interferon gamma.

BACKGROUND: Several clinical studies have focused on the therapeutic effects of interferon gamma (IFN-gamma) in patients with severe atopic dermatitis (AD), although the dosage of recombinant IFN-gamma (rIFN-gamma), therapeutic schedule, and the degree of clinical improvement were different among studies. Although the exact mechanism of action of IFN-gamma therapy in AD is not clear, the beneficial effects of IFN-gamma have been attributed mainly to an immunomodulating effect on the expression of certain immunologic markers. OBJECTIVE: Our purpose was to study the therapeutic effect of two different dosages of rIFN-gamma on AD and to investigate the change of lesional expression of infiltrating inflammatory cell markers associated with rIFN-gamma therapeutic efficacy. METHODS: Fifty-one patients with severe recalcitrant AD were treated with rIFN-gamma. Twenty patients were treated with 0.5 x 10(6) IU/m(2) of rIFN-gamma (low-dose [LD] group); 21 patients received 1.5 x 10(6) IU/m(2) of rIFN-gamma (high-dose [HD] group); and 10 patients received placebo. The patients were injected subcutaneously 3 times a week for 12 weeks. Immunohistochemical study was performed in 20 patients of the HD group in the initial visit and after completion of rIFN-gamma therapy with a panel of 14 monoclonal antibodies as markers of inflammatory cells and cytokines. RESULTS: The disease severity of the 2 groups treated with rIFN-gamma was reduced significantly at the end of treatment compared with that of the placebo group (P<.05). More rapid clinical improvement and more effective treatment outcome were seen in the HD group than in the LD group for the initial 6-week treatment period; however, the clinical improvement in both of the treated groups was stable and maintained after week 8 of treatment. Immunohistochemical findings showed statistically significant reduction in the lesional expression of CD25 and EG2 cells that infiltrated into skin after rIFN-gamma therapy. CONCLUSION: This study demonstrated that rIFN-gamma therapy for AD is safe and effective. In the early phase of therapy, a higher dosage of rIFN-gamma is more effective; and for the maintenance of clinical improvement, a lower dosage of rIFN-gamma is recommended when high cost and effectiveness of rIFN-gamma are considered. The therapeutic efficacy of rIFN-gamma in AD might be in part related to the decreased number of CD25(+) and EG2(+) inflammatory cells infiltrated into skin.

Head and neck dermatitis: the role of Malassezia furfur, topical steroid use and environmental factors in its causation.

The aetiology of head and neck dermatitis (HND), one subgroup of postpubertal atopic dermatitis (AD), is still unclear. The aim of this study was to evaluate the influence on HND of common environmental factors, long-term topical steroid use, and the role of Malassezia furfur infection. Relevant information was obtained from 100 patients with HND attending our dermatology clinic by means of both physical examinations and questionnaires. Corticosteroid-induced vasoconstriction was estimated by visual scoring of laser-Doppler flowmetry. and the following immunological studies were performed: skin prick test, measurement of total IgE, eosinophil cationic protein, and specific IgE antibodies to several fungal antigens including those of M. furfur. The questionnaire revealed that sweating (81%), heat (71%), dryness (70%), psychic stress (67%), and sun exposure (50%) were responsible for aggravation of skin lesions. The vascular response to topical steroid was reduced in HND patients as compared with that of normal healthy controls (P < 0.05). Fifty-four of 80 patients with HND (68%) had anti M. furfur-specific IgE antibodies and 36 of 80 patients (45%) showed positive skin prick tests for M. furfur. The clinical severity and serum total IgE of HND patients were higher in patients with positive response to anti-M. furfur-specific IgE antibodies than in patients with negative response (P < 0.05). These results suggest that HND can be aggravated not only by M. furfur but also by environmental factors such as sweating, heat, dryness, psychic stress and sun exposure. Furthermore, long-term use of topical steroid might be associated with the development of diffuse erythematous lesions with telangiectasia on the head and neck areas.