Although chromium has been the most extensively investigated metal with respect to mutagenicity and carcinogenicity, its genetic effects in humans are only partly understood. Our previous study demonstrated that lung cancer from chromate-exposed workers infrequently (20%) displayed p53 gene mutations as well as a particular mutation pattern. In the present study, we examined the replication error (RER) and loss of heterozygosity (LOH) in 38 lung cancers from 28 chromate-exposed workers (chromate lung cancer group) and in 26 lung cancer patients without chromate exposure (non-chromate lung cancer group), using six microsatellite markers containing CA repeats: D3S647 (3p23), D3S966 (3p21.3), D3S1289 (3p21.1), D5S346 (5q21-q22), D9S161 (9p21), and TP53 (17p13.1). The RER phenotype was defined as the presence of microsatellite instability (MSI) at two or more loci. Thirty (78.9%) of 38 tumors in the chromate lung cancer group exhibited RER. In contrast, only four (15.4%) of 26 tumors in the non-chromate lung cancer group exhibited RER. The frequency of RER in the chromate lung cancer group was significantly higher than that in the non-chromate lung cancer group (P < 0.0001). By contrast, the frequency of LOH at 3p, 5q, 9p, and 17p loci in tumors with chromate exposure was not significantly different from that in tumors without chromate exposure. In the chromate lung cancer group, the period of chromate exposure in workers with RER (24.5 +/- 6.7 yr) was significantly longer than that in workers without RER (17.0 +/- 3.5 yr) (P = 0.0046). In addition, a longer period of chromate exposure was associated with a tendency toward a higher frequency of MSI. This finding suggests that MSI may play a role in chromium-induced carcinogenesis. In addition to our previous study of p53 mutations, the present findings suggest that the carcinogenic mechanism of chromate lung cancer may differ from that of non-chromate lung cancer.

In this pilot study computed tomography-guided transbronchial metallic coil marking with an ultrathin bronchoscope with virtual bronchoscopic simulation might be a useful method for the fluoroscopy-assisted thoracoscopic resection of pulmonary nodules.

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BACKGROUND A distinction between noninvasive, invasive, and metastatic thymoma on the basis of the cytologic features is difficult. The current study investigated whether the expression of MMP and TIMP was correlated with tumor invasiveness and prognosis in patients with thymoma. METHODS Tumor tissue samples were obtained from 42 patients with thymic epithelial tumors between 1974 and 2001 at Tokushima University Hospital. Three‐micrometer‐thick, formalin‐fixed, paraffin‐embedded tissue sections were immunostained using specific antibodies against MMP‐2, MMP‐9, TIMP‐1, and TIMP‐2. RESULTS MMP‐2 expression was detected in 30 tumors (71%), and TIMP‐2 expression was detected in 31 tumors (74%). MMP‐9 expression was detected in 22 of 36 tumors (61%), and TIMP‐1 expression was detected in only 7 tumors (19%). MMP‐2 and TIMP‐2 expression levels were very low (10% and 0%, respectively) in noninvasive tumors but were very high (91% and 97%, respectively) in invasive tumors. In thymic epithelial tumors, the more progressive the clinical stage of tumor, the higher the strongly positive rate of MMP‐2 and TIMP‐2 expression. There was no correlation between positivity for MMP‐9 and stage. Twenty‐five percent of Type AB thymomas and 50% of Type B1 thymomas expressed MMP‐2 and TIMP‐2. Most of Type A, Type B2, Type B3, and Type C thymomas expressed MMP‐2 and TIMP‐2. There were significant differences in disease‐free survival at 5 years between patients without and with MMP‐2 expression (91% vs. 55%, respectively) and patients without and with TIMP‐2 expression (100% vs. 53%, respectively). CONCLUSIONS MMP‐2 and TIMP‐2 are key enzymes for invasiveness of thymic epithelial tumors. The expression of these proteins can predict a poor outcome in patients with thymoma. Cancer 2003. © 2003 American Cancer Society.