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Several molecules have been proven to be associated with responsiveness to chemotherapy. A clinical study on the expression of excision repair cross-complementing (ERCC)-1 and class III β-tubulin was conducted in advanced stage non-small cell lung cancer (NSCLC) patients. We investigated 34 resected stage III NSCLC patients treated with induction chemoradiotherapy using carboplatin-taxane. Immunohistochemistry was performed to evaluate the intratumoral expression of ERCC1 and class III β-tubulin. Nineteen tumors (55.9%) were ERCC1-high and 11 (32.4%) were class III β-tubulin-high. There was no correlation between ERCC1 and class III β-tubulin expression (r=0.208). Regarding the pathological effect of induction therapy, the percentage of ERCC1-positive tumor cells was lower in tumors with a major response than in tumors with a minor response (P=0.0851). The percentage of class III β-tubulin-positive tumor cells was significantly lower in tumors with a major response than in tumors with a minor response (P=0.0105). Regarding patient survival, the overall survival was significantly higher in patients with ERCC1-low tumors than in those with ERCC1-high tumors (P=0.0034). The overall survival was also significantly higher in patients with class III β-tubulin-low tumors than in those with class III β-tubulin-high tumors (P=0.0185). Cox regression analysis also demonstrated that ERCC1 (P=0.0467) and class III β-tubulin statuses (P=0.0237) were significant prognostic factors. Co-evaluations of the intratumoral expression of ERCC1 and class III β-tubulin are clinically useful for identifying patient populations responsive to chemotherapy using carboplatin-taxane.

Benign Mesenchymoma of the chest wall is very rare neoplasm. We report a case of the tumor. The patient is a 64 year-old male, whose tumor was removed on 1978. Histologically, the tumor was diagnosed as benign mesenchymoma. However, 8 years after the last operation, the tumor recurred in the right chest wall. The tumor was 4.5 X 4.0 cm in size and was removed smoothly n Nov. 1986. It was composed of fat tissue, blood vessels and smooth muscles. One year and two months later, the patient is alive without recurrence.

To investigate the relationship between intrahepatic bile duct hyperplasia and cholangiocellular carcinoma, 27 patients with cholangiocellular carcinoma (including biliary cystadenocarcinoma) and 303 controls were histologically examined. Livers with cholangiocellular carcinoma were closely associated with hyperplasia (100%), atypical hyperplasia (77.8%), and carcinoma in situ (51.9%). Transition from hyperplasia to atypical hyperplasia, and from atypical hyperplasia to carcinoma, was often observed. In the controls, hyperplasia was frequent in those older than 30 years of age, whereas carcinoma was frequent in patients from 50 to 80 years of age. Of the intrahepatic bile ducts examined, the large duct showed the highest incidence of hyperplasia, atypical hyperplasia, and carcinoma in situ. All 27 cases of cholangiocellular carcinoma originated in, or near, the hilus of the liver. These findings suggest that cholangiocellular carcinoma frequently develops from bile duct hyperplasia.