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It is unclear whether synchronous multiple tumors arise from multicentric or monoclonal origins. To verify the multicentric origin of synchronous colorectal carcinomas at a genetic level, immunohistochemical and molecular techniques were used to determine the p53 alterations in individual lesions of synchronous colorectal carcinomas. This study was based on a total of 32 colorectal tumors from 16 patients. Twenty-one of the 32 (66%) advanced tumors examined had positive staining for p53. Single-strand conformation polymorphism and polymerase chain reaction direct sequencing were carried out for exons 5 to 8 of p53. All cases had p53 mutations in one or more tumors of synchronous lesions. In nine patients in this series, individual lesions were found to carry a different mutated codon of the p53 gene. In the other seven patients, a p53 mutation was found in one tumor but not in another. These results indicate discordance of the mutation pattern of p53 in individual lesions of multiple colorectal carcinomas and support the idea that most synchronous colorectal carcinomas are genetically distinguishable and are multicentric in origin. We also confirmed the high frequency of p53 mutations in left-sided (71%) and rectal (91%) carcinomas, rather than right-sided (43%; P ‫؍‬ .04) carcinomas, suggesting that the molecular mechanism of synchronous colorectal carcinomas might differ between right-and left-sided tumors in the same patient.KEY WORDS: P53, Single-strand conformation polymorphism, Synchronous colorectal carcinomas.Mod Pathol 2000;13(2):131-139

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The findings of the current study suggest that the range of the sarcomatous component may be a prognostic factor in RCC, and the malignant behavior of sarcomatoid RCC is due to high cell proliferative activity and decreased expressions of E-cadherin and alpha-, beta-, and gamma-catenin in the sarcomatous component.

Background and Objectives Sarcomatoid RCC (renal cell carcinoma) is an uncommon, but not rare, neoplasm which has been shown to have a much worse prognosis than common RCC. The current study was designed to investigate the association of proliferative activity and cell‐cell adhesion molecules with sarcomatoid RCC. Methods Proliferative activity (Ki‐67 labeling index) and expression of cell‐cell adhesion associated molecules (E‐cadherin, α‐, β‐, and γ‐catenin, and p120) were examined using immunohistochemical techniques in 11 cases of sarcomatoid RCC. Results In six patients with sarcomatous component more than 50%, five were died within 24 month after diagnosis. The expression of these molecules within the carcinomatous and sarcomatous components of sarcomatoid RCC was compared. The mean Ki‐67 labeling index in the sarcomatous components (12.6%) is statistically higher than in the carcinomatous components (3.7%) (P < 0.05). The expressions of E‐cadherin, and α‐, β‐, and γ‐catenin were statistically decreased in the sarcomatous components compared to the carcinomatous components. However, no differences were observed regarding p120 immunostaining. Conclusions The findings of the current study suggest that the range of the sarcomatous component may be a prognostic factor in RCC, and the malignant behavior of sarcomatoid RCC is due to high cell proliferative activity and decreased expressions of E‐cadherin and α‐, β‐, and γ‐catenin in the sarcomatous component. J. Surg. Oncol. 2001; 77:123–131. © 2001 Wiley‐Liss, Inc.