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This paper describes augmented reality visualization for the guidance of breast-conservative cancer surgery using ultrasonic images acquired in the operating room just before surgical resection. By combining an optical three-dimensional (3-D) position sensor, the position and orientation of each ultrasonic cross section are precisely measured to reconstruct geometrically accurate 3-D tumor models from the acquired ultrasonic images. Similarly, the 3-D position and orientation of a video camera are obtained to integrate video and ultrasonic images in a geometrically accurate manner. Superimposing the 3-D tumor models onto live video images of the patient's breast enables the surgeon to perceive the exact 3-D position of the tumor, including irregular cancer invasions which cannot be perceived by touch, as if it were visible through the breast skin. Using the resultant visualization, the surgeon can determine the region for surgical resection in a more objective and accurate manner, thereby minimizing the risk of a relapse and maximizing breast conservation. The system was shown to be effective in experiments using phantom and clinical data.

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In a series of 45 poorly differentiated adenocarcinomas (por) and 7 signet‐ring‐cell carcinomas (sig) of the colorectum, K‐ras gene mutation, p53 immunostaining and microsatellite instability (MSI) were analyzed for a comparison with 46 cases of colorectal carcinomas of the well or moderately differentiated type (well/mod). In addition, the mutations of simple repeated sequences in the transforming‐growth‐factor‐β type‐II receptor (T β R‐II) gene and the BAX gene were analyzed as possible targets for DNA replication errors. Mutation of the K‐ras gene in the por, sig and well/mod specimens was detected in, respectively, 22%, 11% and 48%, positive immunostaining for p53 in 41.8%, 28.6% and 60.3%, and MSI in 36%, 30% and 4%. Frameshift mutation of the T β R‐II gene was detected in 27.5% of the por and none of the sig specimens, while corresponding figures for mutation of the BAX gene were 15.7% and 0%. Significant differences between the por and well/mod tumors were found in the occurrence of K‐ras mutation at codons 12 and 13, and MSI. Clinicopathologically, the tumor status of por with MSI was found to significantly correlate with the tumor's location in the proximal colon. In cases without MSI and sig, no frameshift mutation of either the T β R‐II or the BAX gene was found. These results suggest that poorly differentiated and signet‐ring‐cell carcinomas have a genetic background different from that of well or moderately differentiated carcinomas of the colorectum, and that DNA‐replication error is at least partly involved in the carcinogenesis of these specific types of colorectal carcinomas. Int. J. Cancer (Pred. Oncol.) 84:33–38, 1999. © 1999 Wiley‐Liss, Inc.

Recent studies have shown that the cyclin-dependent kinase (CDK) inhibitor p27^Kip1 represents an indicator for patients’ outcome in several human malignancies including gastric cancer. However, the clinicopathologic value of another class of CDK inhibitor, p16^INK4, has not been determined. In a retrospective study, we examined the expression of p16^INK4 by immunohistochemical assay of 80 samples of primary gastric cancers and their adjacent nonneoplastic mucosas. Less than 10% of non-tumor gastric mucosal cells were p16^INK4 positive, whereas the expression of p16^INK4 in gastric cancer cells varied widely from 0 to 100% (mean, 24.5%). The expression of p16^INK4 was not seen in 11.3% (9/80) of the cancer cases, but in 65% (52/80) this protein was even overexpressed when compared with the nonneoplastic mucosa. A clinicopathologic survey indicated that a low or no expression of p16^INK4 was associated with poorly differentiated carcinoma (p = 0.0133), but the level of expression did not correlate with other parameters including patients’ prognosis or with the expression of the pRb protein. In an effort to explore the underlying mechanism for the p16^INK4-negative cases, a prospective study was also performed on 20 cases of gastric cancer to compare the level of the p16^INK4 protein with the methylation status of the p16^INK4 promoter. Gastric cancer tissues with methylation expressed significantly lower levels of the p16^INK4 protein (p = 0.0013) and two of them lacked p16^INK4 expression altogether, whereas all the cancer tissues without methylation expressed it. These findings suggest that the p16^INK4 protein may be associated with differentiation of gastric cancer tissues and that methylation of the p16^INK4 promoter may, in part, account for the loss of p16^INK4 expression.