PLK (polo-like kinase), the human counterpart of polo in Drosophila melanogaster and of CDC5 in Saccharomyces cerevisiae, belongs to a family of serine/threonine kinases. It is intimately involved in spindle formation and chromosome segregation during mitosis. The purpose of this study was to determine whether PLK1 is overexpressed in primary colorectal cancer specimens as compared with normal colon mucosa and to assess its relation to other kinases as a potential new tumor marker. In the present study, immunohistochemical analyses were performed of PLK1 expression in 78 primary colorectal cancers as well as 15 normal colorectal specimens. Furthermore, we examined the relationship between other kinases, Aurora-A and Aurora-C, and PLK1 expression. In normal colon mucosa, some crypt cells showed weakly positive staining for PLK1 in 13 out of 15 cases, the remaining cases being negative. Elevated expression of PLK1 was observed in 57 (73.1%) of the colorectal cancers, statistically significant associations being evident with pT (primary tumor invasion) (P = = = =0.0006, Mann-Whitney U test), pN (regional lymph nodes) (P = = = =0.008, χ χ χ χ 2 test) and the Dukes' classification (P = = = =0.0005, MannWhitney U test). Mean proliferating cell nuclear antigen-labeling index was 52.3%, with a range of 24.1% to 77.3%. Values for lesions with high and low PLK1 expression were 54.7 ± ± ± ±10.3% (mean ± ± ± ±SD) and 45.9 ± ± ± ±11.9% (P = = = =0.002, Student's t test). PLK1 was significantly associated with Aurora-A, but PLK1 staining was more diffuse and extensive than for Aurora-A or Aurora-C. Interestingly, PLK1 overexpression was significantly associated with p53 accumulation in colorectal cancers. Our results suggest overexpression of PLK1 might be of pathogenic, prognostic and proliferative importance, so that this kinase might have potential as a new tumor marker for colorectal cancers. (Cancer Sci 2003; 94: 148-152)

We have demonstrated that the dynamic study for breast lesions by magnetic resonance imaging(MRI)can differentiate benign from malignant lesions objectively.The cases were 57 histopathologically appraised breast lesions, including 20 cases of breast cancer, 28 cases of mastopathy, 8 cases of fibroadenoma and 1 caseof intraductal papillomatosis. We plotted time-signal intensity ratio curves and then determined 95% confidence intervals, plotting the signal intensity ratio for both breast cancer and mastopathy every 30 seconds during dynamic magnetic resonance mammography(MRM)after gadolinium-diethylenetriamine pentaacetic acid(Gd-DTPA)administration, and further established cut-off points to differentiate between them. We then tried of estimate objectively the benign-malignant differentiation to breast lesions by confirming their signal intensity ratio to be more or less than the cut-off points. We advocate this procedure, and call it the " dynamic ratio method. " As a result, we found highly significant differences between breast cancer and mastopathy at 30 and 60 seconds after Gd-DTPA administration(P < 0.0001). We also confirmed that the cut-off point for the dynamic ratio method was equivalent to 1.4 and 1.8 times the precontrast signal intensity value at30 and 60 seconds after administration of Gd-DTPA respectively. By performing this dynamic ratio method preoperatively we can assess objectively not only the malignancy of breast lesions, but also neighboring infiltration, extending intraductal component, and lymph node metastasis. Furthermore, the dynamic ratio method provides detailed information for selecting the appropriate region for breast conserving surgery preoperatively, and can be expected to reduce unnecessary biopsies of benign cases. The dynamic ratio method had a sensitivity of 95.0%, a specificity of 81.1% and a positive predictive value of 73.1%. Also, for detectinginvasive ductal carcinoma, the sensitivity of the dynamic ratio method was 100.0%.

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