These data suggest that antibodies directed against the gamma2 chain of laminin-5 can identify cervical lesions with invasive capacity and thus may be useful as a sensitive marker of early invasion.

Aberrations of 13q occur frequently in prostate cancer and this chromosome contains two known tumor suppressor genes, BRCA2 and Rb1. This study analysed 13q LOH, DNA ploidy, BRCA2 mutation and pRb expression in prostate cancers. In total, 13q deletions were found in 18 of 36 tumors but did not correlate with histological grade, stage or DNA ploidy. Two smallest regions of overlapping deletions were de®ned: one¯anked by D13S218 and D13S153; the other¯anked by D13S31 and D13S137. BRCA2 was less frequently deleted whereas Rb1 did have a high frequency of deletion. None of the two genes was located in any of these two regions. Furthermore, BRCA2 mutation was not found in the ®ve tumors where deletions had involved the BRCA2 locus. Neither did the Rb1 deletion correlate with absent pRb expression. In addition, tetraploidy was found in 14 out of 25 tumors analysed and correlated with aberrant pRb expression. Our results indicate that 13q deletion is an early non-random event. Tumor suppressor genes other than BRCA2 or Rb1 may be the target of 13q deletions. Aberrant pRb expression may not re¯ect the two-hit Rb1 inactivation but may be involved in the tetraploidization of prostate cancer cells.

Assessment of the malignant potential of parathyroid tumors in the absence of metastases can be difficult using morphologic criteria alone. In this study we have examined a total of 58 parathyroid tumors (31 benign, 15 malignant, and 12 equivocal) from 54 patients using immunohistochemistry with monoclonal antibodies directed against the retinoblastoma (RB) protein and the cell cycle-associated antigen Ki-67 to evaluate their role as diagnostic markers. RB protein immunoreactivity was not useful for distinguishing between benign and malignant parathyroid tumors. Analysis of the proliferation marker Ki-67 showed that there was a trend toward more intense staining in the malignant cases. The Ki-67 labeling index was highest in the parathyroid cancers (median 33) and lowest in the sporadic primary adenomas (median 2). An observation that might have clinical implications is that tumors from patients with familial hyperparathyroidism linked to chromosome 1q showed a high Ki-67 index, indicating strong proliferative activity (median 25). This correlates well with the clinical observation of tumors with malignant potential in this syndrome. Because of the considerable overlap between groups of tumors, Ki-67 is not suitable for definitive differentiation between benign and malignant tumors. However, Ki-67 may give valuable information about which patients should be followed more closely.;1999>

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We have investigated p53 expression in 178 thyroid tumors from 162 patients by immunohistochemistry using two antibodies, DO1 and CM1. In addition, 35 tumors were analyzed for expression of WAF1/p21, one of the downstream mediators of p53. Only 15 tumors (8.4%) had greater than 10% of tumor cell nuclei positively stained for p53. Six of 14 Hürthle tumors and three of 34 papillary thyroid carcinomas showed staining of p53 in the cytoplasm. A total of 40 tumors, including all p53 positive tumors, and all anaplastic and poorly differentiated tumors were screened for mutations in exons 5-8 of the TP53 gene by constant denaturing gel electrophoresis and subsequent sequence analysis. A mutation was detected in five tumors only: one anaplastic carcinoma, one poorly differentiated follicular carcinoma (negative by p53 immunohistochemistry), one atypical follicular adenoma, and two papillary thyroid carcinoma metastases, of which the primary tumors had no detectable mutation. We conclude that p53 immunohistochemistry cannot be used for diagnostic and prognostic purposes in thyroid tumors. The tumors with TP53 mutation showed a markedly reduced WAF1/p21 expression. Three anaplastic carcinomas with highly expressed p53, but with no detectable mutation, also showed high expression of WAF1/p21. This may be explained by overexpression of wild-type p53, possibly due to the patients' preoperative treatment, including external radiation of the neck region. The results indicate that WAF1/p21 immunohistochemistry contributes to the information of the functional status of p53, and may facilitate the interpretation of results from p53 immunohistochemistry in these tumors.