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C Kainz

Publications and source records attributed to C Kainz.

165 records · Page 10Linked to original sources

The serum tumor marker M3/M21 in the follow-up of breast cancer patients.

The aim of this study was to evaluate the new serum tumor marker M3/M21 in comparison to CA 15-3, CEA and MCA in the follow-up of breast cancer patients. We investigated 267 serum samples from 35 patients suffering from invasive breast cancer, International Union Against Cancer (UICC) stage pT1 to pT4. Cut-off values for M3/M21, CA 15-3, CEA, and MCA were 25 U/I, 30 U/I, 5 ng/ml and 11 U/I, respectively. Serum tumor marker results were correlated with the results of the clinical and radiological examinations. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of serum CA 15-3, CEA and MCA were 47/85/61/76%, 24/90/55/70% and 39/84/55/73%, respectively. Serum M3/M21 showed a sensitivity of 45%, specificity of 81%, PPV of 73% and NPV of 69%. The combination of CA 15-3 and M3/M21 increased the sensitivity to 55%, with a specificity, PPV and NPV of 83%, 79% and 86%, respectively. CA 15-3 measurements showed a lead time effect in 5 patients, ranging from 3 to 7 (median 4.1) months. The combination of CA 15-3 and M3/M21 provided lead time effects in 7 cases, ranging from 2 to 8 (median 5.7) months. We conclude that the detection of breast cancer recurrence with CA 15-3 is improved by combination with M3/M21.

Antigens, Tumor-Associated, Carbohydrate↗

Numerical chromosomal aberrations in borderline, benign, and malignant epithelial tumors of the ovary: correlation with p53 protein overexpression and Ki-67.

OBJECTIVE: Ovarian tumors of low malignant potential (borderline tumors) have a 5-year survival rate of 69-98%, illustrating that while the prognosis is better than in the typical epithelial carcinoma, a significant number of women still succumb to this disease. The aim of our study was to elucidate the role of numerical chromosomal aberrations in borderline tumors of the ovary in comparison with benign and malignant epithelial tumors in an effort to develop parameters to differentiate prospectively borderline lesions from benign and invasive tumors. METHODS: Cytologic imprints of surgical specimens of 46 ovarian tumors of low-malignant potential, 17 invasive epithelial carcinomas of the ovary, and 18 benign epithelial tumors of the ovary were examined for numerical chromosomal aberrations (trisomy 7, trisomy 12, and trisomy 17) by fluorescence in situ hybridization (FISH). RESULTS: In benign tumors no evidence of trisomy 7 and 17 was present. Trisomy 12 was detected in six cases (33.3%). We did not find p53 protein overexpression in any case. Ki-67 stained positive in three cases (16.7%). In borderline tumors trisomy 12 was detected in 33 patients (71.7%). Numerical aberrations of chromosome 17 were absent in all cases. Fourteen patients (30.4%) showed trisomy 7. No immunohistochemical staining reaction for p53 protein was found. Staining of the proliferation marker Ki-67 was observed in two cases (4.3%). In malignant epithelial tumors of the ovary, trisomy 7, trisomy 12, and trisomy 17 were detected in 14 (82.3%), 11 (64.7%), and 5 (29.4%) cases, respectively. Four tumors (23.5%) showed immunohistochemically detected p53 protein overexpression. Thirteen tumors (76.5%) stained for Ki-67. CONCLUSION: Our results indicate that trisomy 7 argues against benign disease. Trisomy 17 was specific for invasive disease, while trisomy 12 is common in borderline tumors of the ovary.

Adult↗

Prostate specific antigen (PSA) in breast and ovarian cancer.

Prostatic specific antigen (PSA) is commonly used for the diagnosis and monitoring of prostatic adenocarcinoma, and has recently been detected in breast cancer and it is also thought to be produced by ovarian cancer. To examine the prognostic value of PSA tumor expression, we investigated the tumor cytosols of 26 patients with breast cancer and of 16 women with ovarian cancer. We used a chemiluminescence immunoassay for the quantitative determination of PSA (detection limit 0.003 ng/ml). The median PSA level in breast cancer patients was 0.31 ng/mg (minimum 0.003, maximum 4.4). PSA expression was significantly lower in poorly differentiated breast cancers compared to moderately and highly differentiated tumors. Advanced lymph node metastases were also correlated with lower PSA expression. We found no correlation with relapse free or overall survival. Median PSA level in our ovarian cancer patient collective was 0.014 ng/mg (minimum 0.003, maximum 0.046). We found a significant correlation between PSA expression and the estrogen receptor content of the tumor. PSA expression showed no correlation with histological grading, tumor size or other tumor characteristics in ovarian cancer. There was no correlation with relapse free or overall survival in ovarian cancer patients. Our study demonstrates that PSA is expressed in ovarian malignancies but at a lower level compared to breast cancer tissue. PSA was not able to identify a subset of patients with good prognosis in breast and in ovarian cancer patients.

Adenocarcinoma↗