Comparison of one-step nucleic acid amplification (OSNA) method and routine histological investigation for intraoperative detection of lymph node metastasis in Polish women with breast cancer.

Sentinel lymph node (SLN) biopsy is a part of the staging procedure in breast cancer patients. Intraoperative molecular analysis for SLN metastases using the one-step nucleic acid amplification (OSNA) method based on reverse-transcription loop-mediated amplification (RT-LAMP) has already been validated in breast cancer. In this study, we compare the intraoperative OSNA method to our routine histological investigation. To evaluate the performance of OSNA in comparison to histology, analysis of 74 SLN from 60 breast cancer patients was conducted with both methods. Of the 22 histologically positive samples, 14 were attributed to macrometastases (++) in the OSNA-CK19 assay and 8 to micrometastases (+). Two samples negative in histopathology were positive in the OSNA method (micrometastases +). Our results show that OSNA is an excellent method for the detection of metastases in lymph nodes and can be applied as an intraoperative diagnostic approach. Intraoperative molecular analysis for SLN metastases using the OSNA method reduces the number of admission days and duration of surgery. To our knowledge this is the first study referring to Polish women.

A single nucleotide polymorphism in the 5' untranslated region of RAD51 and ovarian cancer risk in Polish women.

BACKGROUND: DNA repair gene polymorphisms are known to influence cancer risk. The RAD51 gene encodes proteins essential for maintaining genomic stability by playing a central role in holmology-dependent recombinational repair of the DNA double-strand breaks. Aims. We investigated the association of polymorphisms in the DNA repair genes RAD51-135G > C and 172G >T with ovarian cancer risk. METHODS: 120 Polish ovarian cancer patients and 120 healthy controls were genotyped for RAD51 (135G > C and 172G > T) by PCR-RFLP. RESULTS: In the present work no association was detected between ovarian cancer risk and 172G > T polymorphism of the RAD51 gene. The 135G > C polymorphism was associated with ovarian cancer risk. We found evidence of an increased ovarian cancer risk in CC homozygotes (OR 12.97 [95% confidence interval {CI} (5.73-29.36)]) but not in heterozygotes (OR 0.55 [95% CI 0.23-1.29]). We demonstrated a significant positive association between the RAD51 variant 135C allele and ovarian carcinoma, with an adjusted odds ratio (OR) of 6.24 (p < .0001). CONCLUSION: The results indicated that the polymorphism 135G > C of RAD51 may be positively associated with ovarian carcinoma in the Polish population. Further studies on the role of the RAD51 gene on ovarian cancer are warranted.

The association between polymorphisms of the RAD51-G135C, XRCC2-Arg188His and XRCC3-Thr241Met genes and clinico-pathologic features in breast cancer in Poland.

BACKGROUND: XRCC2 and XRCC3 genes are structurally and functionally related to RAD51 which plays an important role in homologous recombination, the process frequently involved in cancer transformation. MATERIAL AND METHODS: In the present work the distribution of genotypes and frequency of alleles of the RAD51 G135C polymorphism, XRCC2 Arg 188His and XRCC3 Thr241Met polymorphism in 790 cases of breast cancer were investigated. The control group consisted of 798 cancer-free blood donors (age +/- 5 years) who were sex and ethnicity-matched. The polymorphisms were determined by PCR-RFLP methods. We also correlated genotypes with the clinical characteristics of breast cancer patients. RESULTS: Our results obtained for the 135G>C polymorphism of the RAD51 gene indicated that both the C/C genotype and the C allele are strongly associated with breast cancer. The Arg/His genotype of XRCC2 (OR = 2.16, 95% CI = 1.48-3.16) and Thr/Met of XRCC3 increased the risk of type I breast cancer occurrence (OR = 2.33, 95% CI = 1.60-3.41). We did not find any association with the RAD51, XRCC2/3 gene polymorphism and estrogen and progesterone receptor status. CONCLUSION: The results support the hypothesis that the polymorphism of RAD51 and XRCC2/3 gene may be associated with the incidence of sporadic breast cancer in Polish women.

p16 gene mutations in Barrett's esophagus in gastric metaplasia - intestinal metaplasia - dysplasia - adenocarcinoma sequence.

PURPOSE: Barrett's associated esophageal adenocarcinoma (ADC) is one of the malignancies of most rapidly increasing incidence. The aim of the study was to assess p16 tumor suppressor gene alterations in the ADC premalignant conditions. MATERIAL & METHODS: In the present study two p16 gene mutations (A148T and I49S) analysis with PCR- RFLP method have been performed in oesophageal biopsy specimen in 33 patients with Barrett's gastric metaplasia (GM), 27 - with Barrett's intestinal metaplasia (IM), 8 - with dysplasia and 11 - with ADC. RESULTS: We have detected the I49S mutation in 12% (4/33) patients with GM, 18% (5/27) with IM, 50% - with dysplasia (4/8) and in 27% (3/11) - with ADC. The A148T mutation were found in 3% (1/33) patients with GM, 22% (6/27) - IM, 25% (2/8) - dysplasia and 27% patients with ADC (3/11). The frequency of the A148S mutation was rising in GM - IM - dysplasia - ADC sequence and was significantly lower in GM compared to all other grades taken together (p=0.0256). The frequency of the I49S mutation was rising in GM - IM - dysplasia sequence, to drop in ADC cases. There were no significant differences in frequency of the I49S mutation between studied groups. CONCLUSIONS: These findings are consistent with the hypothesis on the role of the p16 mutations in early phase of Barrett's epithelium progression to ADC. The presence of p16 mutations in esophageal metaplastic columnar epithelium without goblet cells suggest that this pathology may have malignancy potential.

Association between Arg399Gln polymorphism of X-ray repair cross-complementing 1 (XRCC1) gene and sporadic endometrial cancer in the Polish population.

BACKGROUND: Endometrial cancer is one of the most common malignant neoplasms which appear in the uterine body. X-ray repair cross-complementing 1 (XRCC1) protein can be involved in the repair of DNA lesions, which are known to contribute to endometrial cancer. MATERIAL AND METHODS: The genotype analysis of XRCC1 Arg399Gln gene polymorphisms for 456 endometrial cancer patients and 300 controls of cancer-free subjects in the Polish population were performed using the PCR-based restriction fragment length polymorphism (PCR-RFLP). RESULTS: The association between endometrial cancer occurrence and the Gln/Gln genotype of the Arg399Gln polymorphism (odds ratio, OR 2.28; 95% confidence interval, CI 2.02-2.54) was found. The Gln/Gln genotype of XRCC1 increased the risk of type I endometrial cancer occurrence (OR = 2.42, 95% CI = 2.12-2.72). No statistically significant association was found between gene polymorphisms and endometrial cancer risk factors such as BMI, HRT, uterine bleeding, endometrial ultrasound transvaginal, diabetes and hypertension. CONCLUSION: The results support the hypothesis that the Arg399Gln polymorphism of the XRCC1 gene may be associated with the incidence of sporadic endometrial cancer in Polish women.

Vascular endothelial growth factor (VEGF) genotype and serum concentration in patients with pancreatic adenocarcinoma and chronic pancreatitis.

Vascular endothelial growth factor (VEGF) is necessary for microvasculature development and important for growth and spread of pancreatic tumors. Functional polymorphism of VEGF gene at position C-460T and G+405C may influence VEGF serum level. VEGF gene polymorphisms at position C-460T and G+405C were evaluated in 85 patients with pancreatic adenocarcinoma (PA), 72 - with chronic pancreatitis (CP) and 50 healthy volunteers. VEGF genotypes were studied in DNA isolated from blood samples and serum VEGF concentrations were measured. We found an increased frequency of the homozygous +405C/C VEGF genotype in patients with PA (55.3%) compared with CP (25%) and control group (16%; p<0.01). In contrast, the distribution of genotype and allele frequencies of the -460C/T polymorphism in the PA patients did not differ from those in CP and control groups. Serum levels of VEGF were significantly higher in PA patients (mean level: 441 ± 37.2 pg/ml) compared with CP patients (217 ± 13.6 pg/ml; p<0.001) and control group (137 ± 7.7 pg/ml; p<0.001). No relationship between VEGF serum levels and VEGF gene polymorphisms have been found. Our findings suggest that +405C/C VEGF genotype may contribute to pancreatic carcinogenesis. VEGF serum levels, although elevated in PA patients, are not associated with analysed VEGF polymorphisms.

Estrogen receptor alpha (ER-alpha) gene polymorphism in patients from the Lodz region of Poland with sporadic endometrial cancer.

OBJECTIVE: Estrogens play a crucial role in the pathogenesis and progression of endometrial cancer. The gene ER-alpha is polymorphic and gene variability could contribute to the level of protein biosynthesis. METHODS: The aim of this study was to evaluate PvuII and XbaI polymorphism of the ER-alpha gene in 120 postmenopausal women with endometrial cancer in DNA samples obtained from cancer tissue. The polymorphisms were determined by PCR-RFLP methods. RESULTS: The distribution of the genotypes of PvuII and XbaI polymorphism of ER-alpha in both controls and patients did not differ significantly from those predicted by the Hardy-Weinberg distribution. There were no significant differences in genotype distributions and allele frequencies between subgroups assigned to histological stage. CONCLUSIONS: The results suggest that the PvuII polymorphism of ER-alpha gene as well as XbaI polymorphism may not be linked with appearance and development of endometrial cancer.

Tumor necrosis factor alpha and interferon gamma genes polymorphisms and serum levels in pancreatic adenocarcinoma.

Several biochemical pathways can lead to cancer cachexia, one of which involves the elevation of the cytokines, such as tumor necrosis factor alpha (TNF-alpha) and interferon gamma (INF-gamma). It was suggested that TNF-alpha and INF-gamma genes polymorphisms may influence these cytokines serum levels, but published data are still controversial. The aim of our study was to assess the clinical significance of -308G/A TNF-alpha and +874A/T INF-gamma genes polymorphisms as well as TNF-alpha and INF-gamma serum levels in pancreatic adenocarcinoma (PA) and chronic pancreatitis (CP) as regards to healthy volunteers. We studied 41 patients with pancreatic adenocarcinoma, 56 with chronic pancreatitis and 50 healthy volunteers. Peripheral venous blood samples were obtained from all patients for TNF-alpha and INF-gamma serum concentrations measurement. After DNA isolation TNF-alpha and INF-gamma genes polymorphisms have been studied using restriction fragment length polymorphism (RFLP) analysis. Plasma levels of TNF-alpha were significantly higher in PA patients (32.7 pg/ml) compared with CP patients (3.2 pg/ ml) and control group (<1.6 pg/ml; p<0.01). Similarly, plasma levels of INF-gamma in PA patients (12.7 pg/ml) were higher from those in CP and control group (<7.1 pg/ml; p<0.01). In contrast, there were no differences between CP patients and healthy volunteers in INF-gamma levels. We observed a trend toward a correlation between weight loss in PA patients and TNF-alpha serum level (p=0.02). The TNF-alpha and INF-gamma genotype distribution were similar in patients with PA, CP and control group. We have not observed any association between TNF-alpha and INF-gamma serum levels and their genes polymorphisms. Our results suggest that elevated TNF-alpha serum level may have clinical significance in the development of cachexia in PA patients. -308G/A TNF-alpha and +874A/T INF-gamma genes polymorphisms probably do not play important role in pancreatic diseases. Key words: pancreatic adenocarcinoma, tumor necrosis factor alpha, interferon gamma, cytokines, polymorphism.

Microsatellite instability (MSI) and MLH1 and MSH2 protein expression analysis in postmenopausal women with sporadic endometrial cancer.

Microsatellite instability (MSI) seems to be important for the development of various human cancers including sporadic endometrial cancer. The aim of this study was evaluation of microsatellite instability in 60 postmenopausal women with endometrial cancer in DNA samples obtained from cancer tissue and blood of the same patients. Control DNA was obtained from normal endometrial tissue (n = 70). MSI was studied at five loci containing single- or dinucleotide repeat sequences and mapping to different chromosomal locations: BAT-25 (at locus 4q12), BAT-26 (2p16), D2S123 (2p16-p21), D5S346 (5q21-q22) and D17S250 (171q11.2-q12). No differences in the MSI frequencies between blood and cancer tissue obtained from patients were detected. The microsatellite instability status was significantly higher in endometrial cancer tissue [21/60 (35%)] compared to control [8/70 (11%)] (p < 0.05). There were significant differences between MSI presence in the subgroups assigned to the histological grades (p < 0.05). The lack of association between MLH1 and MSH2 protein expression and MSI in endometrial cancer samples was observed. The results suggest that the microsatellite instability seems to be important in the development of sporadic endometrial cancer.

The T/G mutation in exon 8 of hMSH2 gene in the sporadic colon cancer patients.

The DNA mismatch repair (MMR) system guards against genomic instability, therefore the mutations in the human MMR genes cause the majority of the hereditary nonpolyposis colorectal cancer (HNPCC) and a small percentage of the sporadic colon cancer. hMSH2 is one of MMR genes involved in the correction of mispairing during replication and its mutations are associated with both--microsatellite instability and the hereditary and sporadic colon tumourgenesis. The aim of this study was to analyse the T/G mutation (codon 458) in exon 8 of hMSH2 gene in the sporadic colon cancer cells. We also examined the relationship between the T/G mutation of hMSH2 gene, and the selected prognostic factors such as Dukes' stage, histological grade and lymph node metastasis. We analysed samples of tumour from 75 patients with sporadic colorectal cancers. The mutation in the hMSH2 gene ware determined by the RFLP-PCR. We found T/G mutation in exon 8 of hMSH2 gene in 5 patients (6,7%). There was no statistically significant difference between this mutation and selected clinical parameters. The results of our studies revealed that mutations of hMSH2 gene may lead to development of colorectal cancer. No dependence between the mutation of hMSH2 gene and clinical parameters, suggests that the mutation of hMSH2 gene may have a critical significance for the first steps of carcinogenesis in colon epithelial.

The T/C polymorphism of the CYP17 gene and G/A polymorphism of the CYP19 gene in endometrial cancer.

Endogenous estrogen exposure is an important determinant of endometrial cancer risk. The CYP17 and CYP19 genes encode 17 hydroxylase/17,20-lyase and aromatase, respectively, both involved in sex hormone synthesis. The gene CYP17 and CYP19 are polymorphic and gene variability could contribute to the level of protein biosynthesis. In the present work the distribution of genotypes and frequency of alleles of the C/T polymorphism in promoter region of CYP17 and G/A polymorphism at position Val80 in CYP19 in subjects with endometrial cancer were investigated. Paraffin embedded tumour tissues were obtained from 100 women with endometrial cancer. DNA from normal endometrial tissue (n = 106) served as control. The polymorphisms were determined by PCR-RFLP. The distribution of the genotypes of the C/T polymorphism of CYP17 and G/A polymorphism of CYP19 in both control and patients did not differ significantly (p > 0.05) from those predicted by the Hardy-Weinberg distribution. There were no significant differences (p > 0.05) in genotype distributions and allele frequencies between subgroups assigned to histological stage. The results suggest that C/T polymorphism of the CYP17 gene as well as G/A polymorphism of CYP19 may not be linked with onset and development of endometrial cancer.

Analysis of RAD51 polymorphism and BRCA1 mutations in Polish women with breast cancer.

AIM: Breast cancer is one of the major killers worldwide. The objectives of this study were to determine the frequency of BRCA1 germ-line mutations and the RAD51 G/C polymorphism in patients with breast cancer. METHODS: 100 breast cancer women provided blood for mutation analysis. Blood samples age matched healthy individuals (n = 106) served as control. The G/C polymorphism and BRCA1 mutations were determined by PCR-RFLP methods. RESULTS: The distribution of the genotypes of the G/C polymorphism RAD51 in both control and patients did not differ significantly from those predicted by the Hardy - Weinberg distribution. There were no significant differences in the genotype distributions and allele frequencies between node-positive and node-negative patients. In present study one Ex20insC mutations of BRCA1 gene was identified in women with breast cancer. CONCLUSION: Our study implies that the G/C polymorphism of the RAD51 gene may not be directly involved in the development and=or progression of breast cancer.

Usefulness of p16 and K-ras mutation in pancreatic adenocarcinoma and chronic pancreatitis differential diagnosis.

BACKGROUND: The differentiation of chronic pancreatitis (CP) from pancreatic adenocarcinoma (PA) remains a great challenge. The purpose of the study was to compare the prevalence of p16 and K-ras mutation in PA and CP in order to evaluate their usefulness in differential diagnosis of those diseases. METHODS: The study included 44 patients who underwent Whipple resection or distal pancreatectomy for PA (23 subjects) or CP (21 subjects). DNA from pancreatic tissue was analysed for K-ras mutation (codon 12) and p16 mutations with PCR amplifications. RESULTS: The K-ras gene mutation has been shown in 17 (73,9%) cases with pancreatic adenocarcinoma which was significantly more often than in chronic pancreatitis - 9 (42,8%) (p<0,01). Prevalence of p16 mutations in patients with PA was 18 (78,3%) and with CP - 7 (33,3%) (p<0,01). K-ras and p16 mutations together have been observed in 16 (69,6%) cases in patients with PC and only in 3 (14,3%) - with CP (p<0,01). No statistically significant association between K-ras or p16 mutations and tumor size, sex or patient age has been observed. CONCLUSION: It is suggested that simultaneous measurement of K-ras and p16 mutations may provide an additional tool in differential diagnosis of chronic pancreatitis and pancreatic adenocarcinoma.

Laparoscopically assisted vaginal hysterectomy with bilateral salpingo-oophorectomy due to endometrial cancer in a heart transplant recipient. A case report.

INTRODUCTION: Transplant recipients have a higher incidence of cancer compared with the general population. This increased risk is related to the intensity and chronicity of immunosuppression that these patients receive. In this report, we present a case of a heart transplant woman with endometrial cancer who was diagnosed six months after transplantation. CASE REPORT: A 49-year-old woman who had undergone a heart transplant was referred to our department in May 2002 for final treatment. The diagnosis of endometrial cancer was established on the basis of the histopathology findings of the fractional curettage. Her heart transplant had occurred six months before, as a result of idiopathic restrictive cardiomyopathy. The patient received triple immunosuppression with cyclosporin, azathioprine and prednisone and she displayed no signs of acute graft rejection features. Laparoscopically assisted vaginal hysterectomy with adnexa was performed without any complications. Duration of surgery was 85 minutes. The patient was operated on under general anesthesia and intraabdominal pressure was automatically maintained at 10 mmHg with a carbon dioxide insufflator (AESCULAP, Germany). Immunosuppressive therapy was continued without modification. The postoperative course was uncomplicated in our patient. No significant changes in heart rate or blood pressure were observed. The patient was discharged from the hospital on the 11th postoperative day. Microscopic appearance revealed Stage I endometrial cancer. The patient is in good physical condition with normal heart performance and without disease recurrence. CONCLUSION: In our opinion LAVH was a justifiable form of surgical management in the treatment of a heart transplant recipient with an early-stage endometrial cancer.

Antigen levels of the urokinase-type plasminogen activator and its gene polymorphisms in colorectal cancer.

We analysed the distribution of genotypes of two polymorphisms in the urokinase-type plasminogen activator (uPA) gene: C-->T substitution in exon 6 and T-->C substitution in intron 7 in 52 subjects with colorectal cancer. Genotypes were determined in tumour tissue and distant mucosa samples by allele-specific polymerase chain reaction. The antigen levels of uPA in cancer tissue were higher than in distant mucosa as measured by enzyme-linked immunosorbent assay. The level of uPA antigens in cancer samples with the C/C genotype of C-->T polymorphism in exon 6 was higher than in samples with C/T and T/T genotypes. No differences in the level of uPA antigens between the alleles of the intron 7 T-->C polymorphism were found. As uPA can be involved in cancer invasion and metastasis, C/C genotype in exon 6 of uPA gene can be further considered as being related to colorectal cancer progression.

The promoter polymorphism of the matrix metalloproteinase 3 (MMP-3) gene in women with ovarian cancer.

Matrix metalloproteinases (MMPs) comprise family proteolytic enzymes that degrade extracellular matrix components and therefore play an important role in tumour cell invasion and cancer metastasis. Overexpression of matrix metalloproteinase 3 (MMP-3 or stromelysin 1) gene has been demonstrated in various types of cancers and high level of MMP-3 protein in tumour is a poor prognostic factor for patients. The insertion (6A)/deletion (5A) polymorphism (5A/6A polymorphism) located at the promoter of the MMP-3 gene may have functional significance in the regulation of its expression. In the present work the distribution of genotypes and frequencies of alleles of the 5A/6A polymorphism in subjects with ovarian cancer were investigated. Paraffin embedded tumour tissues were obtained from 100 women with ovarian cancer. The genotypes of 5A/6A polymorphism were determined by PCR amplification using the allele specific primers. The distribution of the genotypes of the 5A/6A polymorphism in both control and patients did not differ significantly (p > 0.05) from those predicted by the Hardy-Weinberg distribution. Additionally, there were no significant differences (p > 0.05) in genotype distributions and allele frequencies between subgroups assigned to histological stage. The results suggest that the 5A/6A polymorphism of MMP-3 gene may not be linked with appearance and development to ovarian cancer.

Plasminogen activator inhibitor 1 (PAI-1) levels and gene promoter polymorphisms in subjects with colorectal cancer.

The high level of plasminogen activator inhibitor 1 (PAI-1) in colorectal cancer predicts poor prognosis for patients. The insertion (5G)/deletion (4G) polymorphism (the 4G/5G polymorphism) and G-->A single base substitution (the G/A polymorphism) located at promoter of PAI-1 gene may have functional significance in regulation of its expression. In the present work the level of PAI-1, distribution of genotypes and frequency of alleles of the 4G/5G and G/A polymorphisms in samples of cancer tissue and normal mucosa as well as in blood were investigated. Blood, tumor and normal tissues were obtained from 40 patients with colorectal cancer. The 4G/5G and G/A polymorphism were determined by PCR amplification using the allele specific primers. The PAI-1 level was measured by enzyme linked immunosorbent assay (ELISA). The distribution of the genotypes of both polymorphisms did not differ significantly (p > 0.05) from those predicted by the Hardy-Weinberg distribution. There were no differences in the genotype distributions and allele frequencies between blood, normal mucosa samples and cancer tissue. The 4G/5G and G/A polymorphisms were in linkage disequilibrium. The average level of PAI-1 in tumor samples was significantly (p < 0.05) higher than in normal tissue. The results obtained indicate that a higher level of PAI-1 can be associated with colorectal cancer. On the other hand, in colon cancer, the 4G/5G and G/A polymorphisms are not linked with elevated levels of PAI-1 and therefore may not be used to predict colon cancer prognosis.

A C/T polymorphism in the urokinase-type plasminogen activator gene in colorectal cancer.

Urokinase plasminogen activation system can play an important role in the appearance and progression of many cancers. Urokinase-type plasminogen activator (uPA) is implicated in the control of cell adhesion and invasion, and is regarded as a strong prognostic marker in colorectal cancer. A C-->T substitution (the C/T polymorphism) in the nucleotide sequence encoding the kringle structure of uPA results in an alteration from proline to leucine at position 121. This substitution may be directly or indirectly involved in the decreased affinity for uPA substrates. In the present work the distribution of genotypes and frequencies of alleles of the C/T polymorphism were investigated. Tumour tissues and distal mucosa samples were obtained from 40 patients with colorectal cancer. Blood samples from sex and age matched healthy individuals served as control. The C/T polymorphism was determined by PCR amplification using the allele specific primers. No differences between genotypes of the C/T polymorphism in cancer tissue and distant mucosa of each patient were found. The distributions of the genotypes in both patients and control differed significantly (p < 0.05) from that predicted by the Hardy-Weinberg distribution. A distinct preference of heterozygotes (70% - patients, 65% - controls) was observed in both patients and controls. Additionally, there were no differences in the frequencies of the C and T alleles in both groups. The C/T polymorphism of the uPA gene may not be linked with colorectal cancer.

Female breast carcinomas: nuclear and cytoplasmic proteins versus steroid receptors.

Nuclear and cytoplasmic proteins of human female breast cancer were analysed by one-dimensional sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). Oestrogen receptor and progesterone receptor expression was determined by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method. The electropherograms were developed by silver nitrate staining and quantitative analysis was carried out by video densitometer using the software Gel-Pro Analyzer. Nuclear and cytoplasmic proteins of breast carcinomas and normal tissue differed both qualitatively and quantitatively. Nuclear polypeptides of 108, 53 and 48 kD as well as the 36 kD cytoplasmic polypeptide were specific for tumour samples, while the 51 kD nuclear polypeptide was detected only in normal tissue. Quantitative differences in band density were noted in the 32 kD nuclear polypeptide. This polypeptide was expressed in greatest concentration in infiltrating ductal carcinomas which also indicated the greatest oestrogen receptor gene expression. This relationship appeared to be statistically significant (p < 0.005). No correlations were evident between the 32 kD protein expression and the progesterone receptor gene expression in any of the tissue types examined, nor between the 32 kD protein and the patient's age or tumour grade.

[Choriocarcinoma]. / Kosmówczak.

Choriocarcinoma is a malignant neoplasm with it's origin in trophoblast. It can be found after every pregnancy, but specially after pregnancy complicated by mola hydatidosa (complication in 2-3% of all molas). The main biochemical marker, used in treatment and prognosis is hCG. There are different prognostic systems for choriocarcinoma: presence of metastases, level of hCG in urine and plasma, end of last pregnancy. Surgical and chemical treatment in used. Outcome is generally good and very good.