Overweight and obesity may play a role in the pathogenesis of chronic spontaneous urticaria.

BACKGROUND: Chronic spontaneous urticaria (CSU) is one of the commonest diseases in allergological and dermatological practice. It constitutes an interdisciplinary problem, and its pathogenesis is not always easily determined. It has been suggested that metabolic syndrome and hyperlipidaemia are more frequent in patients with CSU, but the influence of overweight and obesity on the development of CSU has not been thoroughly investigated. AIM: To assess the association between body parameters and the development of CSU. METHODS: The study enrolled 85 patients with CSU, who were divided into three subgroups: patients whose only symptoms were weals, patients whose only symptom was angio-oedema, and patients with urticaria and accompanying angio-oedema. Mean weight, height, body mass index (BMI), body surface area, disease duration and age of disease onset were recorded RESULTS: There was a statistically significant association between CSU and heavier weight, higher BMI, greater affected body surface area and older age at disease onset. Subjects with higher BMI values had a tendency towards longer disease duration. There were no statistically significant differences between the three subgroups. CONCLUSIONS: Our results suggest that CSU, especially if of long duration, may be associated with overweight and obesity, while increased body mass can result in later onset of urticaria symptoms. Further analyses to confirm the presented results and possible association between obesity and CSU occurrence are needed.

Distribution of interstitial cells of Cajal in the neurogenic urinary bladder of children with myelomeningocele.

PURPOSE: C-kit positive interstitial cells of Cajal (ICCs) play an important role in the regulation of the smooth muscle motility, acting as pacemakers to provide the slow wave activity in various organs. Recent studies have shown that c-kit positive ICCs are widely distributed in the urinary tract of animals and humans. The aim of our study was to examine the distribution of ICCs in the children's neurogenic bladder. METHODS: An immunohistochemical study of specimens obtained from neurogenic urinary bladder (from the trigonum and the corpus) of children with meningomyelocele and during autopsy was performed using antibody against c-kit (CD 117). Histological morphometry of immunoexpression of c-kit positive ICCs was performed by means of an image analyzing system. RESULTS: Our investigation demonstrated ICCs located in the vesical muscle layers. The distribution of those cells is different in the trigonum and the corpus of the urinary bladder. No remarkable differences were observed in c-kit immunoexpression between the neurogenic and the control group. CONCLUSION: There was no difference in the distribution of ICCs in the urinary bladder of healthy children as compared to children with myelomeningocele. Biopsy revealed different distribution of ICCs in particular parts of the bladder (trigonum/ corpus) in both groups of children.

Immunoexpression of Ki-67 in pulmonary hypoplasia.

Adequate pulmonary development at birth is the major determinant of postnatal outcome in the perinatal period. Lung hypoplasia is a poorly defined condition. The aim of this study was to investigate expression of Ki-67 in human fetuses with pulmonary hypoplasia compared to fetuses without pulmonary pathology and malformations of other organs used as controls. The analysis comprised 149 formalin-fixed and paraffin-embedded tissue sections from the files of the Clinical Pathology Department of the Research Institute of Polish Mother's Memorial Hospital in Lodz. Tissue sections obtained from lungs during autopsies were divided into two groups. In our studies immunohistochemistry was performed using antibody against Ki-67 as a cell proliferation marker for evaluation of growth fraction in the fetal and neonatal human lungs. The results presented in our study showed higher expression of growth fraction in the control group as compared to study subjects in all stages of lung development. Values of Ki-67 positive cells in the saccular stage of lung development were lower than in the canalicular and alveolar phase in both study and control groups. In conclusion, our results indicate their usefulness to understand better etiology of pulmonary hypoplasia and may be helpful in identifying the most appropriate moment for prenatal interventions.

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.

[Genetics risk factors in chronic obstructive pulmonary disease]. / Genetyczne czynniki ryzyka rozwoju przewlekfej obturacyjnej choroby pluc.

Chronic obstructive pulmonary disease (COPD) is not fully recognized process regarding many risk factors genetics and environmental. Etiology of COPD is not fully understood. There is evidence of a hereditary component in COPD. Patients with hereditary alpha1-antitrypsin deficiency are at risk of developing COPD. A number of genetic association studies have been performed to find susceptibility genes of COPD. Many of genes play an important role in development of COPD. This review examines the impact of alpha1-antitrypsin, matrix metalloproteinases, tumour necrosis factor gene a, microsomal epoxide hydrolase, transforming growth factor b-1, Vitamin D-binding protein and CFTR on COPD extension.

Production of cytokines during interaction of peripheral blood mononuclear cells with autologous ovarian cancer cells or benign ovarian tumour cells.

Cytokines produced by tumour and immune cells may play a significant role in a modulation of immune cells response against tumour. We investigated an ability of peripheral blood mononuclear cells (PBMC) of patients with early and advanced stages of ovarian cancer and from non-cancer patients to produce various cytokines in the presence or absence of autologous ovarian cancer (OC) cells or benign ovarian tumour (BOT) cells. Activated PBMC of patients with advanced stage of cancer produced slight amount of interferon gamma (IFN-gamma) and what's more, the production of IFN-gamma was decreased in the presence of OC cells. PBMC of patients with ovarian cancer or benign ovarian tumour generated comparable amounts of interleukin 6 and 10 (IL-6, IL-10), and transforming growth factor beta1 (TGF-beta1). PBMC of the patients with cancer produced higher amount of tumour necrosis factor alpha (TNF-alpha) than PBMC of non-cancer patients. We demonstrated here that the reciprocal contact of OC cells from advanced cancer with autologous PBMC altered the direction of produced cytokines and leads to the down-regulation of IFN-gamma and TNF-alpha as well as to up-regulation of immunosuppressive (IL-10, TGF-beta1) and pro-inflammatory (IL-6) cytokines production.

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.

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.

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.

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.

Tumor front grading in prediction of survival and lymph node metastases in patients with laryngeal carcinoma.

PURPOSE: Despite innumerous both therapeutic and histopathologic studies that have been performed no morphologic markers are currently available in order to predict the outcome in patients with laryngeal cancer. According to the recent reports nowadays tumor front grading (TFG) is one of the most reliable methods of estimation of the progress of the changes in the peripheral part of tumor and it seems to be one of the technics, which is able to assess the dynamics of the tumor growth quite precisely. In this sudy it was presented direct relation between morphological features of tumor front and survival. MATERIAL AND METHODS: The authors have analysed 120 cases of patients who were operated on the laryngeal squamous cell carcinoma in ENT Department Medical University of Lódz between 1995-2000. Features of the morphologic tumor front grading was performed on H&E-stained sections in the peripheral parts of a tumor. Dependence on tumor grade G, tumor size T, lymph node metastases and survival were analysed. RESULTS: Our study showed that feature such as TFG is very useful in prediction of survival in patients with laryngeal squamous cell carcinoma in comparison to the histological differentiation degree. The statistical analysis showed no significant correlation between TFG score and tumor size T, nodal status N and G feature. CONCLUSIONS: The presented study emphasizes that TFG might influence decisions regarding therapeutic management and could eventually lead to more appropriate and individualized therapy. It is necessary to extend the traditional histopathological diagnosis by TFG, which assesses the dynamics of the malignant process and it seems to be a good prognostic method in prediction of survival of patients with squamous cell carcinoma.

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.

An association between the matrix metalloproteinase 1 promoter gene polymorphism and lymphnode metastasis in breast cancer.

A single guanine insertion (1G/2G polymorphism) in the promoter of the matrix metalloproteinase (MMP-1) gene creates a binding site for the transcription factor and may affect the level of transcription of MMP-1. An elevated level of MMP-1 in cancer cells may facilitate their invasion and contribute to metastasis. To evaluate the contribution of 1G/2G polymorphism in the development and/or progression of breast cancer we genotyped 135 subjects with breast cancer. The 1G/2G polymorphism was determined by the method based on restriction endonuclease digestion. We found that the frequency of the 2G allele was higher in lymphnode-metastasis patients than in the group without metastasis (p < 0.001). We did not find differences between distribution of the genotypes and frequencies of alleles in cancer patients and in healthy subjects served as control. Our results suggest that allele 2G may be associated with lymphnode metastasis in patients with breast cancer and therefore it can be considered as a prognostic marker in this disease.

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.

[Congenital pneumonia in fetuses and newborns ad inflammatory lesions in the placenta]. / Wrodzone zapalenia pluc plodów i noworodków a zapalenia poplodów.

The authors compared the degree of congenital pneumonia in stillborn and neonates died in first two days of life with inflammation lesions of placenta. The coexistence of those two processes and its significant correlation was found, especially among preterm LBW neonates. This finding supports the hypothesis about infection as a probable cause not only of preterm deliveries but infection of fetuses and neonates as well. Analysis of some cases revealed also that general infection of mother could cause transplacental infection of foetuses.

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.

[Clinical-pathomorphologic preparation of patients after surgical treatment of differentiated thyroid cancer to adjuvant treatment with 131I]. / Kliniczno-patomorfologiczne przygotowanie chorych po chirurgicznym leczeniu zróznicowanych raków tarczycy do uzupelniajacego leczenia 131I.

UNLABELLED: Thyroid cancer treatment includes: surgery, radioiodine therapy, thyroxine therapy and radiotherapy. Selection of treatment's strategy depends on histopathological evaluation, age of patient and iodine uptake. The aim of the analysis was to verify how the medical documentation of patients treated by surgical treatment was prepared. All patients were directed to the Department of Endocrinology, Holycross Cancer Center in Kielce. Analysis encompassed 33 patients classified to 131I therapy for the first time. In each case patient's medical documentation and histopathological diagnosis made in Department of Tumor Pathology, Holycross Cancer Center, were compared. RESULTS: A conformity with primary cancer diagnosis was obtained in all but one patient in whom pathological consultation did not confirm oxyphilic carcinoma. In four cases the type of cancer was changed as a result of repeated consultation. pTMN classification was stated in 23 primary pathologic examination cases. After consultation of slides and inspection of surgery protocol, total or partial pTNM stage was obtained in other 9 patients. CONCLUSIONS: Establishment of diagnostic and therapeutic algorithm, accepted on Conference in Szczyrk, 1995 is inadequately executed in small centers. Routine consultation of histopathological slides creates a possibility to make a proper choice of treatment's strategy.

[Differential criteria between papillary and follicular thyroid carcinoma--initial conclusions from a multicenter trial]. / Kryteria róznicowania miedzy rakiem brodawkowatym i pecherzykowym tarczycy--pierwsze wnioski z badania wieloosrodkowego.

Histopathological diagnosis of thyroid cancer is difficult and requires much experience. Pathologists have to know many histopathological variants and be aware of the current diagnostic criteria. The aim of the study was to unify criteria applied all over the country and compare whether the accuracy of diagnosis has changed in the course of the last fifteen years. In a multicenter trial, 36 pathologists from 25 centers reevaluated 232 thyroid tumors operated between 1985-1998. The reference diagnosis was given on the basis of evaluation made by four experienced pathologists. The two-step analysis was performed. At first, the accuracy of the diagnosis of malignant neoplasm was evaluated. Then, the accuracy of the diagnosis of the cancer histotype was analyzed, with estimation of kappa coefficients and their asymptomatic standard error. Comparison of primary and reference diagnoses revealed statistically significant differences--in 17% of cases the primary diagnosis of cancer was not confirmed by experienced pathologists. Kappa coefficient for the diagnosis of cancer histotype was 0.53 + 0.06. On the contrary, the diagnoses made by the participants of the trial did not differ significantly from the reference ones. Kappa coefficient for the diagnosis of cancer histotype was significantly higher than for primary diagnoses with 0.63 +/- 0.10 (p < 0.001). The first results of the multicenter trial indicated that the most frequent diagnostic error made at primary diagnosis was the overdiagnosis of follicular thyroid carcinoma. Thus, a summary of strict criteria for papillary and follicular thyroid carcinoma is also given.

[Criteria for histopathologic diagnosis of thyroid cancer in a quick test of accuracy]. / Kryteria rozpoznania histopatologicznego raka tarczycy w szybkim tescie zgodnosci.

A quick test of accuracy of histopathological diagnosis of thyroid carcinoma was performed in May 2000 during the meeting of Polish thyroid cancer group (Committee for Epidemiology, Diagnosis and Treatment of Thyroid Carcinoma). 29 pathologists participated in the test and evaluated 8 cases of thyroid carcinoma and 14 benign thyroid lesions. All cases were chosen from the current material sent for pathologic evaluation to the Institute of Oncology in Gliwice due to diagnostic difficulties. In total, 591 diagnoses were made and were the subject of the presented analysis. They were compared with reference diagnosis in two aspects. First, the accuracy of the distinction between malignant and benign lesions was evaluated. 72.5% of diagnoses were concordant with the reference. The false diagnosis of cancer in a benign lesion was observed 133 times (22.5% of all diagnoses). A reverse error--a false exclusion of cancer--was seen in 29 diagnoses (4.9%). Chi 2 test revealed a statistically significant difference between the participants' diagnoses and reference ones (p < 0.0001). Overdiagnosis of cancer was the most frequent at the diagnosis of follicular or oxyphilic cancer. With reference to the diagnosis of cancer histotype, concordant diagnoses were seen in 40-47% of cases with the lowest accuracy of the diagnosis of oxyphilic (40% of correct diagnoses) and follicular (50%) cancer. The causes of false diagnoses may be divided in two groups: sample-related causes (sampling of surgical specimens, lack of standard description, insufficient number of samples, poor quality of staining) and diagnostic errors: non-compliance with diagnostic criteria and inappropriate setting of diagnoses, which require immunohistochemical confirmation.