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.

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.

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.

[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.

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.

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.

Inhibitory effects of fumagillin and its analogue TNP-470 on the function, morphology and angiogenesis of an oestrogen-induced prolactinoma in Fischer 344 rats.

The process of angiogenesis occurs in many physiological states, but it is also essential for the growth of solid tumours and metastasis formation. An abnormal arterial vascularization has been shown in prolactin-secreting pituitary adenomas induced by prolonged treatment with oestrogens in Fischer 344 (F344) rats. It is thought that anti-angiogenic agents might be useful in therapy for these tumours. Fumagillin and its analogue TNP-470 are known to inhibit endothelial cell proliferation selectively, but their effect on lactotroph cell secretory function and prolactinoma formation has not yet been described. The aim of the present study was to examine the effects of fumagillin and TNP-470 on prolactin secretion, and morphological and vascular changes within the anterior pituitary in long-term oestrogen-treated male F344 rats in vivo and in vitro. As expected, 7 weeks after s.c. implantation of Silastic tubes containing 10 mg diethyl-stilboestrol (DES), a very high rise in serum prolactin levels was found. Both angiogenesis inhibitors injected s.c. at doses of 10 mg/kg body weight for 24 days attenuated the stimulatory effect of DES on prolactin production and release. They also diminished prolactin cell density and inhibited cell proliferation expressed as the number of anterior pituitary cells labelled with bromodeoxyuridine (BrdU), but the effect of TNP-470 was minor compared with fumagillin. Both angioinhibitors suppressed neo-vascularization within the anterior pituitary with similar potency but, on the other hand, they did not affect DES-induced increases in prolactin secretion from cultured rat pituitary cells and cell proliferation in vitro. In conclusion, our results provide strong evidence for the anti-tumour and anti-prolactin activity of angiogenesis inhibitors in the experimentally oestrogen-induced pituitary adenoma; this might be mediated indirectly through the inhibition of angiogenesis.

The effect of somatostatin analog octreotide on diethylstilbestrol-induced prolactin secretion, cell proliferation and vascular changes in the rat anterior pituitary gland.

The effects of diethylstilbestrol (DES) and of long-acting somatostatin analog, octreotide (SMS) on the rat anterior pituitary microvasculature have been studied by means of computer-assisted image analysis. Additionally, the effects of DES and SMS on prolactin secretion and anterior pituitary cell proliferation have been studied, as well. The vascularization was visualized using Selye's method modified by Poely et al. (1964). The prolactin serum levels were estimated by radio-immunoassay. The proliferation indices were assessed using bromodeoxyuridine incorporation assay. As expected, it was found that DES sharply increased serum prolactin levels and enhanced cell proliferation in the anterior pituitary gland. DES also induced changes in parameters of vascularization. Simultaneous treatment of rats with SMS inhibited the DES-induced elevation of prolactin levels and pituitary cell proliferation. It also suppressed some but not all DES-induced changes in the anterior pituitary vascularization. These data suggest that the angio-inhibitory activity of SMS might be involved in its anti-tumor action on pituitary adenomas, but not as a sole or principal mechanism.

The effect of angiotensin II receptor antagonists on diethylstilbestrol-induced vascular changes in the rat anterior pituitary gland: a quantitative evaluation.

The effects if diethylstilbestrol (DES) and of angiotensin II (Ang II) receptor antagonists, such as losartan (selective AT1 receptor antagonist) or PD 123319 (selective AT2 receptor antagonist) on the anterior pituitary microvasculature were studied by means of computer-assisted image analysis. The vascularization was visualized using Selye's method modified by Poely et al. (1964). It was found that DES induced a sharp increase in vessel area, mean vessel diameter and perimeter, whereas mean vessel number was reduced. These DES-induced changes were inhibited by simultaneous administration of losartan. On the other hand, PD 123319 was less effective. These findings suggest an involvement of Ang II, acting mainly via AT1 receptors, in the mechanism of estrogen-induced vascular changes in the rat anterior pituitary gland.

Helicobacter pylori infection in the etiopathogenesis of duodenal ulcer in children.

The study evaluates the frequency of Helicobacter pylori (H. pylori) infection, as well as systemic cellular immune response to H. pylori in children with duodenal ulcer (DU). The study group comprised 47 children with DU, aged 6-17 (mean 13, 1 +/- 4, 2). H. pylori detection was based on urease test, histology, culture and serologic tests. Endoscopic and morphologic findings were analysed according to Sydney System criteria. In 12 children from the overmentioned group subsets of blood lymphocytes B and T (CD3, CD4, CD8, CD3/DR, CD19) and NK cells, some neutrophils functions (phagocytosis, chemiluminescence) and phagocytes receptors before and one month after H. pylori triple treatment were investigated. H. pylori infection was detected in 44 of the investigated children. In addition, pathologic examination revealed chronic gastritis in 44 children and chronic duodenitis in 42 of them. In immunosystemic examination decreased percentage of CD8 lymphocytes and NK cells, increased CD4/CD8 ratio, decreased mitogen-induced response and changes of function and receptor expression of neutrophils were found. After H. pylori treatment in follow-up endoscopy no ulcers were found and histologic examination did not reveal chronic active gastroduodenitis, while the rate of nonactive gastritis was increased. Eradication of H. pylori infection in 41 children and normalisation of immune parameters in 11 children were obtained. The results of our investigation indicate, that H. pylori infection plays an important role in the pathogenesis of DU in children.

Morphology of the microvascular bed in primary human carcinomas of lung. Part I: Three--dimensional pattern of microvascular network.

Three-dimensional patterns of the microvascular network of four main types of human lung carcinomas (squamous cell carcinoma, oat cell carcinoma, adenocarcinoma and large cell carcinoma) have been described. Investigation has been conducted in 18 autopsy cases by x-ray microangiography, and in 52 autopsy and surgical cases by modified benzidine-nitroprusside method for colouring the erythrocyte column in blood vessel. Specimens for the investigation were collected from standardized places of the tumor margin. Eight essential spatial structures of which the carcinomas' microvascular bed is built have been distinguished. Some characteristic features of microvascular network of highly differentiated squamous cell carcinomas, adenocarcinomas and oat cell carcinoma have been described. It has been concluded also that large cell carcinomas, poorly differentiated squamous cell carcinomas as well as adenocarcinomas do not produce any characteristic and repeated pattern of microvascular bed. One of the main elements of the neoplasm structure influencing the growth rate of the tumor is its peripherial vascular bed. It determines the access of chemotherapeutics, oxygen and components participating in the immunological response also. All of those factors are significant elements while considering the curability.

Morphology of the microvascular bed in primary human carcinomas of lung. Part II. Morphometric investigations of microvascular bed of lung tumors.

A comparative investigations of peripheral microvascular bed in various histological types of human primary lung carcinomas (squamous cell carcinomas, oat-cell carcinomas, adenocarcinomas and large cell carcinomas) have been performed. The study was performed on 52 cases of lung carcinoma (there were 49 cases from autopsy and 3 cases from surgery) and on 8 normal comparative cases for evaluation of unchanged bronchial mucosa. Tissue blocks were obtained from standardized parts of bronchus and contained the intra- and extrabronchial parts of tumour as well as the bordering bronchial mucosa. The relative capacities of: 1. anaplastic cells, 2. connective tissue in stroma, 3. intraluminal space of blood vessels, 4. degenerative anaplastic cells, 5. necrotic detritus, and 6. haemorrhages and erytrorrhages were estimated in carcinomatous tissue by the hit points method. In bronchial mucosa the capacities of: 1. intraluminal space of blood vessels, and 2. haemorrhages and erythrorrhages were recorded. Furthermore, the structure of peripheral microvascular bed was evaluated by constructing the distributive series of diameters of blood vessels. These distributive series were approximated with the analitical function. It was found that the largest capacity of blood vessels (with an extremely developed capillary segment of vascular bed) is in the intrabronchial part of squamous cell carcinomas. In the extrabronchial part of this type of carcinoma, the capacity of blood vessel is about three-times smaller than in the intrabronchial part (3.36% and 9.26%, respectively). The finest blood vessels of extrabronchial part undergo the most considerable reduction, in comparison with the ones in the intrabronchial part of squamous cell carcinoma. Oat-cell carcinomas show the smallest difference in vascularization of intra- and extrabronchial parts of tumor (4.38% and 3.33%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

A clinico-epidemiological study on gastritis in gastric carcinoma and in non-cancerous gastric pathology in Poland.

To investigate the risk of gastric cancer development in subjects with atrophic and nonatrophic gastritis, we studied 221 consecutive gastric cancer patients and 7647 non-cancer subjects for whom endoscopic biopsy of the gastric mucosa was available. In gastritis patients, the relative risk (RR) estimates of gastric cancer were as follows: corpus atrophic gastritis RR = 8.7 (95% CI = 5.4-14.1), antral atrophic gastritis RR = 4.5 (2.4-8.1), chronic atrophic pangastritis RR = 7.6 (3.8-15.3), corpus nonatrophic gastritis RR = 1.6 (0.9-2.7), antral non-atrophic gastritis RR = 1.2 (0.7-2.3), and pangastritis RR = 1.3 (0.6-2.8). The latter was of borderline significance (p = 0.07). In peptic ulcer, a significant excess risk was calculated for subjects with either corpus atrophic gastritis (RR = 3.1 [2.5-3.9] or antral atrophic gastritis (RR = 3.5 [2.6-4.8]). For stomach polyps, the risk was significantly increased only in subjects with corpus atrophic gastritis (RR = 2.1 [1.3-3.5]). The risks for both peptic ulcer and polyps, however, were significantly increased in chronic atrophic pangastritis. A substantial excess risk of gastric cancer was found for atrophy in the corpus (RR = 20.9 [9.0-48.9]) and in the antrum (RR = 14.9 [5.3-41.9]). An increased risk of peptic ulcer was also confirmed in subjects with atrophy in the corpus (RR = 3.0 [1.3-6.9]) and in the antrum (RR = 4.9 [2.0-12.1]).

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.

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.

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.

Histomorphometric investigations of the human heart microvasculature in coronary disease.

Comparative results of morphometric investigations describing the microvasculature of the human left ventricle heart wall muscle have been presented. The control group consisted of 11 autopsied cases of the atherosclerotically non damaged hearts and the second group consisted of 13 autopsied cases of the hearts with double or triple vessel chronic coronary atherosclerosis. The age of subjects ranged from 47 to 85 (median 65). The study was carried out on microscopical slides using digital image analyser. In the control group a significantly lower number and profile area of capillaries was noticed in the subendocardial zone than in the remaining ones. The differences between control and atherosclerotic hearts were most prominent in the subendocardial zone, although they were observed in the subepicardial and intramyocardial zones as well. If the value of each parameter in the subendocardial zone of the control hearts will be fixed equally to 100%, the corresponding values in atherosclerotic group are: the number of capillaries--34%, total area of capillaries--65%, number of collaterals--170%, total area of collaterals--612%, muscle fibre/capillary ratio--137%, the degree of microvasculature anisotropy--164%. On the ground of this study as well as on the qualitative investigations it is postulated that the chronic atherosclerosis of extra-myocardial coronary arteries corresponds to intramyocardial rebuilding of the capillary network worsen the conditions of muscle fibre nutrition.

Diagnostic value of fine needle aspiration biopsy for breast fibroadenoma diagnosis.

The diagnostic value of fine needle aspiration biopsy was estimated in the study. Cytological features, which allow us to diagnose and distinguish fibroadenoma from other breast benign lesions, were also examined. The diagnostic effectiveness was estimated depending on the observance of the described criteria (features) characteristic for the breast fibroadenoma by a comparative analysis of cytological findings in three diagnostic centers.