Academic relationships between Hungarian professors and the Second Vienna Medical School.

This article discusses the impact of the 'second' Vienna Medical School, hallmarked by Karl Rokitansky, Joseph Skoda and Ferdinand Hebra, on the study and practice of medicine in Hungary. Six medical doctors' lives and achievements are outlined, who formed a bridge between Vienna and Budapest through their studies and work. Four of them returned to Hungary and promoted the cause of medicine and medical education there. Lajos Arányi (1812-1877) founded in 1844 the Institute of Pathology at the University of Pest. János Balassa (1814-1868) took the Chair of the Surgical Department. Ignaz Philip Semmelweis (1818-1865), the 'Saviour of Mothers', received a position at the Department of Obstetrics and Gynaecology in Vienna in 1846. Gustav Scheuthauer (1832-1894) became Arányi's successor. Each of them continued to keep contact with their tutors in Vienna, especially with Karl Rokitansky, and followed the clinicopathological conception pioneered by the Vienna Medical School regarding diagnostics, treatment and prevention of diseases. Two physicians remained in Vienna: Mór Kaposi (1837-1902), who became known worldwide posthumously due to the connection between Kaposi's sarcoma and AIDS, was the director of the Department of Dermatology of the Vienna University in 1878. Salomon Stricker (1837-1898) undertook the leadership of the Department of General and Experimental Pathology in 1872.

Changes of protein expression in prostate cancer having lost its androgen sensitivity.

OBJECTIVE: The majority of prostate cancers require androgen hormones for growth, and androgen ablation is an important part of the systemic treatment of advanced prostate cancer. Nevertheless, most of these cancers eventually relapse as they become less sensitive to androgen ablation and anti-androgen treatment. Elucidating the molecular events that are responsible for the conversion of androgen-sensitive cancers to androgen-refractory tumors may reveal new therapeutic opportunities. METHODS: In the present study, we investigated nine androgen-sensitive and nine androgen-refractory prostate cancer samples to evaluate the expression levels of 10 selected proteins that have been implicated in oncogenesis and cancer progression. RESULTS: Our immunohistochemical data show that three of the investigated proteins (i.e., minichromosome maintenance-2, methylguanine-DNA methyltransferase, and androgen receptor) are expressed at significantly different levels in the androgen-refractory cancer samples than in the androgen-sensitive tumors, whereas the expression levels of the seven other studied proteins (i.e., ß-catenin, p27, p21, p16, Ki67, hypoxia-inducible factor 1 alpha, and geminin) are not significantly different regarding the two groups. CONCLUSIONS: Our data suggest that the increased expression of minichromosome maintenance-2 and decreased expression of methylguanine-DNA methyltransferase related to androgen receptor are indicative of the androgen-refractory stage in prostate cancer. Further studies are required to determine whether these expression changes play a causative role in the transition of androgen-sensitive to androgen-refractory prostate cancer.

Molecular profiling of parathyroid hyperplasia, adenoma and carcinoma.

The objective of the study was to examine proliferation and apoptosis associated gene expression in the whole sequence parathyroid lesions to reveal specific features of carcinoma. This study was based on surgically removed parathyroid tissues, gene expression analysis was performed both at gene and protein level. First, mRNA isolation was performed from deep-frozen tissue samples, and further apoptosis pathway-specific cDNA macroarray analysis was carried out. The results were validated with real-time PCR. Subsequently, protein expression was analyzed with immunhistochemistry on Tissue Micro Array multi-blocks derived from several paraffin-embedded samples. cDNA macroarrays revealed elevated expression of both pro-apoptotic (FAS receptor, TRAIL ligand, CASPASE8, and -4) and anti-apoptotic (cIAP1, APOLLON) genes in benign proliferative lesions compared to that in normal gland. TMA studies showed overexpression of KI67, P53, SURVIVIN and APOLLON protein and failure of expression of P27, BCL2, BAX, CHROMOGRANIN-A, SYNAPTOPHYSIN, CYCLIND1, FLIP, TRAIL, CK8, CK18, CK19 in parathyroid carcinoma was detected. These alterations in gene expression of the investigated products could be used in differentiation between beningn and malignant proliferative processes of the parathyroid gland. Authors conclude that a series of alterations in gene expression such as overexpression of APOLLON, P53, KI67 and suppression of P27, BCL2, BAX lead to uncontrolled cell proliferation, but still not leading to increased apoptotic activity in parathyroid carcinoma.

Subacute toxicity assessment of water disinfection byproducts on zebrafish.

Disinfection of raw water is essential to the production of drinking water. However, by-products of disinfection may exert toxic effects. The potential toxic effects of two of these compounds, 4-ethylbenzaldehyde (EBA) and 2,4-difluoroaniline (DFA) were investigated using the zebrafish (Danio rerio) model. The two compounds, dissolved, were introduced in duplicate aquariums containing zebrafish in two different concentrations based on LC50 values. The aquarium water containing EBA or DFA was changed every 96 h throughout the 3 months of treatment. Behavior of the fish in each replicate was inspected twice daily. In course of treatment with both concentrations, fish exposed to DFA displayed behavior associated with visible anxiety, while EBA treated were lethargic and did not evade capture. Application of both concentrations of each component into the aquarium water resulted in dystrophic lesions in the liver, kidney and skin of the fish while preneoplastic lesions and tumors were not observed.

Differential biomarker expression in head and neck cancer correlates with anatomical localization.

We tested the expression of known (p16(ink4), Ki67, p53, EGFR) and a new immunohistochemical (collagen XVII/BP180) biomarker in head and neck squamous cell carcinomas (SCC) of diverse anatomical localization. Tissue microarrays (TMA) of 124 SCC were created, immunostained, and analyzed following whole slide digitalization using the Pannoramic Scan and the TMA Module software (3DHISTECH Kft, Budapest, Hungary). Statistical analysis of scoring results was carried out using Pearson's chi-square test. We observed the significant elevation of p16(ink4) and Ki67 expression in supraglottic, tonsillar and tonsillo-lingual SCCs compared to those affecting the oral cavity, oropharynx without tonsils, larynx without supraglottis and the hypopharynx. This differential antigen expression may reflect the diverse route of embryologic differentiation followed by the affected regions except those of the tonsils and the supraglottis which show similar antigenic pattern but diverse developmental path. All the other biomarkers tested including p53, collagen XVII and EGFR were detected in the majority of cancers including high grade cases, but did not reveal any significant regional difference. Based on our results oropharyngeal squamous cell carcinomas may not be regarded as one entity. Concerning the oral cavity and the oropharynx, cancers affecting the tonsils (palatine and lingual) show significantly elevated p16(ink4) and Ki67 expression; so as the cancers of the supraglottis compared to the rest of larynx. Consequently, tonsillar and supraglottic cancers show similar biomarker profiles. Correlation of differential biomarker expression with diverse biological behavior in head and neck cancers need further investigations.

Effect of formaldehyde on cell proliferation and death.

Formaldehyde (HCHO) may reach living organisms as an exogenous agent or produced within cells. The so-called formaldehydogenic compounds like S-adenosyl-L-methionine, N-hydroxymethyl-L-arginine, 1'-methyl ascorbigen, methanol, E-N-trimethyl lysine and methylamine are special exogenous sources of HCHO. Endogenous HCHO can be formed from hydroxymethyl groups during enzymatic methylation and demethylation processes. HCHO, as a highly reactive compound, is considered to be involved in the induction of apoptosis, consequently in the pathogenesis of atherosclerosis and neurodegenerative processes. The biological action of HCHO is dose-dependent. In vitro studies on tumour cell and endothelial cell cultures showed that HCHO in the concentration of 10.0 mM caused necrotic cell death, 1.0 mM resulted in enhanced apoptosis and reduced mitotic activity, while 0.5 and 0.1 mM enhanced cell proliferation and reduced apoptotic activity. Among formaldehydogenic compounds N-hydroxymethyl-L-arginine, 1'-methyl ascorbigen and the HCHO donor resveratrol may be considered as potential inhibitors of cell proliferation. Endogenous HCHO in plants apparently play a role in regulation of apoptosis and cell proliferation. The genotoxic and carcinogentic effects of HCHO is due to production of DNA-protein cross-links. Low doses of HCHO, reducing apoptotic activity may also accumulate cells with such cross-links. Experimental data point to the possible therapeutic use of methylated lysine residues and methylated arginine residues in the case of neoplasms.

P21, p27, bax, cathepsin and survivin pathways in macular dystrophy corneas.

The purpose of our study was to elucidate pathways of genetically programmed cell death (apoptosis) in corneas with macular dystrophy. 10 corneal buttons (10 patients) with macular dystrophy and 8 buttons (8 patients) from enucleated eyes with chorioideal melanoma (controls) were analysed histologically. Immunohistochemical analysis was performed to investigate the presence of p21, p27, bax, cathepsin and survivin proteins. The number of positive cells was determined by analysis of 100 cells and given in percentages. The bax protein was present in 25.6% of epithelial cells in macular dystrophy corneas but was absent in controls. P21 and p27 were found in 35.7 and 87.5% of epithelial cells of macular dystrophy corneas, respectively, but again not in control tissue. In contrast, a lower percentage of cathepsin-positive (30.7% vs 58.8%) and survivin-positive cells (37.6% vs 52.1%) were present in epithelial cells of macular dystrophy corneas than in control epithelial cells. The difference reached statistical significance in the expression of p21 and p27 genes (p<0.05 in both). P21 was positive in 3% of keratocytes, p27 in 1% of endothelial cells of macular dystrophy corneas but negative in controls (0%). Bax, cathepsin and survivin immunopositivity was not detected in keratocytes or endothelial cells of either group. We conclude that the down-regulation of p21, p27 and cathepsin in epithelial cells of macular dystrophy corneas may be related to defense mechanisms against apoptotic cell death.

Joint effects of cigarette smoking and irradiation in pregnant mice and their offspring.

BACKGROUND: We have previously reported that irradiation of mice in utero significantly increased the tumor incidence in the offspring of irradiated mothers. The joint effects of irradiation and cigarette smoking (CS) on tumor incidence and on the process of carcinogenesis were investigated. MATERIALS AND METHODS: Pregnant C57Bl/6J female mice were irradiated with a single dose of gamma-ray (1 Gy or 3 Gy) and/or exposed to CS of IR3 non-filtered cigarettes before or during pregnancy, tumors were investigated both with histological and immunohistochemical methods. RESULTS: Longer exposure (60 days) of the mice to CS before pregnancy and irradiation during pregnancy significantly increased the tumor incidence in the mothers and their offspring. Parallel activation of Caspase-8 and inactivation of Caspase-9 was found. CONCLUSION: Joint exposure of mice to prolonged CS before pregnancy and irradiation during pregnancy significantly increased the tumor incidence both in the mothers and their offspring.

GnRH receptor and androgen receptor status and outcome of advanced prostate carcinomas.

BACKGROUND: The effect of gonadotropin-releasing hormone (GnRH) analogs on prostate carcinoma is partly a result of breaking the pituitary-gonadal axis, and partly the direct action on tumor cells expressing the GnRH receptor (GnRHR). The aim of this study was to detect the extent of correlation between the expression of GnRHR and also the androgen receptor (AR) and the efficacy of total androgen blockade (TAB). PATIENTS AND METHODS: Needle biopsy samples of twenty advanced prostate carcinoma patients were investigated histologically regarding Gleason score, AR and GnRHR status of the tumor cells. An affinity purified polyclonal antibody reacting with GnRHR and a monoclonal antibody for AR were applied for immunoperoxidase reactions. TAB was started in each case. Pathological, radiological and laboratory-prostate-specific antigen (PSA) data obtained before the start of TAB and survival, PSA values, and radiological findings after three years of TAB were related to AR and GnRHR. RESULTS: Regarding the clinical, radiological and laboratory findings before and after three years of TAB, 13 patients (group A) were considered to show a favourable' and 7 (group B) to show a 'poor' outcome. Twelve patients out of 14 with AR-positive tumor cells and all nine patients with GnRHR-positive tumor cells, as well as all eight patients with both AR- and GnRHR-positive tumor cells belonged to group A. The majority of AR-negative, GnRHR-negative or both AR- and GnRHR-negative cases belonged to group B. CONCLUSION: The presence of GnRHR and AR or both of these receptors indicates a more favourable outcome of advanced prostate carcinoma when treated with TAB, compared to GnRHR- and AR-negative cases. GnRHR and AR negativity may indicate a need for supplementary chemo- or radiotherapy.

Platinum-based chemotherapy in lung cancer affects the expression of certain biomarkers including ERCC1.

Chemotherapies are widely used in the treatment of lung cancer. However, little is known about their effect in the expression of different tissue markers. Seventeen lung cancer tissue blocks obtained by bronchoscopic biopsies together with their corresponding surgical biopsies after neoadjuvant chemotherapy were studied. They included 9 adenocarcinomas (ADC) and 8 squamous cell carcinomas (SCC). Immunohistochemistry was performed on formalin-fixed, paraffin-embedded tissues to study the expression of Ki-67, p53, Bcl-2, Bax, Fas-ligand and ERCC1 (excision repair cross-complementation group 1). Out of 17 NSCLC 6 expressed proapoptotic markers and 4 expressed antiapoptotic markers, while in 7 cases the apoptotic markers did not show detectable changes after neoadjuvant chemotherapy. Six of 17 bronchoscopic NSCLC cases expressed increased level of Ki-67 after neoadjuvant treatment. Eight bronchoscopic NSCLC tissues (6 SCC, 2 ADC) expressed ERCC1. All but one ADC became ERCC1 negative after neoadjuvant therapy. There was no newly expressed ERCC1 positive case in the surgical biopsy group. Platinum-based neoadjuvant chemotherapy had no effect on the apoptotic activity of 17 patients' tumor specimen, however, 6 of 17 bronchoscopic NSCLC cases expressed increased level of Ki-67 after neoadjuvant treatment, in 3 cases the level of Ki-67 became decreased, while 8 cases had no detectable change of proliferation activity. The results of the present study suggest that platinum-based chemotherapy probably induces a selection of tumor cells with more aggressive phenotype, and also affects the expression of tissue marker (ERCC1) that could have predictive value.

[Examination of somatostatin receptor expression in recurrent childhood medulloblastomas]. / A szomatosztatinreceptor-expresszió változásának vizsgálata recidiváló medulloblastomában.

Medulloblastoma is the most common malignant pediatric central nervous system tumor. Despite the adequate therapy the tumor often recurs. The primary medulloblastoma expresses somatostatin receptor-2 (SSTR-2), but so far we had no experience about the receptor status in recurrent tumors. The presence of SSTR-2 may have an important role in the early detection and treatment of recurrent medulloblastomas. Our aim was to examine the state of SSTR-2 expression in recurrent childhood medulloblastomas. We examined SSTR-2 expression by immunohistochemistry in primary and recurrent medulloblastoma samples of ten children treated with recurrent medulloblastoma at Semmelweis University, Departments of Pediatrics, between 1998 and 2004. All primary and recurrent tumors have been operated at the National Institute of Neurosurgery. We examined the intensity and the percentage of SSTR-2-positive tumor cells in the primary and recurrent tumor samples. All primary tumors were receptor-positive and SSTR-2 was also expressed in all recurrent medulloblastomas. In our samples the percentage of SSTR-2-positive tumor cells was 30-90%. As a positive in vivo control Octreoscan images were available in two cases. In these cases the results of immunohistochemistry and Octreoscan imaging seemed to correlate. As a conclusion, SSTR-2-positive recurrent tumors can be detected early by Octreoscan imaging, and the presence of SSTR-2 establishes the opportunity of applying somatostatin analogues (octreotide) in the treatment of recurrent childhood medulloblastoma.

Apoptosis regulation and spontaneous apoptosis index of testicular germ cell tumors are associated with differentiation and resistance to systemic treatment.

BACKGROUND: Cisplatin-based chemotherapy can cure more than 80% of metastatic germ cell testicular tumors (GCT). Germ cells are particularly susceptible to apoptosis and it is reasonable to presume that GCTs are curable because of an intact and effective apoptotic pathway. PATIENTS AND METHODS: The expression of p53 and p21 was investigated in conjunction with the spontaneous apoptotic index in 20 refractory and 50 chemosensitive GCTs, with a complete follow-up. To detect a differentiation-dependent alteration in the apoptotic pathway, all of the histological tumor types were examined separately. RESULTS: Embryonal carcinoma components showed significantly higher p53 expression compared to other histological subtypes of GCTs. p21 was barely detectable in the majority of tumors. Seminomatous components showed no p21 expression. Mature teratomas and syncytiotrophoblasts showed significantly higher p21 expression than other tumor subtypes. Embryonal carcinomas showed significantly higher apoptotic indices than other non-seminomatous components. On the other hand, choriocarcinomas and mature teratomas showed the lowest spontaneous apoptotic potential. The apoptotic index correlated with the fraction of p53-positive cells, but not with the p21 expression rate. The refractory group showed significantly lower p53 expression, higher p21 expression and a higher apoptosis index than the sensitive group. CONCLUSION: Our results suggest that the p53 and p21 expression levels and the apoptosis index seem to be important factors in the issue of the chemosensitivity of GCTs. The protein expression pattern reflects a differentiation-dependent preference for G1/S-phase arrest in terminally differentiated syncytiotrophoblasts and mature teratoma cells, while p53 mediated apoptosis induction is meaning to less differentiated tumor types.

P53, CD95, cathepsin and survivin pathways in Fuchs' dystrophy and pseudophakic bullous keratopathy corneas.

Our purpose was to elucidate the pathways of apoptosis of corneas with Fuchs' dystrophy and pseudophakic bullous keratopathy. Sixteen corneal buttons (14 patients, median age 73 years) with Fuchs' dystrophy, 13 with pseudophakic bullous keratopathy (PBK) (13 patients, median age 69 years) and 8 buttons (8 patients, median age 59 years) from enucleated eyes with chorioideal melanoma (controls) were analysed histologically. Immunohistochemical analysis was performed to investigate the expression of p21, p27, p63, survivin, CD95, cathepsin, bax, bcl-2 and Ki67. Positive immunohistochemical reactions were detected in epithelial cells of the corneas, but keratocytes and endothelial cells were not positive in any of the groups or stainings. The number of p27 and survivin positive epithelial cells was significantly lower (p=0.048 and 0.041) and the number of cathepsin positive epithelial cells was significantly higher (p=0.004) in Fuchs' dystrophy corneas compared to controls. In pseudophakic bullous keratopathy, p21 and p27 positive epithelial cells were present in a significantly lower (p=0.02 and 0.005) number than in controls. We conclude that genetically programmed cell death is related to the p27, cathepsin and survivin pathways in Fuchs' dystrophy and to the p21 and p27 pathways in pseudophakic bullous keratopathy.

Expression of p21(waf1/cip1), p27 (kip1), p63 and androgen receptor in low and high Gleason score prostate cancer.

The aim of this study was to investigate the expression of p21(waf1/cip1), p27(kip1), p63 and androgen receptor proteins in relation to serum prostate specific antigen levels in low and high Gleason score prostate cancers. Biopsies of patients suffering from prostate adenocarcinoma of low (3 + 3 to 3 + 4) and high (5 + 4 to 5 + 5) Gleason scores (13 cases each group) were immunostained for positive regulators of cell cycle control (p21(waf1/cip1) and p27(kip1)), and essential markers of normal prostate gland ontogeny (p63) and growth (androgen receptor) to find differentially expressed markers of malignant progression. Serum prostate specific antigen levels were also monitored at the time of biopsy and following anti-androgen therapy. All cases except one in each group were androgen receptor positive. P63 and p21(waf1/cip1) proteins detected in normal basal cell nuclei were lost in all but one studied tumors respectively. P27(kip1) protein, however, was detected in all low Gleason score prostate cancers, but it was found in only 7/13 high score cases. Prostate specific antigen levels, either pre- or post-treatment, did not show strict correlation with the p27(kip1) results. The low to high grade dedifferentiation of prostate adenocarcinoma is accompanied with the down-regulation of p27(kip1) protein, which may be an important molecular sign of the lost cell cycle control.

The clinical and pathological symptoms of pregnancy epulis.

Examination of the oral cavity in 2260 pregnant women revealed 12 cases of pregnancy epulis, an incidence of 0.48%. In 9 of these 12 cases, spontaneous regression and recovery occurred 1-4 months after delivery. Despite the continuous conservative therapy, several surgical interventions were necessary in the remaining 3 pregnant women, due to the large size of the epulis and the bleeding that was difficult to stop. The authors provide a detailed description of the clinical symptoms (bleeding, difficulty of oral closure, loosening and migration of teeth) caused by large, multiple epulis instances during two pregnancies of one woman, together with the surgical interventions, the histopathologic examination and the immunohistochemical characteristics of the epulis.

Fermented wheat germ extract (avemar) inhibits adjuvant arthritis.

Anti-inflammatory efficacy of the fermented wheat germ extract (FWGE, Avemar) in the rat adjuvant arthritis (AA) model was examined. To Wistar rats with AA, different doses of FWGE and anti-inflammatory drugs (indomethacin, dexamethasone) as monotherapies were administered and FWGE and either diclofenac or dexamethasone were also given in combination. Besides plethysmographies of the paws, histological investigations of synovial tissues were also performed along with detection of CD4+ and CD8+ T lymphocytes. Gene expressions of COX-1 and 2 were determined by real-time polymerase chain reaction (PCR). FWGE monotherapy significantly inhibited the development of the secondary (immune-mediated) response in AA, and dexamethasone and indomethacin exerted inhibitory effects in a degree comparable to that of FWGE. Histological analysis of the affected joints confirmed the results. FWGE inhibited COX-1 and -2, while indomethacin enhanced COX-2 gene expressions. FWGE had an additive interaction with diclofenac. It is concluded that FWGE has significant anti-inflammatory efficacy confirmed by plethysmography, histology, and real-time PCR.

DNA and RNA isolated from tissues processed by microwave-accelerated apparatus MFX-800-3 are suitable for subsequent PCR and Q-RT-PCR amplification.

Over the past decade, methods of molecular biology have appeared in diagnostic pathology and are routinely applied on formalin-fixed, paraffin-embedded histological samples, processed via conventional embedding methods. Due to its reagent- and cost-effectiveness, embedding techniques that utilize microwave acceleration in one or more steps of histoprocessing are increasingly used by numerous laboratories. The demand arises that tissues processed this way should also be suitable for the requirements of molecular pathology. In this study, both conventionally embedded and MFX-800-3 machine-processed tissue samples from the same source were used for isolation of DNA and RNA and for performing PCR and real-time PCR. PCR amplification of the beta-globin gene, as well as the real-time PCR amplification of the ABL mRNA was successful in all cases. Our conclusion is that samples processed by the vacuum assisted automatic microwave histoprocessor MFX-800-3 are perfectly applicable for DNA and RNA isolation and provide appropriate templates for further PCR and realtime PCR studies.

Skull base chordoma mimicking a preauricular neoplasm in a child: clinicopathological features and biological behaviour.

INTRODUCTION: The extreme rarity of chordomas in childhood, the slow growing nature of these tumours and the diverse symptoms may cause many diagnostic problems. PATIENT: A 9-year-old girl presented with an unusual manifestation of a skull base chordoma. The clinical and pathological features were analysed. RESULT: In the present case, the initial symptoms of the skull base tumour were completely misleading. The otodynia, the masticatory difficulties and the mass in the preauricular region were not characteristic of skull base chordomas. The female sex, the young age, the large tumour size and the atypical histological pattern of the tumour all indicated a very poor prognosis. CONCLUSION: The rarity of this tumour in childhood and the atypical lateral and intracranial spread resulted in a serious delay of the diagnosis and in a fatal outcome.

[Changes in gene expression in the course of proliferative processes in the parathyroid gland]. / Génexpresszió-változások a mellékpajzsmirigy proliferatív folyamata során.

The aim of this study was to investigate the changes in expression pattern of the most important genes connected with apoptosis in proliferative apoptotic lesions (hyperplasia, adenoma), applying cDNA microarray technique, in order to promote the possible diagnostic or therapeutic utilisation of any difference in gene expression compared to the healthy (normal) parathyroid gland. Samples were taken from surgically removed 2 hyperplasias, 2 adenomas and 2 normal parathyroid glands. The Apoptosis Gene Array (Superarray) was used. This contains 112 genes, in tetraspot arrangement. The probes measured 250-600 base pairs. Streptavidin was bound to the array. CDP Star TM chemiluminescent substrate was used for detection. The samples deriving from hyperplasia or adenoma were compared to samples from normal parathyroid glands. The following genes were overexpressed in both hyperplasia and adenoma: CHEK1, ATM, BCL-XL, FAS, TNF, cIAP1, TRAIL, FADD, CASP 4,5,6,8, CD120b, CD137, LTA, TANK, TARF2, CAD, LIGHTR, DR3LG. CASP1,10, BFAR, BOD, BCL2L2, TRANCE were underexpressed in both hyperplasia and adenoma. Genes overexpressed only in hyperplasia were: MDM2, MCL1, BCL2A1, BLK, RIPK2, CD40LG, TRAF5, HUS1, BNIP3. Underexpressed only in hyperplasia: BOK, CIDEA, TRAF1, TRIP. Overexpressed only in adenoma: APOLLON, RIPK1, LTB, LTBR, CASP2,13, cIAP2, CIDEB. Underexpressed only in adenoma: TRAF4 and FASLG. Overexpresion or underexpression meant 1.5-fold difference from normal average values. As a result of this study, both pro-apoptotic and antiapoptotic genes were identified in hyperplasia and adenoma of the parathyroid gland. It seems that increased proliferation is connected also with increased apoptotic activity, but tumor cell candidates are able to survive, by activation of signal pathways resulting in overexpresion of anti-apoptotic genes.