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Carbohydrate metabolism disorders increase the risk of carcinogenesis. Diabetes mellitus alters numerous physiological processes that may encourage cancer growth. However, treating impaired glucose homeostasis may actually promote neoplasia; maintaining proper glucose plasma concentrations reduces metabolic stresses, however, certain medications may themselves result in oncogenic effects. A number of previous studies have demonstrated that metformin reduces the cancer risk. However, the use of sulfonylurea derivatives correlates with an increased risk of developing a malignancy. Another form of treatment, insulin therapy, involves using various forms of insulin that differ in pharmacodynamics, pharmacokinetics and efficacy. Previous studies have indicated that certain insulin variants also affect the cancer risk. The results from analyses that address the safety of long-lasting insulin types raise the most concern regarding the increased risk of malignancy. Rapid development of novel diabetic medications and their widespread use carries the risk of potentially increased rates of cancer, unnoticeable in limited, randomized, controlled trials. In the present review, the results of clinical and epidemiological studies are evaluated to assess the safety of anti-hyperglycemic medications and their effect on cancer risk and outcomes.

The most important molecular mechanisms promoting carcinogenesis in patients with diabetes mellitus (DM) include oxidative stress, excessive generation of free radicals and nitrous oxide, damage to cellular membranes and DNA, overproduction of lactate, overabundance of protein glycosylation storage products, overexpression of pathological enzyme isoforms, and leakage of cytochromes from organelles. Additionally, dysfunctional signal transduction pathways, especially in pathways involving phosphoinositide 3‑kinase (PI3K)/phosphatase and tensin homolog (PTEN)/Akt, RAS/Raf/ERK, and mammalian target of rapamycin (mTOR), have been implicated in malignant transformation and progression. Obesity and metabolic disorders, such as DM, may contribute to a dysfunctional immune system with a suppressed immune response by inducing a chronic inflammatory state, abnormal humoral and cellular mediated immunity, and lower counts and activity levels of natural killer (NK) cells and natural killer T cells (NKT cells). Recent advances in molecular biology will allow for better understanding of abnormal cellular pathways, as well as elucidating how metabolic disorders contribute to oncogenesis. Knowledge gained through these studies may lead to more efficacious oncologic therapies.

Rhabdomyosarcoma (RMS) is the most frequent soft tissue sarcoma in children. It is localized in the head and neck region in 40% of cases. Treatment of RMS is complex, including multi-drug chemotherapy, radiotherapy and surgery. The progress that has been accomplished in oncology in recent decades significantly improved outcomes. The 5-year survival rate raised from 25% in 1970 to 73% in 2001, according to IRS-IV data. The outcome is influenced by primary tumor localization, clinical staging, histological tumor type and age at the moment of diagnosis. The relatively rare incidence of these tumors resulted in difficulties in creating more standardized therapeutic protocols. Comparison of outcomes in large patients groups led to an increase in the number of patients with complete remission. Although survival rates of RMS patients have improved, searching for new therapeutic modalities and substances is still essential to improve outcomes in cases of more advanced stages and unfavorable tumor localizations.

Obstructive sleep apnea (OSA) is a common disorder characterized by pauses in regular breathing. Apneic episodes lead to recurrent hypoxemia-reoxygenation cycles with concomitant cellular intermittent hypoxia. Studies suggest that intermittent hypoxia in OSA may influence tumorigenesis. This review presents recent articles on the potential role of OSA in cancer development. Relevant research has focused on: molecular pathways mediating the influence of intermittent hypoxia on tumor physiology, animal and epidemiological human studies linking OSA and cancer. Current data relating OSA to risk of neoplastic disease remain scarce, but recent studies reveal the potential for a strong relation. More work is, therefore, needed on the impact of OSA on many cancer-related aspects. Results may offer enlightenment for improved cancer diagnosis and treatment.

Introduction: Sleep-disordered breathing is an important risk factor for neurobehavioral impairment in children. This study was conducted to estimate the prevalence of sleep-disordered breathing in a population of first graders and to determine the association between behavior problems, body mass index (BMI) and snoring., Material and Methods: A population-based, cross-sectional study was conducted using a parent-reported questionnaire. The study evaluated 2,474 first-graders. Data including age, weight, height, BMI, snoring intensity, and problems with child behavior were analyzed., Results: Of 3,480 eligible children, 2,474 (71.1%) returned completed questionnaires. Of these, 72% were reported to be non-snorers, 28% snorers, and 6.4% habitual snorers. There was a positive linear association between behavior impairment and snoring severity measured on a 5-point scale, with highly significant differences between each of five snoring intensity groups (p<0.00001). Compared to non-snorers, snorers in the normal-weight and overweight subgroups had significantly more aggressive behavior (p<0.0001; p=0.002, respectively) and more concentration problems (p<0.0001; p=0.03, respectively). There was no significant difference in aggressive behavior and concentration problems intensity in the screened groups of obese and normal subjects (p=0.70; p=0.79, respectively)., Discussion: Behavior problems were positively associated with increasing snoring frequency. However, there were no differences in the prevalence of behavioral or concentration problems between obese and non-obese first-graders studied.

The natural history of clear cell renal cell cancer is highly unpredictable with various progressors and with populations where small renal masses may be accompanied by metastatic disease. Currently, there is a critical need to determine patient risk and optimize treatment regimes. For these patients, molecular markers may offer significant information in terms of prognostic and predictive values, as well as determination of valid therapeutic targets. Until now, only a few of the many identified clear cell renal cell cancer biomarkers have been clinically validated in large cohorts. And only several biomarkers are integrated in predictive or prognostic models. Therefore, a large cohesive effort is required to advance the field of clear cell renal cell cancer prognostic biomarkers through systematic discovery, verification, validation and clinical implementation.

Metastasis is a complex process that propagates cells from the primary or initial site of the cancer occurrence to distant parts of the body. Cancer cells break from the cancer site and circulate through the bloodstream or lymph vessels, allowing them to reach nearly all parts of the body. These circulating tumour cells (CTCs) contain specialized metastasis-initiating cells (MICs) that reside in the biological heterogeneous primary tumour. Researchers have hypothesized that metastasis of renal cell carcinoma is initiated by circulation of MICs in patients' blood and bone marrow. Based on the cancer stem/progenitor cell concept of carcinogenesis, understanding the molecular phenotypes of metastasis-initiating cells (MICs) in renal cancer could play a vital role in developing strategies for therapeutic interventions in renal cancer. Existence of MICs among CTCs in renal carcinoma has not been proven in large scale. However, some studies have reported that specialized markers are found on the surface of circulating cells from the primary tumour. In mice, MICs have been isolated from CTCs using such markers, which have then been transplanted into xenograft model to show whether they give rise to metastasis in different organs. Considering these findings, in this review we have attempted to summarize the studies connected with MICs and their gene expression profiles that are responsible for metastasis in renal cancer., Competing Interests: The authors indicate no potential conflict of interest.

Vascular anomalies are divided according to the contemporary system of classification into two groups: tumors and malformations. However, there is no consensus on juvenile angiofibroma's place in that system. The general characteristics of selected markers of angiogenesis and tissue remodeling are presented in the series in the context of current knowledge in the field of pathophysiology of vascular lesions. The mentioned markers are currently the subjects of multidirectional studies in oncology, as they take part in the process of neoangiogenesis and proliferation of tumors. Nevertheless, they have not been widely examined in vascular lesions. The indirect goal of that series is to indicate the possible research direction on vascular lesions to determine their molecular profile, to create a more specific system of classification, and above all to develop new diagnostic and treatment methods.

At present, only eight cases of tracheal adenoid cystic carcinomas (ACCs) mimicking thyroid tumors have been reported. Since there are no guidelines available regarding their diagnosis and treatment, they present a significant clinical challenge. In the present study, patient treatment was analyzed to deliver the first concise summary of treatment options in patients with ACC mimicking a thyroid tumor. In addition, all available data regarding molecular abnormalities of this disease have been discussed. The current study presents a case of a 17-year-old patient with a tracheal ACC mimicking a thyroid tumor. The patient was diagnosed in 2007 with a pathological mass between the left lobe of the thyroid and the trachea, and underwent surgery and radiotherapy. In 2010, multiple lesions in the lungs were diagnosed and pulmonary metastasectomy was performed. Following surgery, the patient has been disease-free for almost 30 months. Thyroid tumor biopsy may reveal ACCs. This pathological report requires further investigation of the head and neck in order to confirm if the disease is of tracheal origin. Patients may present with a neck swelling, hoarseness of voice or dysphagia. Surgery must be considered as first-line therapy for all patients with local disease as it may be curative. For palliative treatment chemoradiotherapy based on cisplatin may be effective. The identification of cytogenetics, tumor suppressor genes, oncogenes, epigenetic alterations and mitochondrial abnormalities specific for ACCs is critical to the development of targeted therapies. Thus far, large studies have only reported the transcriptional activator Myb and mammalian target of rapamycin signaling pathway to be disrupted in ACCs.

The last few years have brought advances in the understanding of the molecular biology of metastatic clear cell renal cell carcinoma (RCC). Both preclinical research and clinical trials brought together results from the latest advancements in RCC diagnostic and staging. Understanding of the complex molecular alterations involved in the development and progression of RCC enables development of immunohistochemical and genetic diagnostic tools and is also opening the doors for experimental targeted therapies. At the same time, improvements of medical and molecular imaging improves the sensitivity and specificity of metastatic disease diagnosis. Moreover, independent validation of molecular profiles across high-throughput platforms, methods, laboratories and cancer populations has recently been successfully performed in RCC. Generation of informative, clinical diagnostic tools is likely to contribute to development of novel personalized diagnostic and treatment protocols and ensure prolonged survival of RCC patient in the near future.

Introduction: Nasal obstruction is often reported by patients. It is a consequence of a subjective feeling of impaired airflow through the nasal cavity. Currently, objective measures of nasal patency rates are very limited. Functional tests only analyze nasal breathing; they do not simultaneously assess airflow through the mouth., Objective: The aim of this study is to present a new functional test that assesses a single-stage nasal and oral breathing route., Methods: The NOFA (Nasal-Oral Flow Analyzer) is a three-channel flow meter used to perform continuous and simultaneous measurements of nasal and oral respiratory parameters. We present the application of the device and the proposed study protocol., Results: The respiratory tracks of four selected patients are presented. Different breathing patterns are visible: exclusive nasal, exclusive oral, and mixed nasal-oral ventilation pattern., Conclusions: The preliminary results suggest the potential use of the NOFA in ENT practice. Further studies are necessary to evaluate the usefulness of this device in the diagnosis of patients with upper respiratory tract disorders., (Copyright © 2013 Polish Otorhinolaryngology - Head and Neck Surgery Society. Published by Elsevier Urban & Partner Sp. z.o.o. All rights reserved.)

Background: A high level of endogenous erythropoietin (EPO) may be associated with a smaller infarct size determined by the release of necrosis markers. Sleep-disordered breathing (SDB) is a well-known risk factor for cardiovascular diseases. In contrast, protective effects of SDB have also been described. The potential role of increased levels of EPO and vascular endothelial growth factor (VEGF) is suggested in this process. The study aimed to explore the EPO and VEGF serum levels in SDB and non-SDB patients during the acute phase of myocardial infarction., Methods: Thirty-seven patients undergoing successful primary percutaneous coronary intervention in the acute myocardial infarction have been examined for the levels of EPO, VEGF, and troponin I (Tn). In the following, patients had an overnight polysomnography to determine breathing disturbances during sleep., Results: Both on admission day (day 1) and day 3 of hospitalization, EPO levels showed statistically significant differences in both SDB-positive and SDB-negative patient groups (p = 0.003 and p = 0.018, respectively). There was no statistically significant difference in VEGF levels. No correlation was found between the EPO and Tn levels., Conclusions: SDB patients tend to have higher levels of EPO during acute myocardial infarction. No statistically significant differences in VEGF levels were observed.

Ovarian cancer is characterized by the highest mortality rate among gynecologic malignancies. Therefore, there is a growing need for innovative therapies and techniques for monitoring and prevention of this disease. The exact cause of most ovarian tumors usually remains unknown. Ovarian cancer is believed to be caused by a range of different variables. This review is an attempt to summarize some genetic factors involved in the disruption of certain signaling pathways responsible for ovarian tumor transformation and development. Those factors considerably contribute to accurate diagnostics, treatment and prognosis in ovarian cancer.

Background: The main goal of the study was the analysis of somatostatin receptor (SSTR) expression on juvenile nasopharyngeal angiofibroma (JNA) cells and a subsequent analysis of the utility of SST analog-based scintigraphy in JNA diagnostics., Methods: Nine JNA cases were analyzed. All tissue samples were analyzed for the expression of SSTRs. In 2 cases, scintigraphy was performed after the intravenous (IV) administration of an SST analog. MRI of the craniofacial region was subsequently performed., Results: The SST analogues were accumulated in areas matching pathologic tissue in the nasopharynx. Immunohistochemical evaluation of the tissue samples proved the overexpression of SSTRs., Conclusions: SSTRs are overexpressed on JNA cells. The SST analog (99m)TC-octreotide is effectively bound to JNA cells. SST analogues might be used in the diagnostics and treatment of primary, recurrent, or residual JNA., (Copyright © 2011 Wiley Periodicals, Inc.)

Vulvar carcinoma is a rare female genital neoplasm. Although numerous molecular defects in vulvar carcinomas have been reported until now, no molecular markers that could be applied in daily clinical work have been identified so far. However, there is emerging evidence that specific mutations and gene expression patterns may be used as diagnostic tools in oncology. In this article we systematically review genetic alterations that may contribute to the development and progression of vulvar carcinoma. We conclude by suggesting molecular markers of potential clinical value in the diagnostics of this type of cancer.

Objective: The thorough knowledge about anatomy and morphology of the stapedial artery is of such importance to the laryngologist. In rat this artery persists throughout life. The following study was performed to analyze the morphology and course of stapedial artery in rat., Methods: 30 Wistar rats weighing 300-400 g were used to analyze the stapedial artery. After the anesthetic induction with ether, the lethal doses of thiopental were administered. The stapedial arteries were dissected after latex injection and an immersion and preservation in 9% formalin solution., Results: The stapedial artery branches off internal carotid artery and course through the stapes. After that it gives middle meningeal artery and continues in a bony canal laterally to the tegmen tympani. In the orbit stapedial artery gives off ophtalmic artery to supply mainly the orbit structures (muscles, lacrimal gland and eyeball) and the infraorbital artery with palatine artery. Additionally, the ophtalmic artery gives off the central retinal artery., Conclusion: Our study reveals that the stapedial artery and its distal branches are the only vessels supplying all tissues of the orbit, including the eyeball in rats.

Mitochondria are subcellular organelles that produce adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS). As suggested over 70 years ago by Otto Warburg and recently confirmed with molecular techniques, alterations in respiratory activity and mitochondrial DNA (mtDNA) appear to be common features of malignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells, but very few reports document the prevalence of inherited mitochondrial DNA polymorphisms in cancer patients compared to healthy control populations. Here we report the abundance of the 10398G polymorphism in a Polish breast cancer population and its frequency in controls. Amongst individuals with breast cancer the G single nucleotide polymorphism (SNP) is present in 23% of affected females compared to 3% of controls. This difference is highly statistically significant (P = 0.0008). It is therefore possible that the 10398G SNP constitutes an inherited predisposition factor for the development of breast cancer.

For osteoblastoma, with its predilection for the spinal column and appendicular skeleton, the skull is an unusual site, and paranasal sinus involvement is very rare. Herein, we report on a case in which the disease was located within the sphenoid bone. To the best of our knowledge, this is the 4th reported case of osteoblastoma with a sphenoid origin (1). We report an osteoblastoma of the sphenoid sinus in a 12-year-old girl who presented with exophthalmos. Computed tomography (CT) demonstrated an expansile lesion of the sphenoid which caused the orbital contents to be compressed and deviated to the right. In the magnetic resonance imaging scan, the lesion was found to invade the cranial base in the frontal and temporal region, approximating to the cavernous sinus and internal carotid artery on the right. Bilateral fronto-orbital craniotomy was performed. Histologically, the lesion was composed of proliferating osteoblasts along with vascular stroma. The tumor was described as an aggressive osteoblastoma. In the follow-up CT four months later, a pathological mass was observed in the area of the nasal septum, and a signal void was present on all sequences in the densely sclerotic areas. A second resection was performed. The patient has been disease-free for 61 months. Herein, we present the diagnosis and management of this unusual lesion. The histopathology and the imaging characteristics are shown.

Mitochondria are cell organelles mostly known for their production of ATP through oxidative phosphorylation. As suggested over 70 years ago by O. Warburg and recently confirmed with molecular techniques, alterations in respiratory activity and mitochondrial DNA appear to be a common feature of malignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells. MtDNA mutation pattern may enhance the specificity of cancer diagnostics, detection and prediction of tumor growth rate and patients' outcome. Therefore it may be used as a molecular cancer bio-marker. Nevertheless recently published papers list a large number of mitochondrial DNA mutations in many different cancer types, but their role in cell pathophysiology remains unsummarized. This review covers the consequences of mitochondrial genes mutations for human cell physiology and proliferation. We underline effects of mtDNA mutation-resulting amino acid changes in the respiratory chain proteins' structure, and propose changes in mitochondrial protein function. Mutations are critically evaluated and interpreted in the functional context and clinical utility of molecular mitochondrial research is summarized and new perspectives for 'mitochondrial oncology' suggested.

Objective: Salivary tumors can manifest as abnormalities of the gland itself and/or changes in salivary flow. However, effects of salivary tumors on saliva secretion have not been studied in much detail. The aim of the present study was to evaluate effects of benign parotid tumors on unstimulated saliva secretion from the affected gland., Methods: Unstimulated parotid saliva was collected bilaterally using the swab method in patients with unilateral pleomorphic adenoma (n=14) or Warthin's tumor (n=6). Pre-weighted cotton rolls were placed at the opening of each parotid duct for 15min., Results: The range of salivary flow was similar to that found in studies on unstimulated parotid saliva. Salivary flow did not differ between the involved and non-involved side. No difference was found between the involved and non-involved side when the patients with pleomorphic adenoma or Warthin's tumor were separately analyzed., Conclusion: The present results suggest that the most common benign parotid tumors do not alter unstimulated salivary flow from the affected gland.

Endometrial carcinoma is among the most frequently diagnosed gynecological malignancies in highly developed countries. Research has been conducted for 20 years to define the molecular pathology of this disease and much is already known, but adequate prognostic, diagnostic, and monitoring markers are still missing. Recently, mitochondrial research opened a new perspective. The participation of abnormalities of those organelles and mutations of the mitochondrial genome has been defined in some types of cancer and is still under investigation. MtDNA mutations are also found in endometrial adenocarcinoma, although their impact on cell physiology has not been determined so far. Some processes involving mitochondria are widely known and described in numerous papers. These include electron transport and apoptosis, but others await further research. A forward genetics approach has been used in a wide spectrum of projects in which cancer tissue samples were collected from subjects with defined diagnoses and metabolic abnormalities and mtDNA mutations were checked. Thanks to this approach, characteristic patterns of mitochondrial disruption have been assigned to specific types of cancer. This review focuses on the molecular characteristics of endometrial adenocarcinoma with special focus on mitochondrial abnormalities. Research on cancer molecular pathology in endometrial adenocarcinoma may lead to the development of specific screening and/or diagnostic markers.

Aims: Neuroimaging studies suggest a significant overlap between brain regions involved in the regulation of olfaction and mood. The aim of the present study was to search for correlations between depressive symptomatology measured by the 15-item Geriatric Depression Scale (GDS) and olfactory function assessed with Sniffin' Sticks in non-demented older adults (aged 53-79 years)., Methods: Taste detection thresholds were also measured by means of electrogustometry on the anterior tongue., Results: No correlation was found between the GDS scores (range: 0-12) and olfactory thresholds or olfactory identification scores. Similarly, there was no relationship between depressive symptoms and electrogustometric thresholds. Subjects (n = 25) scoring > or = 5 on the GDS were classified as 'depressed' and all other individuals (n = 60) were classified as 'non-depressed'. The two groups did not differ in terms of the olfactory measures and electrogustometric threshold., Conclusion: Depressive symptoms are not associated with any major olfactory deficit in non-clinical older adults.

Data reported until today suggested a pivotal role of nuclear DNA mutations in the process of carcinogenesis. Recently more and more authors claim that disruption of mitochondrial DNA should not be excluded from this analysis. mtDNA have been reported in many cancers of head and neck region. Mitochondrial D-loop has been proven to be mutation hot - spot with majority of mutations in the positions 303 to 315 of poly-C tract. Data show that 37% of patients with premalignant lesions and 62% with carcinoma in situ are positive for mtDNA mutations. Moreover mutations in genes encoding ND2, ND5, COIII, CYTB, and ATP6 were observed in 17% of patients. Mutations in mitochondrial rRNA genes occured in similar number of cases. Neoplastic cells undifferentiation and disease progression is accompanied by multiplication of mtDNA number and increased mtDNA content. mtDNA content corellates with the stage of the disease. mtDNA mutations faciliate cell proliferation and inhibit apoptosis by increasing the production of ractive oxygen species (ROS). Cells harbouring mutated mtDNA have increased proliferation rate, as increased ROS concentration may act as an endogenous growth factor.

Recently published papers report a large number of mitochondrial DNA mutations in many different cancer types, but their significance for electron transport chain proteins remains unknown. This review covers structural mutations of mitochondrial genes, choosing prostate cancer, esophageal cancer and epithelioma as research models. As all mitochondrial genes encode subunits of the electron transport chain, the review focuses on the consequences of structural mutations on cell metabolism.

Unlabelled: Glutathione S-transferase (GST, EC 2.5.1.18) is one of the most important enzymes protecting cells against toxic, electrophilic compounds. It occurs in isoenzymes, expression of which changes in various pathological conditions including neoplasia. The aim of the present study was to analyze the expression pattern of GST pi, mi4 and alpha in human tongue and floor of mouth squamous cell carcinomas., Material and Methods: The studies were conducted on tissue samples obtained from surgery. RT-PCR was used to determine the GSTs-mRNA expression, and Western blotting to study GST pi protein expression., Results: Indicated statistically significant differences in GST pi mRNA expression in tumor and control tissues. GST pi expression was raised in tumors on both mRNA and protein levels, whereas mRNA-GSTmi4 and alfa expression was diverse., Conclusion: Increased level of GST pi expression indicates its role in carcinogenesis.

Aims: The aim of the present study was to evaluate a possible relationship between taste responses to sweet solutions and alcoholic status., Methods: The rated intensity and pleasantness of sucrose taste was compared in male alcoholics (n = 45) and non-alcoholic controls (n = 33)., Results: The rated intensity, but not pleasantness, of water taste (0% sucrose) was higher in the alcoholics. The two groups did not differ with respect to the rated intensity or pleasantness of sucrose solutions (1-30%). The proportion of sweet-likers, i.e. subjects rating 30% sucrose as most pleasant, was similar in both groups (the controls: 57.6%, the alcoholics: 62.2%). A subgroup of alcoholics with a paternal history of alcoholism (n = 22) rated the highest sucrose concentration as more pleasant compared to alcoholics without alcoholic fathers. The proportion of sweet-likers among the alcoholics with a paternal history of alcoholism (77.3%) was significantly higher than that found in the alcoholics without a familial history of alcoholism (47.8%)., Conclusions: The present results suggest the following: (i) alcohol dependence is not associated with any major alterations in taste responses to sucrose solutions, (ii) sweet liking is a phenotypic marker of male alcoholics with a paternal history of alcoholism.

Introduction: Submucosal arytenoidectomy is one of many surgical techniques used in the treatment of the median bilateral vocal fold paralysis. The technique evolved from the large extralaryngeal operation to the endoscopic, intralaryngeal procedure. Gradually it excluded tracheostomy from the methods of treatment of dyspnoea caused by bilateral vocal fold paralysis., Materials and Methods: We present two patients with bilateral vocal fold paralysis with dyspnoea, caused by the neoplastic mass primarily localised in the left lung. In both cases the nonmicrocellular carcinoma was diagnosed. Both patients had the left recurrent laryngeal nerve palsy for more than 18 months and the right nerve palsy for 10-14 days before admission, with concomitant dyspnoea., Results: Both patients were successfully extubated, 24 hours after the operation. The breathing improved significantly. None of the patients had to be reintubated or tracheotomized., Conclusions: The Authors conclude, that the arytenoidectomy with laterofixation should be the method of choice in the treatment of the bilateral vocal fold paralysis caused by the lung cancer. The method does not exclude the upper airway from the respiratory tract which is of special importance for the patients with the lung problems.

Introduction: Esthesioneuroblastoma is a malignant tumour arising from the olfactory epithelium located in the upper part of the nasal cavities. Recent clinical and preclinical studies shed more light on etiopathogenesis, diagnosis, and treatment of this rare malignancy., Material and Methods: A systematic review of PubMed/Medline and available Polish literature., Results: Molecular studies indicate basal progenitor cells of the olfactory epithelium as the origin of esthesioneuroblastoma. Tumour symptoms are related to its location and typically include: epistaxis, nasal obstruction, olfactory and ophtalmic disturbances as well as craniofacial pain. Esthesioneuroblastoma should be differentiated from embryonic rhabdomyosarcoma, Ewing's sarcoma, melanoma, lymphoma, and pericytoma. A combination of surgery and radiotherapy seems to be the optimum approach to treatment. More aggressive treatment regimens are promising but require further studies., Conclusions: Esthesioneuroblastoma is a rare malignant tumour arising from the olfactory epithelium. Early diagnosis and interdisciplinary approach to treatment is vital in the management of the tumour.

Carcinoma planoepitheliale of larynx is the most common cancer present in the upper part of the respiratory system. The molecular mechanism of this cancer generation is unknown and there is no a specific marker for its early diagnosis. The properties, physiological function, as well as the results of studies on genetic polymorphism indicate that glutathione-S-transferase (GST) may play an important role in etiology of this cancer. In the present work the studies on expession of GST isoenzymes pi, alfa, mu4, and mu5 in larynx cancer (carcinoma planoepitheliale laryngis) were performed. Specimens of larynx cancer and their corresponding normal adjacent tissues were obtained from patients by surgery. Expression was studied on the level of mRNA using RT-PCR method. The results indicated raised expression of GST pi (the major isoform in larynx) and lowered expression of GSTs mu4 and alfa in cancer as compared with the control tissue. No expression of GST mu5 was observed in tumor and normal larynx tissues. Obtained results indicate various mechanism in regulation of GSTs expression in cancerous and normal larynx tissues. They also indicate a special role of GST pi in larynx carcinogenesis.

The aim of the study was to investigate the kinetic properties and identify the subtypes of Ca2+ currents in the cardiac postganglionic sympathetic neurones of rats. Neurones were labelled with a fluorescent tracer--Fast-Blue, injected into the pericardial cavity. Voltage-dependent Ca2+ currents were recorded from dispersed stellate ganglion cells that showed Fast Blue labelling. Only high threshold voltage-dependent Ca2+ currents were found in the somata of cardiac sympathetic neurones. Their maximum amplitude, mean cell capacitance and current density were respectively: 0.67 nA, 19.3 pF and 36.4 pA/pF (n = 21). The maximum Ca2+ conductance was 51.3 nS (n = 14). Half activation voltage equalled +11.0 mV and the slope factor for conductance 11.1 (n = 14). As tested with a 10 s pre-pulse, the Ca2+ current began to inactivate at -80 mV. Half inactivation voltage and slope factor for steady-state inactivation were -36.6 mV and 14.1 (n = 9), respectively. Saturating concentration of L channel blocker (nifedipine), N channel blocker (omega-conotoxin-GVIA), P/Q channel blocker (omega-Agatoxin-IVA) and N/P/Q channel blocker (omega-conotoxin-MVIIC) reduced the total Ca2+ current by 26.8% (n = 7), 57.1% (n = 12), 25.9% (n = 6) and 69.4% (n = 6), respectively. These results show that the somata of cardiac postganglionic cardiac sympathetic neurones contain significant populations of N, L and P/Q high threshold Ca2+ channels.