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Downregulation of guanine nucleotide-binding protein beta 1 (GNB1) is associated with worsened prognosis of clearcell renal cell carcinoma and is related to VEGF signaling pathway.

Clear-cell renal cell carcinoma (ccRCC) is characterized by genetic abnormalities, while the role of Guanine Nucleotide-Binding Protein Beta 1 (GNB1) in ccRCC has not been studied. We thus aimed to evaluate the expression and prognostic value of GNB1 in ccRCC.

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MiR429 expression level in renal cell cancer and its correlation with the prognosis of patients.

To test the hypothesis that miR429 expression in renal cancer patients is increased and plays a role in the pathogenesis of the disease.

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EGFR mutations and tumor metastases in patients with nonsmall cell lung cancer in the South of Russia.

To assess the frequencies of somatic EGFR mutations in the tumor tissues of patients with non-small cell lung cancer (NSCLC) residing in the South of Russia (SR), and to define the relationship between genetic subtypes of NSCLC and the emergence of different types of metastases.

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Carcinogenic potential of antitumor therapies - is the risk predictable?

The growing number of successfully cured cancer patients has created a new field in oncogenesis. The life expectancy of such patients has increased, however this favorable event may create enough time for epigenetic events to occur which can cause a new carcinognic event, i.e. a secondary malignancy. The terms in use are second primary malignancies as well as therapy-related neoplasms in case the treatment of the first neoplasm is a direct cause. Second primary malignancies can be hematological neoplasms or solid tumors, with solid tumors having higher frequency. Hematological malignancies, especially t MDS (therapy-related myelodysplastic syndrome) and t AML (therapy-related acute myeloid leukemia), are causally associated with cytotoxic chemotherapy, while secondary solid tumors are related to radiotherapy. The pathogenic mechanisms of clonal selection in second malignancies are in connection with induction of fusion oncogenes, induction of genetic instability, selection of resistant cell clones and hereditary predisposition. The most common oncogenic agents are external (antineoplastic systemic treatments including radiation therapy), patient-specific factors (genetic, demographic, hormonal) and tumorspecific factors (tissue radiosensitivity, immunodeficiency). There are special features in the clinical picture, biological characteristics and evolution of the second neoplasm - different latency period, aggressive course and treatment resistance. Risks, types and characteristics of secondary malignancies are analyzed in specific groups of patients. For example, the peak of t-AML is several years after a primary malignancy and for solid tumors, the risk increases progressively during the observation period. In this review, the authors outline that the risk of second malignancies is predictable and can be controllable by adequate monitoring of patients as well as by personalized treatment of the first neoplasm.

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DNA Diffusion Assay Applied to Plant Cells.

DNA diffusion assay is a simple, sensitive and reliable technique which allows the assessment of programmed cell death (PCD) or necrosis events based on nuclear morphology. It consists in isolating nuclei from plant material, which are then embedded in agarose and subjected to lysis in alkaline buffers. Under these conditions, and due to the presence of abundant alkali-labile sites in the DNA, small pieces of DNA diffuse in the agarose gel giving a specific halo appearance when stained with fluorescent dyes like DAPI (4',6-diamidino-2-phenylindole). Here, we describe an optimized protocol for DNA diffusion assay applied to different types of plant cells/tissues, indicating all the critical steps required for a successful experimental procedure.

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Detection of Reactive Oxygen and Nitrogen Species (ROS/RNS) During Hypersensitive Cell Death.

Reactive oxygen and nitrogen species (ROS/RNS) are signaling molecules involved in a plethora of physiological processes in plants. Especially, ROS and nitric oxide (NO) are key players that are required for programmed cell death (PCD). The PCD associated with the hypersensitive response (HR) has been well characterized and the role of H2O2 and NO as key signaling molecules inducing HR has been established. Localization of ROS and NO production in plant tissues in response to pathogens can be imaged by confocal laser microscopy by using specific fluorescent probes. Deciphering the time and spatial regulation of ROS and NO is very important to establish the cellular response of plants to adverse conditions. This chapter is mainly focused on the imaging of ROS and RNS accumulation in vivo in plant tissues undergoing PCD.

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Markers of Developmentally Regulated Programmed Cell Death and Their Analysis in Cereal Seeds.

Programmed cell death (PCD) is a key process for the development and differentiation of multicellular organisms, which is characterized by well-defined morphological and biochemical features. These include chromatin condensation, DNA degradation and nuclear fragmentation, with nucleases and proteases playing a relevant function in these processes. In this chapter we describe methods routinely used for the analysis of hallmarks of developmentally regulated PCD in cereal seed tissues, which are based on agarose and polyacrylamide gel electrophoresis, in situ staining of DNA fragmentation, and cell-free assays of relevant enzymatic activities.

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Comparative study of selenium and selenium nanoparticles with reference to acute toxicity, biochemical attributes, and histopathological response in fish.

Recent studies have demonstrated that selenium (Se) and selenium nanoparticles (Se-NPs) exhibited toxicity at a higher concentration. The lethal concentration of Se and Se-NPs was estimated as 5.29 and 3.97 mg/L at 96 h in Pangasius hypophthalmus. However, the effect of different definite concentration of Se (4.5, 5.0, 5.5, and 6.0 mg/L) and Se-NPs (2.5, 3.0, 3.5, and 4.0 mg/L) was decided for acute experiment. Selenium and Se-NPs alter the biochemical attributes such as anti-oxidative status [catalase (CAT), superoxide dismutase (SOD), and glutathione-S-transferase (GST) activities], neurotransmitter enzyme, cellular metabolic enzymes, stress marker, and histopathology of P. hypophthalmus in a dose- and time-dependent manner. CAT, SOD, and GST were significantly elevated (p < 0.01) when exposed to Se and Se-NPs, and similarly, a neurotransmitter enzyme (acetylcholine esterase (AChE)) was significantly inhibited in a time- and dose-dependent manner. Further, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and malate hydrogenase were noticeably (p < 0.01) affected by Se and Se-NPs from higher concentration to lower concentration. Stress markers such as cortisol and HSP 70 were drastically enhanced by exposure to Se and Se-NPs. All the cellular metabolic and stress marker parameters were elevated which might be due to hyperaccumulation of Se and Se-NPs in the vital organ and target tissues. The histopathology of liver and gill was also altered such as large vacuole, cloudy swelling, focal necrosis, interstitial edema, necrosis in liver, and thickening of primary lamellae epithelium and curling of secondary lamellae due to Se and Se-NP exposure. The study suggested that essential trace element in both forms (inorganic and nano) at higher concentration in acute exposure of Se and Se-NPs led to pronounced deleterious alteration on histopathology and cellular and metabolic activities of P. hypophthalmus.

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Methylmercury Intoxication Promotes Metallothionein Response and Cell Damage in Salivary Glands of Rats.

Environmental and occupational mercury exposure is considered a major public health issue. Despite being well known that MeHg exposure causes adverse effects in several physiologic functions, MeHg effects on salivary glands still not completely elucidated. Here, we investigated the cellular MeHg-induced damage in the three major salivary glands (parotid, submandibular, and sublingual) of adult rats after chronic, systemic and low doses of MeHg exposure. Rats were exposed by 0.04 mg/kg/day over 60 days. After that, animals were euthanized and all three glands were collected. We evaluated total Hg accumulation, metallothionein I/II (MT I/II), α-smooth muscle actin (α-SMA), and cytokeratin 18 (CK18) immune expression. Our results have showed that MeHg is able to disrupt gland tissue and to induce a protective mechanism by MT I/II expression. We also showed that cell MT production is not enough to protect gland tissue against cellular structural damage seen by reducing marking of cytoskeletal proteins as CK18 and α-SMA. Our data suggest that chronic MeHg exposure in low-daily doses is able to induce cellular damage in rat salivary glands.

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Tumor expression of survivin, p53, cyclin D1, osteopontin and fibronectin in predicting the response to neo-adjuvant chemotherapy in children with advanced malignant peripheral nerve sheath tumor.

Selected cell-cycle regulators and extracellular matrix proteins were found to play roles in malignant peripheral nerve sheath tumor (MPNST) biology. We aimed to analyze whether initial tumor tissue expressions of survivin, p53, cyclin D1, osteopontin (OPN) and fibronectin (FN) correlate with the response to neo-adjuvant CHT (naCHT) in children with advanced inoperable MPNST.

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