Serum cathepsin K and cystatin C concentration in patients with advanced non-small-cell lung cancer during chemotherapy.

A pathogenic implication of cathepsin K (Cath K) and its inhibitor - cystatin C (Cyst C) occur to be of growing importance in the mechanisms of tumor invasiveness in lung cancer. This study was conducted to investigate the prognostic role and the effects of chemotherapy on serum Cath K and Cyst C (ELISA) in patients with advanced stage non-small cell lung cancer (NSCLC). The study entered 40 patients (32 men) and 15 healthy volunteers (control group). Peripheral blood samples were taken before and after four cycles of chemotherapy. The mean serum Cyst C levels were significantly higher in patients with advanced NSCLC than in controls (p=0.003). The levels of Cath K in serum of NSCLC are comparable to those in controls. No correlation was found between Cath K and Cyst C concentrations and the histological type and staging of lung cancer. Patients with T4-stage had a lower level of Cyst C, than those with T2 (p=0.033). No correlation was found between the concentrations of Cath K, Cyst C and the effect of chemotherapy. However, Cyst C level positively correlated with serum creatinine concentration (R=0.535; p=0.005) in patients who responded to chemotherapy and with patient's age (R=0.456; p=0.018) in whole group. When the cut-off values of serum Cath K and Cyst C (23.35 pmol/l, 1.29 mg/l, respectively) were used, the prognoses of high and low groups were not different. Concluding, patients with lung cancer have a higher serum concentration of Cyst C compared to healthy people. In our opinion, determination of Cath K and Cyst C concentrations has no clinical significance in the prognosis of the survival time in lung cancer

Bone as a source of organism vitality and regeneration

The most important features that determine the vital role of bone include: a) a continuous supply of calcium, which is indispensible for every cell of the entire organism at all times, and b) the delivery of circulating blood cells and some adult stem cells to keep the body vigorous, ready for self-reparation, and continuously rebuilding throughout life. These functions of bones are no less important than protecting the body cavities, serving as mechanical levers connected to the muscles, and determining the shape and dimensions of the entire organism. The aim of this review was to address some basic cellular and molecular knowledge to better understand the complex interactions of bone structural components. The apprehension of osteoblast differentiation and its local regulation has substantially increased in recent years. It has been suggested that osteocytes, cells within the bone matrix, act as regulatory mechanosensors. Therefore immobility as well as limited activity has a dramatic effect on bone structure and influences a broad spectrum of bone physiology-related functions as well as the functions of many other organs. Lifelong bone rebuilding is modulated through several pathways, including the Wnt pathway that regulates bone formation and resorption. In the adult skeleton, bone is continuously renewed in response to a variety of stimuli, such as the specific process of remodeling dependent on RANK/ /RANKL/OPG interactions. Better understanding of bone biology provides opportunities for the development of more effective prevention and treatment modalities for a variety of bone diseases, including new approaches to adult stem cell-based therapies. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 4, pp. 558–569

Immunohistochemical markers of cancerogenesis in the lung.

Lung cancer is the leading cause of cancer deaths for people of both sexes worldwide. Early diagnosis of precancer lesions may be of crucial significance to lowering lung cancer mortality. The World Health Organization has defined three preneoplastic lesions of the bronchial epithelium: squamous dysplasia and carcinoma in situ, atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. These lesions are believed to progress to squamous cell carcinoma, adenocarcinoma and carcinoid tumors, respectively. Apart from WHO classification, two other lesions such as bronchiolization and bronchiolar columnar cell dysplasia (BCCD) can be observed and thought to be preneoplastic lesions leading to adenocarcinoma. In this review we summarize the data of morphological and cell cycle related proteins changes in both central and peripheral compartments of lung. Many molecular changes, which accompany the multistep process of the development of invasive types of cancer, may be observed thanks to the application of immunohistochemical markers. A deeper knowledge of molecular and genetic changes accompanying pre-cancer states may show new directions of early diagnostics of cancer development

Immunohistochemical markers of cancerogenesis in the lung.

Lung cancer is the leading cause of cancer deaths for people of both sexes worldwide. Early diagnosis of precancer lesions may be of crucial significance to lowering lung cancer mortality. The World Health Organization has defined three preneoplastic lesions of the bronchial epithelium: squamous dysplasia and carcinoma in situ, atypical adenomatous hyperplasia and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. These lesions are believed to progress to squamous cell carcinoma, adenocarcinoma and carcinoid tumors, respectively. Apart from WHO classification, two other lesions such as bronchiolization and bronchiolar columnar cell dysplasia (BCCD) can be observed and thought to be preneoplastic lesions leading to adenocarcinoma. In this review we summarize the data of morphological and cell cycle related proteins changes in both central and peripheral compartments of lung. Many molecular changes, which accompany the multistep process of the development of invasive types of cancer, may be observed thanks to the application of immunohistochemical markers. A deeper knowledge of molecular and genetic changes accompanying pre-cancer states may show new directions of early diagnostics of cancer development

Mutations in the KRAS gene in ovarian tumors.

RAS genes are the most frequently mutated oncogenes detected in human cancer. In this study we analyzed the presence of mutations at codon 12 of the KRAS gene in 78 women with ovarian tumor, including 64 invasive ovarian cancers and 14 borderline ovarian tumors, using an RFLP-PCR technique and we evaluated whether such alterations were associated with the selected clinicopathological parameters of the patients. KRAS codon 12 gene mutations were found in 6,2% of ovarian cancer tissue and in 14,3% of the borderline ovarian tumor. KRAS mutations were found with a significantly higher frequency in mucinous and borderline tumors compared to serous tumors (

Mutations of the KRAS oncogene in endometrial hyperplasia and carcinoma.

The aim of this study was to examine the prevalence and clinicopathological significance of KRAS point mutation in endometrial hyperplasia and carcinoma. We analysed KRAS in 11 cases of complex atypical hyperplasia and in 49 endometrial carcinomas using polymerase chain reaction associated with restriction fragment length polymorphism (PCR-RFPL). Point mutations at codon 12 of KRAS oncogene were identified in 7 of 49 (14,3%) tumor specimens and in 2 of 11 (18,2%) hyperplasias. No correlation was found between KRAS gene mutation and age at onset, histology, grade of differentiation and clinical stage. We conclude that KRAS mutation is a relatively common event in endometrial carcinogenesis, but with no prognostic value

Flake Graphene-Based Nanomaterial Approach for Triggering a Ferroptosis as an Attractive Theranostic Outlook for Tackling Non-Small Lung Cancer: A Mini Review

Lung cancer is a highly aggressive neoplasm that is now a leading cause of cancer death worldwide. One of the major approaches for killing cancer cells is related with activation of apoptotic cell death with anti-cancer drugs. However, the efficiency of apoptosis induction in tumors is limited. Consequently, the development of other forms of non-apoptotic cell death is up to date challenge for scientists worldwide. This situation motivated us to define the aim of this mini-review: gathering knowledge regarding ferroptosis—newly defined programmed cell death process characterized by the excessive accumulation of iron—and combining it with yet another interesting nanomaterial-based graphene approach. In this manuscript, we presented brief information about non-small lung cancer and ferroptosis, followed by a section depicting the key-features of graphene-based nanomaterials influencing their biologically relevant properties

Mutations in the KRAS gene in ovarian tumors.

RAS genes are the most frequently mutated oncogenes detected in human cancer. In this study we analyzed the presence of mutations at codon 12 of the KRAS gene in 78 women with ovarian tumor, including 64 invasive ovarian cancers and 14 borderline ovarian tumors, using an RFLP-PCR technique and we evaluated whether such alterations were associated with the selected clinicopathological parameters of the patients. KRAS codon 12 gene mutations were found in 6,2% of ovarian cancer tissue and in 14,3% of the borderline ovarian tumor. KRAS mutations were found with a significantly higher frequency in mucinous and borderline tumors compared to serous tumors (p<0,01). Mutation frequency was correlated with the histological type of tumor, but not with stage, grade or patients age

Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes

Before this study, there had been no research evaluating the relationship between a lysosomal exoglycosidase profile and secretory function in the salivary glands of rats with streptozotocin- (STZ-) induced type 1 diabetes. In our work, rats were divided into 4 groups of 8 animals each: control groups (C2, C4) and diabetic groups (STZ2, STZ4). The secretory function of salivary glands—nonstimulated and stimulated salivary flow, α-amylase, total protein—and salivary exoglycosidase activities—N-acetyl-β-hexosaminidase (HEX, HEX A, and HEX B), β-glucuronidase, α-fucosidase, β-galactosidase, and α-mannosidase—was estimated both in the parotid and submandibular glands of STZ-diabetic and control rats. The study has demonstrated that the activity of most salivary exoglycosidases is significantly higher in the parotid and submandibular glands of STZ-diabetic rats as compared to the healthy controls and that it increases as the disease progresses. Reduced secretory function of diabetic salivary glands was also observed. A significant inverse correlation between HEX B, α-amylase activity, and stimulated salivary flow in diabetic parotid gland has also been shown. Summarizing, STZ-induced diabetes leads to a change in the lysosomal exoglycosidase profile and reduced function of the salivary glands