Classical and up-to-date models of hematopoietic Lineage determination are briefly reviewed with the focus on myeloid-based models challenging the existence of the common progenitor for T cells, B cells and NK cells. The analysis of immunophenotype of leukemic blast cells seems to be a promising approach for interpreting some controversies in the schemes of normal hematopoiesis. The literature data as well as our own findings in the patients with various types of acute leukemias are in favor of the concept postulating that common myeloid-lymphoid progenitors giving rise to T and B cell branches retain the myeloid potential. The similarity of some immunophenotypic features of blast cells in pro-B acute lymphoblastic leukemia and acute monoblastic leukemia is consistent with monocyte origin postulated in the studies of normal hematopoiesis. Study of acute leukemias may be the challenging area of research allowing for new insight into the origin of hematopoietic cell lineages.

In recent years, the new direction such as identification of informative circulating markers reflecting molecular genetic changes in the DNA of tumor cells was actively developed. Smoking-related DNA adducts are very promising research area, since they indicate high pathogenetic importance in the lung carcinogenesis and can be identified in biological samples with high accuracy and reliability using highly sensitive mass spectrometry methods (TOF/TOF, TOF/MS, MS/MS). The appearance of DNA adducts in blood or tissues is the result of the interaction of carcinogenic factors, such as tobacco constituents, and the body reaction which is determined by individual characteristics of metabolic and repair systems. So, DNA adducts may be considered as a cumulative mirror of heterogeneous response of different individuals to smoking carcinogens, which finally could determine the risk for lung cancer. This review is devoted to analysis of the role of DNA adducts in lung carcinogenesis in order to demonstrate their usefulness as cancer associated markers. Currently, there are some serious limitations impeding the widespread use of DNA adducts as cancer biomarkers, due to failure of standardization of mass spectrometry analysis in order to correctly measure the adduct level in each individual. However, it is known that all DNA adducts are immunogenic, their accumulation over some threshold concentration leads to the appearance of long-living autoantibodies. Thus, detection of an informative pattern of autoantibodies against DNA adducts using innovative multiplex ELISA immunoassay may be a promising approach to find lung cancer at an early stage in highrisk groups (smokers, manufacturing workers, urban dwellers).

Evidence indicates that prolactin plays a crucial role in the normal function and development of the prostate, but abnormal high levels of the hormone are associated with hyperplasia and cancer of the gland. Aims: the present study was designed to describe the progressive specific histological abnormalities in the prostate of rats with chronic hyperprolactinemia. Prolactin was administered during 4; 12 or 24 weeks, and the resulting prostatic alterations were compared with control rats, and also with those treated with testosterone, or the combination of prolactin + testosterone. Rats treated with prolactin, testosterone or prolactin + testosterone expressed precancerous histological abnormalities in the dorsolateral and ventral portions of the prostate as early as in 4 weeks of treatment, but in all cases the malignancy increased after 12 or 24 weeks of treatment. Conclusion: our study confirms that chronic hyperprolactinemia is a cause of prostate precancerous pathologies.

Індекс рубрикатора НБУВ: Р562.3-5

Рубрики:

Саркома

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Індекс рубрикатора НБУВ: Р56-52

Рубрики:

Онкологія

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Індекс рубрикатора НБУВ: Р569.715.2

Рубрики:

Пухлини яєчників

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Study was aimed to analyze the dynamics of changes and study interrelations between content of ferritin, transferrin, active gelatinases (MMP-2 and -9) in blood serum and tumor tissue, free iron, rate of superoxide radicals generation in tumor, activity ofNADPH-oxidase and iNOS in neutrophils rats with sensitive and resistant strains of Guerin carcinoma (GC). In order to obtain resistant tumor, 12 courses of cisplatin chemotherapy have been carried out on rats bearing GC. Levels of transferrin and free iron were determined by analysis of EPR spectra from computerized radiospectrometer EPR RE-1307 at temperature of liquid nitrogen. Rate of superoxide radicals and nitric oxide generation in tumor and neutrophils of blood was determined by EPR using spin traps at room temperature. Content of ferritin in tumor homogenate and blood serum of rats with GC was determined by ELISA method using corresponding kits. Concentration of active forms of MMP-2 and -9 in obtained samples was determined using method of zymography. Unregulated generation of superoxide radicals and NO by mitochondria of tumor cells and NADPH-oxidase and iNOS neutrophils via oxidation of iron-containing proteins causes the accumulation of "free iron" complexes in blood and tumor tissue of rats able to evoke oxide-induced damages of macromolecules. It has been shown that for resistant strain of carcinoma, as compared with sensitive one, significantly higher concentrations of active forms of MMP-2 and -9 in blood serum of rats are typical. Dynamics of gelatinases activity changes in tumor tissue corresponds in general with dynamics of changes in serum. In tumor tissue of rats the indices of gelatinases activity positively correlate with rate of superoxide radicals generation, content of "free iron" complexes, ferritin and activity of transferrin. Cytostatic agent increased levels of reactive oxygen species (ROS) and self-amplify rate of superoxide radicals generation. In turn, activation of MMPs via superoxide-depending regulation allows tumor ceils to facilitate migration, invasion and finally - formation of metastatic centers. Mentioned above tumor "oxide phenotype" determines high level of its aggressiveness and forms corresponding level of drug resistance. Conclusions: Thus, high levels of superoxide radicals oxidize transport proteins and form free iron pool. Iron ions, via Haber - Weiss mechanism, initiate generation of the hydroxyl radicals, which also enhance oxidation processes.

Індекс рубрикатора НБУВ: Р361 + Р56-1

Рубрики:

Дія іонізуючого випромінювання на організм (медична радіобіологія)

Онкологія

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Endometrial cancer (EC) is the second most common malignancy associated with hereditary non-polyposis colorectal cancer (HNPCC) family. The development of HNPCC is associated with defects in DNA mismatch repair (MMR) pathway resulting in microsatcllite instability (MSI). MSI is present in a greater number of EC than can be accounted for by inherited MMR mutations, therefore alternative mechanisms may underline defective MMR in EC, including polymorphic variation. Aim: we checked the association between EC occurrence and two polymorphisms of MMR genes: a 1032G>>A (rs4987188) transition in the hMSH2 gene resulting in a Giy22Asp substitution and a - 93G>>A (rs 1800734) transition in the promoter of the hMLHl gene. Material and methods: These polymorphisms were genotyped in DNA from peripheral blood lymphocytes of 100 EC patients and 100 age-matched women by restriction fragment length polymorphism PCR. A positive association (OR 4,18; 95 % CI 2,23 - 7,84) was found for the G/A genotype of the -93G>>A polymorphism of the hMLH 1 gene and EC occurrence. On the other hand, the A allele of this polymorphism was associated with decreased EC occurrence. The Gly/Gly genotype slightly increased the effect of the -93G>>A-G/A genotype (OR 4,52; CI 2,41 - 8,49). Our results suggest that the -93G>>A polymorphism of the hMLH 1 gene singly and in combination with the Gly322Asp polymorphism of the hMSH2 gene may increase the risk of EC.

Індекс рубрикатора НБУВ: Р569.433.2 + Р411.1

Рубрики:

Пухлини шлунку і дванадцятипалої кишки

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Індекс рубрикатора НБУВ: Р569.133.1

Рубрики:

Пухлини молочних (грудних) залоз

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Індекс рубрикатора НБУВ: Р569.133.1

Рубрики:

Пухлини молочних (грудних) залоз

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Індекс рубрикатора НБУВ: Р411.022.3 + Р569.411

Рубрики:

Лімфатичні лейкози

Пухлини кісткового мозку і крові

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Індекс рубрикатора НБУВ: Р411.022.2-5 + Р569.411-5

Рубрики:

Мієлоїдні лейкози

Пухлини кісткового мозку і крові

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Індекс рубрикатора НБУВ: Р411.022.3 + Р569.411

Рубрики:

Лімфатичні лейкози

Пухлини кісткового мозку і крові

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

Aim - the expression differences of SCN8A (which encodes type VIII alpha subunit of voltage gated sodium channel) and NDUFC2 (which encodes C2 subunit of Complex I enzyme moxidative phosphorylation) genes were evaluated in paired colorectal cancer (CRC) tissues which was relied on our partial transcriptome analysis data in cancer cell lines. A total of 62 paired tissues of CRC patients (34 male, 28 female) were included in the study. The mRNA levels of SCN8A and NDUFC2 genes were determined by using real-time PCR (qRT-PCR and semiquantitative PCR). SCN8A gene expression level was significantly lower in tumor tissues (p = 0,0128) and in the patients with tbe age below 45 years (p = 0,0049). There were also meaningful relationships between the gender, grade of CRC, tumor location, histopatbological classification, and SCN8A expression. There was no NDUFC2 differential expression. However, the tumors taken from rigbt colon had significantly lower NDUFC2 expression. Conclusion: although the voltage gated sodium channels (VGSCs) and Complex I (Cl) were associated to a number of diseases including different types of cancers, tbe different subunits of Cl and individual members of VGSCs seem to be cancer type-specific in varying proportions.

Symptomatology of oncological diseases consists not only of local symptoms caused by the primary malignancy or its metastases, but also by general systemic signs that are not directly connected with the tumor. These symptoms are mostly associated with auto-immunity or endocrine influences. In many cases, the source of paraneoplastic syndromes (PNS) is unknown. Nearly 15 % of on-cological patients demonstrate these syndromes but it is diagnosed much more rarely. The survey of the numerous PNS is offered. The significance of the PNS differs for oncologists and other physicians who encounter it m their practice. The reason of those differences, as well as the connection between PNS and cancer toxicity is discussed. The experience of antitoxic therapy (hemosorption, lymphosorption, enterosorption) used in our clinic in the previous years is overviewed.

Exposure to ionizing radiation is associated with increasing risk of various types of hematological malignancies. The results of major studies on association of leukemias and radiation exposure of large populations in Japan and in Ukraine are analyzed. The patterns of different types of leukemia in 295 Chernobyl clean-up workers diagnosed according to the criteria of up-to-date World Health Organization classification within 10 - 25 years following Chernobyl catastrophe are summarized. In fact, a broad spectrum of radiation-related hematological malignancies has been revealed both in Life Span Study in Japan and in study of Chernobyl clean-up workers in Ukraine. The importance of the precise diagnosis of tumors of hematopoietic and lymphoid tissues according to up-to-date classifications for elucidating the role of radiation as a causative factor of leukemias is emphasized. Such studies are of high importance since according to the recent findings, radiation-associated excess risks of several types of leukemias seem to persist throughout the follow-up period up to 55 years after the radiation exposure.

Індекс рубрикатора НБУВ: Р562.9 + Р56-5

Рубрики:

Інші види пухлин

Онкологія

Шифр НБУВ: Ж14160 Пошук видання у каталогах НБУВ 

In recent years gold nanoparticles (AuNPs) have received considerable attention for various biomedical applications including diagnostics and targeted drug delivery. However, more research is still needed to characterize such aspects of their use in clinical oncology as permeability, retention and functional effect on tumor cells. Aims - this study was designed to describe the effect of non-functionalized AuNPs on LNCaP prostate cancer cells growth. Material and Methods: LNCaP cells were cultured in RPMI-1640 medium containing AuNPs covered by polyvinylpyrrolidone of average size 26,4 nm (10,0 mu g/ml). Counts of cells were calculated and their morphology was examined. Results: AuNPs conglomerates have been visualized in cultured cells. After 4-day incubation in presence of AuNPs significant retardation of LNCaP cells growth was observed both in 5 alpha-dihydro testosterone stimulated and non-stimulated cultures. No morphological changes of live LNCaP cells were seen in any experiment. Conclusion: given absence of morphological changes in live cells and dribble and relatively constant numbers of dead cells, it was concluded that inhibitory effect of AuNPs on LNCaP cells growth was caused by alterations of proliferation.