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  1. 13 Archivum Immunologiae et Therapiae Experimentalis

  2. 7 Biotechnologia

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  1. 2 Gozdzicka-Jozefiak A.

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1

Quantitative real-time PCR in cancer research

100%
Mocellin S., Rossi C. R., Marincola F. M.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 5
301-313
EN
In the era of the Human Genome Project, quantitation of gene expression by tumor/host cells is of paramount importance to investigate gene patterns responsible for cancer development, progression and response/resistance to treatment. Quantitative real-time PCR (qrt-PCR) technology has recently reached a level of sensitivity, accuracy and practical ease that support its use as a routine bioinstrumentation for gene level measurement. Several applications have been already implemented in the field of cancer research, and others are being validated, showing that this molecular biology tool can provide both researchers and clinicians with precious information concerning the behaviour of tumors. The knowledge of the biochemical principles underlying this biotechnology can be of great value to correctly interpret qrt-PCR data.
2

Ki-67 reactivity in primary fallopian tube cancers

100%
Rabczynski J., Kochman A., Kowalski P., Ziolkowski P.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 4
281-285
EN
Forty-four cases of primary cancer of the fallopian tube (PFTC) were analyzed as to Ki-67 expression, grade, stage and the cancer histological type. Among patients with an average age of 57.5 years (range 38?70 years), 27 patients were FIGO I, 7 were FIGO II and 10 were FIGO III. Histological classification of PFTC revealed 18 cases of endometroid type, 9 serous, 7 undifferentiated, 6 urothelial, 2 clear-cell and 2 of other type. Histological grading revealed 11 cases of G1, 16 of G2 and 17 of G3 tumors. The quantity of Ki-67 positive cells was counted on 300 cancer cells in random high-power fields (10x40) and recorded as the labeling index (LI, %). Positive staining for Ki-67 was shown in the nuclei in all cases. Ki-67 LI values ranged from 14. 2 to 97.2% (median 36. 1). Ki-67 LI values were graded as 36. 1% as high and <36. 1% as low. We did not find any significant differences in Ki-67 LI values among tumors of various clinical stages, histological grades and histological types. The p value was statistically significant only for stage as a prognostic factor.
3

Contribution of molecular biology to cancer diagnosis and treatment

100%
Radzikowski C.
Biotechnologia
|
1996
|
issue 4
26-41
EN
The aim of this lecture is to find a bridge between a current understanding of early events during oncogenesis and the complexity of cancer disease, whose development and course is a consequence of interactions on various levels, local as well as systemic between cancer cells and cellular components of patients surveillance and homeostasisi systems.
4

Malformations of angiogenesis in the low differentiated human carcinomas. Immunohistochemical study

80%
Zoltowska A., Stepinski J., Lewko B., Zamorska B., Roszkiewicz A., Serkies K., Kruszewski W.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 1
59-62
EN
Our previous observations showed that the perivascular mesenchyma of the thin-walled vessels (capillaries) in cancers may be the source of organ-specific stem cells. We suggested that the cells forming vascular channels in altered stroma participate in the tumor development. This study was designed to examine the distribution of the vessels and their appearance in the breast, lung and colon cancers. Using immunohistochemical methods, we have shown that in the low differentiated tumors both CD31 and factor VIII antigens may be expressed in capillaries chiefly on the periphery of neoplastic foci. Many of these vessels were discontinuous, with interruptions or unformed tubules. Sporadically, CD31 protein and factor VIII antigens were not expressed in capillaries inside the very low differentiated cancer cases. It is difficult to assess by immunohistochemichal means whether the vascular malformations are the primary or secondary phenomena in the malignancy and why these abnormalities were especially visible in some low differentiated cancers.
5

Nucleotide excision repair, NER - a relationship with cancer risk

80%
Butkiewicz D., Rusin M., Pawlas M., Czarny M., Chorazy M.
Postępy Higieny i Medycyny Doświadczalnej
|
2002
|
vol. 56
|
issue 4
485-498
EN
DNA damage repair, responsible for maintaining the genome integrity, plays a central role in cancer biology. Individual DNA repair capacity is genetically determined. Inherited defect in nucleotide excision repair (NER) genes leads to three distinct and extremely rare disorders: xeroderma pigmentosum, associated with high risk of skin cancer, Cockayne syndrome, and trichothiodystrophy. The recently identified common polymorphism in several NER genes may also influence a risk of cancer in general population. The review presents current knowledge about a role of genetic variation of NER genes in cancer predisposition.
6

Role of response gene to complement 32 in disease

80%
Vlaicu S. I., Cudrici C., Ito T., Fosbrink M., Tegla C. A., Rus V., Mircea P. A., Rus H.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 2
115-122
EN
The role of response gene to complement (RGC)-32 as a cell cycle regulator has been attributed to its ability to activate cdc2 kinases and to induce S-phase entry and mitosis. However, recent studies revealed novel functions for RGC-32 in diverse processes such as cellular differentiation, inflammation, and fibrosis. Besides responding to C5b-9 stimulation, RGC-32 expression is also induced by growth factors, hormones, and cytokines. Transforming growth factor ? activates RGC-32 through Smad and RhoA signaling, thus initiating smooth muscle cell differentiation. Accumulating evidence has drawn attention to the deregulated expression of RGC-32 in human malignancies, hyper-immunoglobulin E syndrome, and fibrosis. RCG-32 expression is up-regulated in cutaneous T cell lymphoma and colon, ovarian, and breast cancer, but down-regulated in invasive prostate cancer, multiple myeloma, and drug-resistant glioblastoma. A better understanding of the mechanism by which RGC-32 contributes to the pathogenesis of these diseases will provide new insights into its therapeutic potential. In this review we provide an overview of this field and discuss the most recent research on RGC-32.
7

Cancer stem cells: the theory and perspectives in cancer therapy

80%
Gil J., Stembalska A., Pesz K. A., Sasiadek M. M.
Journal of Applied Genetics
|
2008
|
vol. 49
|
issue 2
193-199
EN
The cancer stem cell theory elucidates not only the issue of tumour initiation and development, tumour's ability to metastasise and reoccur, but also the ineffectiveness of conventional cancer therapy. This review examines stem cell properties, such as self-renewal, heterogeneity, and resistance to apoptosis. The ?niche' hypothesis is presented, and mechanisms of division, differentiation, self-renewal and signalling pathway regulation are explained. Epigenetic alterations and mutations of genes responsible for signal transmission may promote the formation of cancer stem cells. We also present the history of development of the cancer stem cell theory and discuss the experiments that led to the discovery and confirmation of the existence of cancer stem cells. Potential clinical applications are also considered, including therapeutic models aimed at selective elimination of cancer stem cells or induction of their proper differentiation.
8

Mitochondrial DNA mutations in human neoplasia

80%
Czarnecka A. M., Golik P., Bartnik E.
Journal of Applied Genetics
|
2006
|
vol. 47
|
issue 1
67-78
EN
Many models of tumour formation have been put forth so far. In general they involve mutations in at least three elements within the cell: oncogenes, tumour suppressors and regulators of telomere replication. Recently numerous mutations in mitochondria have been found in many tumours, whereas they were absent in normal tissues from the same individual. The presence of mutations, of course, does not prove that they play a causative role in development of neoplastic lesions and progression; however, the key role played by mitochondria in both apoptosis and generation of DNA-damaging reactive oxygen species might indicate that the observed mutations contribute to tumour development. Recent experiments with nude mice have proven that mtDNA mutations are indeed responsible for tumour growth and exacerbated ROS production. This review describes mtDNA mutations in main types of human neoplasia.
9

Inhibition of angiogenesis in the treatment of tumors

80%
Ostrowski K., Kinsner A.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 1
27-32
EN
Angiogenesis is essential for tumor progression, growth and metastases. Many substances present in a normal organism can inhibit or stimulate the process of new vessel formation in tumors. The use of natural or synthetic angiogenesis inhibitors as anticancer drugs is currently under intense investigation. Such agents can have lower toxicity and are less likely to generate drug resistance than conventional cytotoxic drugs. Clinical trials are now underway to develop optimum treatment strategies for antiangiogenic drugs. This paper reviews the present achievements in preclinical and clinical studies with antitumor drugs based on inhibitors of angiogenesis.
10

Heterocyclic aromatic amines and their role in the induction of carcinogenesis

80%
Woziwodzka A., Piosik J.
Biotechnologia
|
2009
|
issue 4
133-151
EN
Cancer is one of the most frequent causes of human death worldwide. It is a consequence of inherited DNA impairments or mutations induced by several exogenous factors. Diet is one of the most important exogenous factors, which is responsible for one-third cancer incidents in humans. Heterocyclic aromatic amines (HCA) arise during thermal processing of food. Based on the results on rodents and epidemiological data IARC classified HCA as probably (class 2A) or possibly (class 2B) carcinogenic to humans. After metabolic activation by cytochrome P450, N-hydroxy derivatives of HCA demonstrate strong mutagenic activity as they can form adducts with DNA. Experiments on laboratory animals indicated that HCA induce digestive tract, breast and lung cancers. Epidemiological data also confirm the association between HCA consumption and cancer appearance in humans. Although it is impossible to completely eliminate HCA from diet, there are several ways to limit the exposure to HCA and decrease their negative impact on human organisms.
11

Prognostic significance of p53 protein accumulation in cancer cells obtained from selected group of patients with sporadic colorectal cancer

80%
Paluszkiewicz P., Karski J., Berbe H., Pawlowska-Wakowicz B., Cybulski M., Karski M., Paszkowska A.
Journal of Applied Genetics
|
1999
|
vol. 40
|
issue 2
135-144
EN
p53 gene instability frequently causes accumulation of mutant protein in neoplastic cells. The goal of this study was to evaluate of p53 protein accumulation in tumour cells in relation to colorectal cancer outcome. p53 protein accumulation was tested immunohistochemically using DO-7 and Pab-1620 antibodies. In the group of 80 selected patients with sporadic colorectal cancer, p53 protein accumulation in tumour cells was found significantly more often (52.6% of cases) in cancers localised in the colon, nonmucinous and poorly differentiated. In 5-year follow-up, a shorter survival time was observed in the group of patients with p53 protein accumulation in cancer cells (P<0.05). The differences in p53 protein accumulation found in cancer cells in relation to tumour localisation and their histological type indicate the possibility of p53-independent carcinogenesis in mucinous and right-sided cancers. We indicate the importance of performing the immunohistochemical tests for prediction of the outcome of sporadic colorectal cancers.
12

The influence of beta-carotene, retinoids, RAR and RXR receptors on proliferation and neoplastic transformation of cells

71%
Staniaszek K., Gozdzicka-Jozefiak A.
Biotechnologia
|
2008
|
issue 3
28-45
EN
Beta carotene is a member of a class of substances called carotenoids. Beta carotene, alpha carotene and beta cryptoxanthin can serve as dietary precursors of retinoids (RA, all-trans retinol or provitamin A). Biological effects of retinoids and expression of RA responsive gene are mediated by different receptors, namely RAR and RXR in homodimeric or heterodimeric form. Expression levels of the retinoic acid receptors are significantly different in neoplastic tissues compared with non-neoplastic tissues for many types of tumors.
13

Isolation, composition and biological activities of mushroom polysaccharides on the example of Hericium erinaceum

71%
Malinowska E., Krzyczkowski W., Herold F.
Biotechnologia
|
2008
|
issue 1
109-121
EN
In recent years mushroom polysaccharides have been extensively investigated according to their unique biological activity. Among them polysaccharides from Hericium erinaceum (Hydnaceae) are well known as anti-tumor and cholesterol reducing agents as well as growth and differentiation of adrenal nerve cells stimulators. In Poland, H. erinaceum is restricted only to several areas and is considered endangered species. Thus mycelium and culture broth obtained from submerged in vitro culture could be an excellent source of polysaccharides. The review describes methods of isolation, purification and analysis of mushroom polysaccharides and summarizes data about biological activities of Hericium erinaceum polysaccharides.
14

Dendritic cells and their application in cancer immunotherapy - achievements and future prospects

71%
Rossowska J., Pajtasz-Piasecka E.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 5
501-518
EN
Dendritic cells (DC) are generally believed to play a key role in the initiation of immune response. A potential usefulness of these cells in antitumor immunotherapy is strongly considered in every stage of cancer treatment. Studies on tumor tissue infiltration by immune cells shown, that DC represented only a small percentage of leukocytes. The influence of tumor environment resulted in reduction of DC number, their inability to migrate across endothelial barriers, or impaired maturation and efficiency of tumor antigens presentation. Thus, decreased number of DC in tumors could be associated with a bad prognosis. Many attempts concentrate on the creation of the DC-based vaccines, which would generate strong anticancer cell mediated immunity. They include studies on stage of differentiation of the administered DC; effective way for antigen loading; optimum route and schedule of DC delivery into tumor bearing host; effective vectors for the therapeutic genes; effects of the therapy based on cytokine secreting DC; influence of DC on co-operation between innate and acquired immunity as well as on the generation of specific antitumor response. This review is focused on two important areas aiming for the preparation of DC vaccine for effective stimulation of immune response: - loading of DC with tumor antigens (or other ways of DC preparation to successful antigen presentation) - as an encouraging evidence of therapeutic efficacy, and - genetic modification of DC with cytokines resulting in the stimulation or alteration of the antitumor DC activity - as a promising anticancer strategy.
15

DNA Tumor Vaccines

71%
Wlazlo A. P., Ertl H. C. J.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 1
1-12
EN
A new generation of vaccines are being developed to induce immune responses that fight off infectious agents, or erradicate cancerous cells. The new vaccines are based on a plasmid vector, which in transfected mammalian cells cause constitutive high-level expression of the target antigen. Expression of the target antigen, in turn, can induce a full-range of immunologic responses, including cell-mediated killing, cell-mediated cytokine release and the production of antigen-specific antibodies. Through molecular techniques, these nucleic acid vaccines can enhanced to increase target antigen expression and faciliatate antigen presentation. Additionally, genetic adjuvants expressed simultaneously with the target antigens can induce the immune responses to disease-associated antigens. The ease with which these genetic vaccines can be generated and the potency of their ability to generate immune-mediated responses make them highly effective, which creates hope for developing effective treatment and prevention of various diseases, most notably cancer.
16

Usefulness of polymorphic markers in exclusion of BRCA1/BRCA2 mutations in families with aggregation of breast/ovarian cancers

71%
Gorski B., Debniak T., Jakubowska A., Cybulski C., Huzarski T., Byrski T., Zlowocka E., Lubinski J.
Journal of Applied Genetics
|
2003
|
vol. 44
|
issue 3
419-423
EN
Founder mutations can account for a large proportion of BRCA1/BRCA2 gene abnormalities in a given population. However there is still a need to study the entire gene in many families, even in countries where founder mutations have been identified. It is possible to decrease the number of cases which are studied by complex and expensive sequencing/Southern blot analyses of BRCA1/BRCA2 genes by exclusion of common BRCA1/BRCA2 alleles in a given family by using polymorphic dinucleotide markers. The goal of our study was to assess the effectiveness of this method in exclusion of BRCA1/BRCA2 constitutional mutations. In each family, blood samples for genetic analyses were taken from two affected relatives from the same generation. Six polymorphic microsatellite markers linked to BRCA1/BRCA2 genes were analysed. Results obtained with these markers were verified by applying BRCA1 testing for the most common founder mutations in Poland and using ?exon by exon? sequencing of coding fragments of the BRCA2 gene. Polymorphic markers useful in BRCA1/BRCA2 analyses included only 3 of 6 examined ? D17S855, D13S260 and D13S267. Occurrence of common alleles of BRCA1 was excluded in 3 families and BRCA2 in 5 out of 30 families. Results obtained by testing for BRCA1 Polish founder mutations and BRCA2 sequencing were in agreement with BRCA1 findings based on polymorphic markers. The only exception was family 994 with BRCA1 exon 5 300T/G mutation, in which BRCA1 mutation carrier was excluded by using D17S855. Among 14 families without BRCA1 Polish founder mutations in this gene were excluded in 2 families and BRCA2 mutation was excluded in one family.
17

Antigen non-specific activation of CD8+ T lymphocytes by cytokines: relevance to immunity, autoimmunity and cancer

71%
Ramanathan S., Gagnon J., Ilangumaran S.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 5
311-323
EN
Development of T lymphocytes and their survival in the periphery are dependent on signals emanating from cytokine receptors as well as the T cell antigen receptor (TCR). These two signaling pathways play distinct and complementary roles at various stages of T cell development, maturation, survival, activation and differentiation. During immune response to foreign antigens initiated by TCR signaling, cytokines play a key role in the expansion of activated T cells. Even though the initial activation of T cells occurs via the TCR, this requirement can be overcome under certain circumstances. During lymphopenia, cytokines trigger memory CD8+ T cells to undergo antigen non-specific homeostatic expansion, whereas na?ve CD8+ T cells require both cytokines and TCR signaling. Recent reports show certain combinations of cytokines can induce proliferation and effector functions of na?ve CD8+ T cells without concomitant stimulation via the TCR. While such antigen non-specific stimulation of na?ve T cells might significantly boost the adaptive immune response, it could also have an undesirable effect of triggering potentially autoreactive cells. Understanding the mechanisms and the regulation of cytokine-driven stimulation of na?ve CD8+ T cells may lead to novel strategies of intervention for autoimmune diseases. On the other hand, in vitro expansion of na?ve CD8+ T cells by certain combinations of cytokines could be used to generate tumor-specific cells with ideal properties for cellular immunotherapy of cancer.
18

Gene therapy of cancer

71%
Gorny A., Wiznerowicz M., Mackiewicz A.
Biotechnologia
|
1995
|
issue 1
74-90
EN
Progress in genetic engineering has to lead to the development of efficient methods of transfer and expression of genes in eucariotic cells.This technology has been employed to kill cancer cells.Five major strategies of cancer gene therapy have been proposed and are currently verified in clinical trials.They include: (1) genetic cellular vaccines, (2) siuicide genes, (3) multidrug resistance genes, (4) HLA genes tansfer into cancer cells, and (5) repair of defective suppresor genes and/or removal of activated oncogene.
19

Fatty acid synthase-catalyzed de novo fatty acid biosynthesis: from anabolic-energy-storage pathway in normal tissues to jack-of-all-trades in cancer cells

71%
Menendez J. A., Lupu R.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 6
414-426
EN
In 1994, Kuhajda and colleagues unambiguously identified the oncogenic antigen-519, a prognostic molecule found in breast cancer patients with markedly worsened prognosis, as fatty acid synthase (FAS), the key enzyme for the de novo fatty acid biosynthesis. It now appears that human carcinomas and their pre-neoplastic lesions constitutively overexpress FAS and undergo significant endogenous fatty acid biosynthesis. Moreover, FAS blockade specifically induces apoptotic cancer cell death and prolongs survival of cancer xenograft hosts. Therefore, FAS signaling seems to play a central role in the maintenance of the malignant phenotype by enhancing cancer cell survival and proliferation. This review documents the rapidly changing perspectives on the function of FAS in cancer biology. First, we describe molecular mechanism by which aberrant transduction cascades driven by oncogenic changes subvert the down-regulatory effects of dietary fatty acids, resulting in tumor-associated FAS insensitivity to nutritional signals. Second, we speculate on the putative function that hypoxia can play as the epigenetic factor that triggers and maintains FAS overexpression in cancer cells by inducing changes in gene expression and in metabolism for survival. Third, we explore the role that FAS exhibits in cancer evolution by specifically regulating cancer-related proteins such as Her-2/neu oncogene and estrogen receptor. Finally, we reveal previously unrecognized functions of FAS on the response of cancer cells to chemo-, endocrine-, and immuno-therapies. These findings, all together, should ultimately enhance our understanding of how FAS-dependent endogenous fatty acid metabolism, once considered a minor anabolic-energy-storage pathway in normal cells, has become a jack-of-all-trades in cancer cells.
20

Assessment of selected costimulatory, adhesion, and activatory molecules and cytokines of Th1/Th2 balance in acute lymphoblastic leukemia in children

71%
Luczynski W., Stasiak-Barmuta A., Krawczuk-Rybak M., Malinowska I.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 4
357-363
EN
Recent years have seen a rise in the importance of cytokine production and co-stimulatory/activatory molecule expression in the immune response in leukemia. The aim of our study was to assess the function of T lymphocytes in children with acute lymphoblastic leukemia (ALL) during remission induction based on selected cytokine and co-stimulatory/activatory molecule expression. The study group consisted of 50 children with ALL (B cell precursor). Peripheral blood samples were taken before treatment (day 0), after the prednisone prophase (day 8), and during (day 15) and after (day 33) remission induction. The percentages of T cells with interferon (IFN)-g (Th1), interleukin (IL)-4 (Th2) and IL-2 receptor (IL-2R), CD28, CTLA-4, CD38, ICAM-1, and HLA-DR expression were assessed by tricolor flow cytometry. At the time of diagnosis we noted higher percentages of T cells with adhesion molecule ICAM-1, activation molecule CD38 expression, and an increased population of Th2 cells (IL-4) compared with the control group. During and after remission induction we observed a decreased population of CD38+ T cells, elevated percentages of helper T lymphocytes with IL-2R expression, and a rise in helper T lymphocytes producing IFN-g (Th1). During fever/infection, higher levels of activated T lymphocytes (CD4+HLA-DR+, CD8+HLA-DR+), a rise in Th1, and no change in Th2 populations were observed. The results suggest T cell activation and Th2 predominance at the time of diagnosis and during remission induction in ALL in children. These results confirm the involvement of cellular immunity in the leukemic process and can be used in immune therapy in leukemia.
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