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1

The role of genetic factors in the pathogenesis of thyroid neoplasms

100%
Ferenc T., Maciaszczyk K., Gesing A., Lewinski A.
Postępy Higieny i Medycyny Doświadczalnej
|
1997
|
vol. 51
|
issue 4
367-384
EN
This paper summarizes the current knowledge on the role of genetic factors in the development of thyroid neoplasms. The introduction of the methods and concepts of molecular genetics (as, e.g. recombinant DNA technology) have elucidated etiopathogenesis of the majority of thyroid tumours and, in the future, can make the diagnosis easier. Mutations of genes involved in the control of cellular growth and/or differentiation (ras, c-myc, RET, met) affect the development of thyroid neoplasms. Loss of heterozygosity (LOH) may suggest the presence of tumor suppressor genes and has been reported in thyroid follicular carcinomas. Activation of tyrosine kinase, whether by specific oncogene amplification or by rearrangement, appears to be highly specific for the transformation of thyroid follicular cells into papillary tumours. Cytogenetic studies have shown frequent clonal abnormalities in thyroid follicular adenomas and carcinomas.
2

The role of antisense oligodeoxynucleotides in the investigationa of the molecular phenomenas activated by oncogenes: therapeutical implications

80%
Skorski T., Nieborowska-Skorska M.
Biotechnologia
|
1995
|
issue 1
44-55
EN
Antisense oligodeoxynucleotides are well known as specific inhibitor of targeted genes expression. In this paper we demonmstrate that antisenses could be applied for investigation of the molecular mechanisms activated by oncogenes These studies may identify new targets for antisense treatments of tumors.
3

Neoplastic cell transformation by viruses

80%
Schmidt M., Olejnik A., Gozdzicka-Jozefiak A.
Biotechnologia
|
2002
|
issue 1
87-104
EN
Tumor-inducing viruses occur in several taxonomic groups. All RNA tumor viruses belong to retrovirus family, but the DNA tumor viruses come from several different groups. Their oncogenic potential is associated with their replication strategy, and in a vast majority of cases oncogenic transformation occurs only if the viral life cycle is aborted. The oncogenic phenotype results from discrete changes in the expression of key cellular control genes: oncogenes and tumor suppressor genes. Most often, the retroviruses cause the activation of oncogenes, and DNA tumor viruses usually target tumor suppressor genes.
4

Antisense oligonucleotides: from the bench to the patients

80%
Skorski T., Nieborowska-Skorska M., Szczylik C., Calabretta B.
Biotechnologia
|
1996
|
issue 4
108-115
EN
We describe here tha current state of progress toward gene-directed antisense-based cancer therapy targeting BCR/ABL, oncogene, primarily from the viewpoint of initial proof-of-concepts studies in animal models of human leukemias and phase I clinical investigations.
5

Transgenic mice as a tools for analysis of neoplastic transformation of T and B lymphocytes

80%
Kobzdej M., Strzadala L.
Postępy Higieny i Medycyny Doświadczalnej
|
1996
|
vol. 50
|
issue 2
113-129
EN
This article describes the significance of the mouse transgenic model in elucidation of the role and the oncogenic potential of such genes as N-ras, pim-1, bcl-2, myc and p53. The role of gene targetting by homologous recombination in the study of preneoplastic state in the mice model was also discussed.
6

The perspectives the antisense strategy applicatgion in the clinical medicine

80%
Ratajczak M. Z., Skorski T., Bialek A.
|
EN
In this review paper the different aspects and perspectives of antisense strategy applications in clinical medicine are discussed.
7

Apoptosis-the programmed cell death

80%
Gora-Tybor J., Robak T.
Postępy Higieny i Medycyny Doświadczalnej
|
1994
|
vol. 48
|
issue 3
209-225
EN
Apoptosis is structurally distinct programmed cell death pathway.It takes place during embryogenesis, after withdrawal of the trophic hormones and in the course of normal tissue turnover.Defective regulation of apoptosis may play a very important role in the aetiology of cancer and other diseases.In this paper these and other problems concerning with apoptosis are reviewed.
8

Immunoglobulin repertoire of rearranged VH segments in human blood

80%
Kraj P.
|
|
vol. 49
|
issue 1
9-22
9

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

70%
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.
10

Heparin and atherosclerosis

61%
Stajszczak M., Gminski J.
Postępy Higieny i Medycyny Doświadczalnej
|
1994
|
vol. 48
|
issue 3
275-290
EN
Heparin is a highly sulfated glycosaminoglycan with many functions such as antilipemic and antithrombotic.In spite os these activities heparin is able to inhibit vacsular smooth muscle cells proliferation and mmigration what seems to be very important event in the pathogenesis of atherosclerosos.The molecular mechanism of the action of heparin on smooth muscle cells is not yet understood.Heparin inhibits growth factors binding to their receptors,oncogenes expressionand has influence on the extracellular matrix protein deposition in the artery wall.
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