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Antisense oligonucleotides: from the bench to the patients

100%

Skorski T. , Nieborowska-Skorska M. , Szczylik C. , Calabretta B.

1996

nr 4

108-115

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.

The perspectives the antisense strategy applicatgion in the clinical medicine

100%

Ratajczak M. Z. , Skorski T. , Bialek A.

1995

nr 1

35-43

In this review paper the different aspects and perspectives of antisense strategy applications in clinical medicine are discussed.

Immunoglobulin repertoire of rearranged VH segments in human blood

100%

Kraj P.

tom 49

nr 1

9-22

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

88%

Menendez J. A. , Lupu R.

nr 6

414-426

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.

Heparin and atherosclerosis

75%

Stajszczak M. , Gminski J.

nr 3

275-290

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.