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1

37kDa oncofetal antigen is an autoimmunogenic homologue of the 37kDa laminin receptor precursor

100%

Barsoum A. L., Rohrer J. W., Coggin J. H.

Cellular and Molecular Biology Letters

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2000

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tom 05

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nr 2

The laminin receptor precursor (LRP) has been the center of intense controversy and interest for over a decade. Chief among these controversies is the putative multifunctional aspect of this molecule: as a ribosomal-associated protein (p40) and/or as the precursor for the 67kDa high-affinity laminin receptor (67LR), neither of which have been definitively established. Other controversies include the presence of more than one 67kDa laminin receptor protein. However, interest in the molecule is sustained because of its vital function in the cell as a component of the translational machinery and due to its constant up-regulation in cancer cells with the invasive and metastatic phenotype and in association with poor prognosis. Recently, while studying the autoimmunogenicity of a species conserved 37-44 kDa oncofetal antigen (37kDa OFA), the authors of this paper, using amino acid sequencing of isolated OFA-peptides, cDNA cloning and sequencing and antigens-antibodies cross reactivity as well as antigens-T cell recognition reactions, identified the 37kDa OFA as precursor or immature laminin receptor protein.

2

Urokinase plasminogen activator [uPA] and soluble urokinase plasminogen activator receptor [suPAR] serum level in patients with malignant lymphomas

100%

Hus I., Cioch M., Jawniak D., Manko J., Dmoszynska A., Chrapko M., Hus M.

Bulletin of the Veterinary Institute in Puławy. Supplement

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2002

3

Expression of CD200 and CD200R regulatory molecules on the CD83plus monocyte-derived dendritic cells generated from patients with laryngeal cancer

84%

Klatka J., Grywalska E., Klatka M., Rahnama M., Polak A., Rolinski J.

Folia Histochemica et Cytobiologica

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2013

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tom 51

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nr 1

4

TGF beta signalling and its role in tumour pathogenesis

84%

Kaminska B., Wesolowska A., Danilkiewicz M.

Acta Biochimica Polonica

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2005

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tom 52

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nr 2

Transforming growth factor beta (TGF-β) is a multifunctional cytokine involved in the regulation of cell proliferation, differentiation and survival/or apoptosis of many cells. Knock-out experiments in mice for the three isoforms of TGF-β have demonstrated their importance in regulating inflammation and tissue repair. TGF-β is implicated in the pathogenesis of human diseases, including tissue fibrosis and carcinogenesis. TGF-β receptors act through multiple intracellular pathways. Upon binding of TGF-β with its receptor, receptor-regulated Smad2/3 proteins become phosphorylated and associate with Smad4. Such complex translocates to the nucleus, binds to DNA and regulates transcription of specific genes. Negative regulation of TGF-β/Smad signalling may occur through the inhibitory Smad6/7. Furthermore, TGF-β-activated kinase-1 (TAK1) is a component of TGF-β signalling and activates stress-activated kinases: p38 through MKK6 or MKK3 and c-Jun N-terminal kinases (JNKs) via MKK4. In the brain TGF-β, normally expressed at the very low level, increases dramatically after injury. Increased mRNA levels of the three TGF-β isoforms correlate with the degree of malignancy of human gliomas. TGF-βs are secreted as latent precursors requiring activation into the mature form. TGF-β may contribute to tumour pathogenesis by direct support of tumour growth and influence on local microenvironment, resulting in immunosuppression, induction of angiogenesis, and modification of the extracellular matrix. TGF-β1,2 may stimulate production of vascular endothelial growth factor (VEGF) as well as plasminogen activator inhibitor (PAI-I), that are involved in vascular remodelling occurring during angiogenesis. Blocking of TGF-β action inhibits tumour viability, migration, metastases in mammary cancer, melanoma and prostate cancer model. Reduction of TGF-β production and activity may be a promising target of therapeutic strategies to control tumour growth.

5

Local reaction from eosinophils in the development of Morris hepatoma after hrecTNF-alpha administration

67%

Terlikowski S., Nowak H. F., Poludniewski G.

Folia Histochemica et Cytobiologica. Supplement

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1996

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tom 34

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nr 1

6

Nuclear factor-kappaB: a key regulator in health and disease of lungs

59%

Batra S., Balamayooran G., Sahoo M. K.

Archivum Immunologiae et Therapiae Experimentalis

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2011

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tom 59

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