Wyniki wyszukiwania

1

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

100%

Menendez J. A., Lupu R.

Archivum Immunologiae et Therapiae Experimentalis

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2004

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tom 52

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nr 6

2

Dietary carotenoids in normal and pathological tissues of corpus uteri

84%

Czeczuga-Semeniuk E., Wolczynski S.

Folia Histochemica et Cytobiologica

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2008

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tom 46

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nr 3

283-290

3

Increased pressure stimulates aberrant dendritic cell maturation

84%

Craig D. H., Schaubert K. L., Shiratsuchi H., Kan-Mitchell J., Basson M. D.

Cellular and Molecular Biology Letters

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2008

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tom 13

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nr 2

260-270

Patients with malignancy typically exhibit abnormal dendritic cell profiles. Interstitial tumor pressure is increased 20-50mmHg over that in normal tissue. We hypothesized that elevated pressure in the tumor microenvironment may influence dendritic cell (DC) phenotype and function. Monocyte-derived immature and mature DC isolated from healthy human donors were exposed to either ambient or 40 mmHg increased pressure at 37°C for 12 hours, then assessed for expression of CD80, CD86, CD83, CD40, MHC-I and MHC-II. IL-12 production and phagocytosis of CFSE-labeled tumor lysate were assessed in parallel. Elevated pressure significantly increased expression of all co-stimulatory and MHC molecules on mature DC. Immature DC significantly increased expression of CD80, CD86, CD83 and MHC-II, but not MHC-I and CD40, versus ambient pressure controls. Pressure-treated immature DC phenotypically resembled mature DC controls, but produced low IL-12. Phenotypic maturation correlated with decreased phagocytic capacity. These results suggest increased extracellular pressure may cause aberrant DC maturation and impair tumor immunosurveillance.

4

Tumor-specific pyruvate kinase isoenzyme M2 involved in biochemical strategy of energy generation in neoplastic cells

84%

Guminska M., Ignacak J., Kedryna T., Stachurska M. B.

Acta Biochimica Polonica

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1997

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tom 44

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nr 4

The differences in properties of pyruvate kinase (EC 2.1.7.40) from normal tissues and animal or human tumors are described and their significance for various metabolic abnormalities is reviewed. The tumor variant gamma3 from M2 isoenzyme of pyruvate kinase sensitive to L-cysteine inhibition, when over-expressed, can be used as a marker of tumorigenic transformation. It seems that this variant represents a tumor-specific oncoprotein, involved in a novel metabolic strategy of energy generation during increased cell proliferation.

5

Alterations of tumor and normal tissue of human lung cancer resection specimens after isolation perfusion

67%

Nowak K., Hanusch C., Kolbel H. C., Schwarzbach M., Post S., Beck G., Gebhard M. M., Metzger R., Hohenberger P.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

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nr 5

6

Analysis of expression of AIF and PARP-1 in cancerogenesis of HPV-positive cervix

67%

Warowicka A., Kwasniewska A., Sobieraj M., Gozdzicka-Jozefiak A.

Bulletin of the Veterinary Institute in Puławy

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2011

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tom 55

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nr 3

The mRNA expression of AIF and PARP-1 in HPV negative non-tumour epithelial cells and HPV-positive cervical cancer cells using the real-time PCR method was examined. An increased level of AIF and PARP-1 mRNA in cervical cancer cells in comparison to normal epithelial cells was demonstrated. These results suggest that changes in the mRNA expression level of AIF and PARP-1 might be involved in cervical cancer development. The analysis of these two factors may represent a new molecular tool for cervical cancer prevention in women with HPV persistent infection.

7

The effect of phytoestrogen coumestrol and estradiol on c-myc protooncogen expression in cultured stromal cells of human proliferative endometrium

67%

Tomaszewski J., Putowski L., Gogacz M., Kotarski J., Jakowicki J. A.

Folia Histochemica et Cytobiologica. Supplement

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1997

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tom 35

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nr 2

8

Mitochondrial DNA mutations in human neoplasia

67%

Czarnecka A. M., Golik P., Bartnik E.

Journal of Applied Genetics

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2006

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tom 47

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nr 1

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.

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