| 1. |
- Arner, ESJ, et al.
(författare)
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The thioredoxin system in cancer
- 2006
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1044-579X. ; 16:6, s. 420-426
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Tidskriftsartikel (refereegranskat)
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| 2. |
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| 3. |
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| 4. |
- Bjerkvig, Rolf, et al.
(författare)
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Cancer stem cells and angiogenesis
- 2009
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Ingår i: Seminars in Cancer Biology. - London : Academic Press. - 1044-579X .- 1096-3650. ; 19:5, s. 279-284
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Forskningsöversikt (refereegranskat)abstract
- Most cancers contain tumor cells that display stem cell-like characteristics. How and when such cells appear in tumors are not clear, but may involve both stochastic as well as hierarchical events Most. likely, tumor cells that display stem cell-like characteristics can undergo asymmetric cell division giving rise to tumor cells that trigger angiogenic programs. As normal stem cells the cancer stem-like cells seem to adapt to hypoxic environments and will use metabolic pathways that involve increased conversion of glucose to pyruvate and lactate, and a concomitant decrease in mitochondrial metabolism and mitochondrial mass. The molecular pathways responsible for inducing glycolysis are now being explored. These pathways seem to mediate multiple metabolic functions in cancer stem-like cells, leading to a highly migratory and angiogenesis-independent phenotype. Future challenges will be to identify and validate molecular targets involved in anaerobic metabolic pathways active in cancer stem-like cells and to determine how these pathways differ from regulatory pathways involved in normal stem cell function.
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| 5. |
- Cao, YH
(författare)
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Angiogenesis in malignancy
- 2009
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 19:5, s. 277-278
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 6. |
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| 7. |
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| 8. |
- Cole, MD, et al.
(författare)
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25 years of the c-Myc oncogene
- 2006
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1044-579X. ; 16:4, s. 241-241
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 9. |
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| 10. |
- Dalianis, T, et al.
(författare)
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Welcome to the Polyomaviridae
- 2009
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 19:4, s. 209-210
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 11. |
- Edsjö, Anders, et al.
(författare)
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Neuroblastoma as an experimental model for neuronal differentiation and hypoxia-induced tumor cell dedifferentiation.
- 2007
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Ingår i: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 17:3, s. 248-256
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Forskningsöversikt (refereegranskat)abstract
- Neuroblastoma is a childhood tumor derived from precursor or immature cells of the sympathetic nervous system. Neuroblastomas show a tremendous clinical heterogeneity, encompassing truly benign as well as extremely aggressive forms. In vivo as well as in vitro data have shown that the degree of sympathetic neuronal tumor cell differentiation influences patient outcome. Unraveling mechanisms governing neuroblastoma cell differentiation is therefore a central issue in the neuroblastoma research field. In this communication, we discuss some of the in vitro models frequently used to study human neuroblastoma cell differentiation. We also review recent data demonstrating that oxygen shortage, hypoxia, shifts neuroblastoma cells toward an immature, stem cell-like phenotype and discuss the potential clinical impact of hypoxia on neuroblastoma behavior.
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| 12. |
- Fan, Xiaolong, et al.
(författare)
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Glioma stem cells: Evidence and limitation.
- 2007
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Ingår i: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 17:3, s. 214-218
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Forskningsöversikt (refereegranskat)abstract
- Gliomas, in particular the high-grade anaplastic glioma and glioblastoma multiforme (GBM), are manifested by morphological, genetic and phenotypic heterogeneity. Most of the studies hitherto have been performed on bulk glioma cells, with limited understanding on the origin and the relative contribution of particular glioma cell populations to glioma growth and progression. Recent studies have demonstrated the existence of a small fraction of glioma cells endowed with features of primitive neural progenitor cells and tumor-initiating function. Such cells have been defined as glioma stem cells. However, questions remain as to whether the currently identified glioma stem cells are the cell-of-origin for glioma initiation and progression, or the results of such processes. In this review, we discuss the current evidence and limitation in identifying glioma stem cells and the potential origin of glioma stem cells in the context of post-natal neural cell regeneration and their transformation mechanisms. The implication of these findings for glioma diagnosis and treatment will also be reviewed.
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| 13. |
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| 14. |
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| 15. |
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| 16. |
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| 17. |
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| 18. |
- Hoglund, P, et al.
(författare)
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Natural killer cells in cancer
- 2006
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1044-579X. ; 16:5, s. 331-332
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 19. |
- Höglund, Mattias
(författare)
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Bladder cancer, a two phased disease?
- 2007
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Ingår i: Seminars in Cancer Biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 17:3, s. 225-232
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Forskningsöversikt (refereegranskat)abstract
- The processes of intraepithelial migration, intraluminal seeding, and field cancerization as models for initiation, spread, and recurrences of urothelial cell carcinoma (UCC) are reviewed in light of recent molecular investigations. The accumulated molecular data on synchronous and metachronous tumors indicate that the majority of recurrent and multiple tumors are monoclonal. Molecular data has also shown the presence of chromosomal and genetic changes in precursor lesions as well as in normal urothelial cells. Genetic-histological mapping of cystectomized bladders has shown that overt tumors occur as local events in areas of genetically altered urothelium. A model is put forward in which the tumor process is initiated by genetically altered but histologically normal cells that produce fields of altered cells by intraepithelial displacement. By the accumulation of further genetic changes the fields of altered urothelium reaches a state of criticality, which locally may produce frank tumors.
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| 20. |
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| 21. |
- Klein, E, et al.
(författare)
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Burkitt lymphoma
- 2009
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 19:6, s. 345-346
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 22. |
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| 23. |
- Kost-Alimova, M, et al.
(författare)
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Modeling non-random deletions in cancer
- 2007
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1044-579X. ; 17:1, s. 19-30
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Tidskriftsartikel (refereegranskat)
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| 24. |
- Lindberg, U, et al.
(författare)
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Actin is where it's at
- 2008
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1044-579X. ; 18:1, s. 1-1
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 25. |
- Lindberg, Uno, et al.
(författare)
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The microfilament system and malignancy
- 2008
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Ingår i: Seminars in Cancer Biology. - : Elsevier BV. - 1044-579X .- 1096-3650. ; 18:1, s. 2-11
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Forskningsöversikt (refereegranskat)abstract
- Increased motile activity, increased rate of cell proliferation and removal of growth inhibiting cell-cell contacts are hallmarks of tumorigenesis. Activation of cell motility and migration is caused by activation of receptors, turning on the growth cycle. Increased expression of metalloproteinases, breaking cell:cell contacts and organ confines, allows the spread of malignant cancer cells to other sites in the organism. It has become increasingly clear that most transmembrane proteins (growth factor receptors, adhesion proteins and ion channels) are either permanently or transiently associated with the sub-membraneous system of actin microfilaments (MF), whose force generating capacity they control. Although there has been great progress in our understanding of the physiological importance of the MF-system, as will be exemplified in this issue of SCB, many aspects of actin microfilament formation and its regulation are still unclear. Redox control of the actin (MF)-system in cell motility and migration and its perturbations in pathophysiology, including cancer, is an emerging field of research.
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| 26. |
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| 27. |
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| 28. |
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| 29. |
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| 30. |
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| 31. |
- Sonkoly, Enikö, et al.
(författare)
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MicroRNAs and immunity : novel players in the regulation of normal immune function and inflammation.
- 2008
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Ingår i: Seminars in Cancer Biology. - : Elsevier BV. - 1044-579X .- 1096-3650. ; 18:2, s. 131-40
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Tidskriftsartikel (refereegranskat)abstract
- The discovery of microRNAs (miRNAs) is one of the major scientific breakthroughs in recent years and has revolutionized the way we look at gene regulation. Although we are still at a very early stage in understanding their impact on immunity, miRNAs are changing the way we think about the development of the immune system and regulation of immune functions. MiRNAs are implicated in establishing and maintaining the cell fate of immune cells (e.g. miR-181a and miR-223), and they are involved in innate immunity by regulating Toll-like receptor signaling and ensuing cytokine response (e.g. miR-146). Moreover, miRNAs regulate central elements of the adaptive immune response such as antigen presentation (e.g. miR-155) and T cell receptor signaling (miR-181a). Recent evidence showing altered miRNA expression in chronic inflammatory diseases (e.g. miR-203 and miR-146) suggests their involvement in immune-mediated diseases. Furthermore, miRNAs have been implicated in viral immune escape and anti-viral defense (e.g. miR-196). In this review, we will summarize the latest findings about the role of miRNAs in the development of the immune system and regulation of immune functions and inflammation.
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| 32. |
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| 33. |
- Zhivotovsky, B, et al.
(författare)
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The Warburg Effect returns to the cancer stage
- 2009
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1096-3650 .- 1044-579X. ; 19:1, s. 1-3
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 34. |
- Åman, Pierre, 1953
(författare)
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Fusion oncogenes.
- 2005
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1044-579X. ; , s. 159-61
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 35. |
- Åman, Pierre, 1953
(författare)
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Fusion oncogenes in tumor development.
- 2005
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Ingår i: Seminars in cancer biology. - : Elsevier BV. - 1044-579X. ; 15:3, s. 236-43
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Forskningsöversikt (refereegranskat)abstract
- Currently, all identified fusion oncogenes are found in rare tumor forms, and most of them only in specific tumor types. Some fusion oncogenes are frequent in healthy individuals suggesting that they rarely induce tumor growth. Multiple double-strand breaks that cluster in time and space increases the risk for formation of fusion oncogenes genes. The normal cell type specific spatial distribution of chromatin and genes in interphase nuclei may affect the risk for fusion of specific genes. Transcriptional orientation, splicing of reading frames, size and sequences of breakpoint introns are other risk factors. The biological activity of fusion oncoproteins is the most important factor for penetrance. The effects in specific target cells may explain the tumor type specificity of most fusion oncogenes.
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