| 1. |
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
|
|
| 11. |
|
|
| 12. |
|
|
| 13. |
|
|
| 14. |
|
|
| 15. |
|
|
| 16. |
- Einarsdottir, H, et al.
(author)
-
Diffusion-weighted MRI of soft tissue tumours
- 2004
-
In: European radiology. - : Springer Science and Business Media LLC. - 0938-7994 .- 1432-1084. ; 14:6, s. 959-963
-
Journal article (peer-reviewed)
|
|
| 17. |
|
|
| 18. |
|
|
| 19. |
- Girnita, L., et al.
(author)
-
Increased expression of insulin-like growth factor I receptor in malignant cells expressing aberrant p53 : Functional impact
- 2000
-
In: Cancer Research. - 0008-5472 .- 1538-7445. ; 60:18, s. 5278-5283
-
Journal article (peer-reviewed)abstract
- We investigated the functional impact of p53 on insulin-like growth factor I receptor (IGF-IR) expression in malignant cells. Using the BL-41tsp53-2 cell line, a transfectant carrying temperature-sensitive (ts) p53 and endogenous mutant p53 (codon 248), we demonstrated a drastic down-regulation of plasma membrane-bound IGF-IRs on induction of wild-type p53, However, a similar response was obtained by treatment of BL-41tsp53-2 cells expressing mutant ts p53 with a p53 antisense oligonucleotide. Thus, even if the negative effect of wild-type p53 predominates under a competitive condition, these data indicate that mutant p53 may be important for up-regulation of IGF-IR, To further elucidate this issue, three melanoma cell lines (BE, SK-MEL-5, and SK-MEL-28) that over expressed p53 were investigated. The BE cell line has a hot spot mutation (codon 248) and expresses only codon 248-mutant p53, SK-MEL-28 has a point mutation at codon 145. SK-MEL-5 cells did not exhibit any p53 mutations, but the absence of p21(Waf1) expression suggested functionally aberrant p53. Our data suggest that interaction with Mdm-2 may underlie p53 inactivation in these cells, Using p53 antisense oligonucleotides, we demonstrated a substantial down-regulation of cell surface expression of IGF-IR proteins in all melanoma cell lines after 24 h, This was paralleled by decreased tyrosine phosphorylation of IGF-IR and growth arrest, and, subsequently, massive cell death was observed (this was also seen in BL-41tsp53-2 cells with mutant conformation of ts p53). Taken together, our results suggest that up-regulation of IGF-IR as a result of expression of aberrant p53 may be important for the growth and survival of malignant cells.
|
|
| 20. |
|
|
| 21. |
|
|
| 22. |
|
|
| 23. |
|
|
| 24. |
|
|
| 25. |
|
|
| 26. |
|
|
| 27. |
|
|
| 28. |
- Lin, YB, et al.
(author)
-
Telomerase promoter mutations and copy number alterations in solitary fibrous tumours
- 2018
-
In: Journal of clinical pathology. - : BMJ. - 1472-4146 .- 0021-9746. ; 71:9, s. 832-839
-
Journal article (peer-reviewed)abstract
- Solitary fibrous tumour (SFT) is an infrequently metastasising mesenchymal tumour defined by the NAB2–STAT6 fusion gene. Activating mutations in the telomerase reverse transcriptase (hTERT) gene promoter has been reported to associate with adverse patient outcome in SFTs.MethodsWe analysed the hTERT gene for promoter mutations and copy number alterations in 43 primary extrameningeal SFTs (9 malignant and 34 benign tumours according to WHO 2013 criteria), six local recurrences and three metastatic lesions.ResultsActivating −124 C>T (n=12) or −148 C>T (n=2) mutations were found in 33% of the tumours and associated with older age (P=0.006), necrosis (P=0.009), higher mitotic rate (P=0.003), nuclear atypia (P=0.002), malignant histological diagnosis (P=0.04) and worse progression-free survival (P=0.023). We also observed frequent (24%) hTERT promoter mutations in histologically benign tumours without metastasis (mean follow-up >9 years), and in 14%–18% of low-risk SFTs as determined by three risk-stratification models. Mutations were seen in 2/6 metastatic tumours and metastatic lesions. hTERT copy number gain was seen in 11/28 hTERT promoter wild-type cases.ConclusionsActivating hTERT promoter mutations associate with aggressive histopathological features, indicating a role in tumour progression. Given the comparatively high prevalence of hTERT promoter mutations in low-risk and non-metastasising lesions, further studies are required to clarify the prognostic value of hTERT promoter analysis before implementing the analysis in clinical diagnostics.
|
|
| 29. |
|
|
| 30. |
- Nilsson, G, et al.
(author)
-
Detection of EWS/FLI-1 by Immunostaining. An Adjunctive Tool in Diagnosis of Ewing's Sarcoma and Primitive Neuroectodermal Tumour on Cytological Samples and Paraffin-Embedded Archival Material
- 1999
-
In: Sarcoma. - : Hindawi Limited. - 1357-714X .- 1369-1643. ; 3:1, s. 25-32
-
Journal article (peer-reviewed)abstract
- Purpose.Recently we showed that the 68-kDa fusion protein derived from theEWS/FLI1hybrid gene can be specifically detected by Western blotting using a polyclonal antibody to the C-terminal of FLI1 on biopsy material from Ewing's sarcoma. The aim of this study was to investigate whether this antibody also could be used for immunocytochemistry and immunohistochemistry in diagnosis of Ewing's sarcoma.Methods.Immunostaining on paraffin-embedded archival material, fine-needle aspirates and tumour touch imprints from Ewing's sarcomas and primitive neuroectodermal tumours (PNET) for detection of the fusion protein was performed. Most cases were also analysed by Western blotting.Tumours of differential diagnostic importance were also included.Results. Eighty per cent (12/15 cases) of the Ewing tumours exhibited a positive immunoreactivity for the FLI1 antibody. The signal was mainly localised in the nuclei of the tumour cells, which seems reasonable sinceEWS/FLI1is a transcription factor. The signal was found to be specific since it did not appear when the blocking peptide was added to the antibody solution.Moreover, two other types of small-round cell tumours (i.e. neuroblastoma and alveolar rhabdomyosarcoma) were negative as well as most normal tissues.Discussion.Immunostaining of histological and cytological specimens with the FLI1 antibody can be of diagnostic relevance in Ewing tumours carrying t(11;22).The absence of immunoreactivity in non-Ewing cells is most likely due to a low expression of the wild-type FLI1 protein.
|
|
| 31. |
|
|
| 32. |
|
|
| 33. |
|
|
| 34. |
|
|
