| 1. |
|
|
| 2. |
- Kalhori, S., et al.
(författare)
-
Resonant ion-pair formation in electron collisions with rovibrationally cold H-3(+)
- 2004
-
Ingår i: Physical Review A. Atomic, Molecular, and Optical Physics. - 1050-2947 .- 1094-1622. ; 69:2, s. 022713-
-
Tidskriftsartikel (refereegranskat)abstract
- Experimental and theoretical cross sections for the resonant ion-pair formation (RIP) in electron collisions with rovibrationally cold H-3(+) ions are presented. Absolute cross sections for the RIP process producing H- ions are measured for center-of-mass energies between 2-20 eV using the CRYRING, heavy-ion storage ring. Theoretical cross sections are obtained using wave-packet propagation on both one- and two-dimensional models of relevant diabatic-potential energy surfaces and couplings of H-3(+) and H-3.
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
- Ahlén, J, et al.
(författare)
-
Malignant Fibrous Histiocytoma, Aggressive Fibromatosis and Benign Fibrous Tumors Express mRNA for the Metalloproteinase Inducer EMMPRIN and the Metalloproteinases MMP-2 and MT1-MMP
- 2001
-
Ingår i: Sarcoma. - : Hindawi Limited. - 1357-714X .- 1369-1643. ; 5:3, s. 143-9
-
Tidskriftsartikel (refereegranskat)abstract
- Purpose:Extracellular matrix metalloproteinase inducer (EMMPRIN) has been shown to stimulate fibroblasts to production of matrix metalloproteinases (MMPs). MMPs comprise a family of proteolytic enzymes implicated in the degradation of extracellular matrix which has been proposed to be one of the essential steps in tumor invasion and metastases. In the present study we investigated the expression and location of mRNAs forEMMPRIN, matrix metalloproteinase-2 (MMP-2), and membrane-type 1 matrix metalloproteinase (MT1-MMP) in mesenchymal tumors with different tendencies to recur or metastasize.Subjects:Eight malignant fibrous histiocytomas (MFH), seven aggressive fibromatosis (AF), and six benign fibrous tumors (BF).Method:The mRNA-expression ofEMMPRIN,MMP-2andMT1-MMPwere studied using mRNAin situhybridization technique.Results:The mRNA-expression ofEMMPRIN,MMP-2andMT1-MMPrespectively were found at varying frequency and level in all tumor types. The mRNAs corresponding toEMMPRINandMMP-2were seen in neoplastic cells as well as in endothelial cells both inside and outside the tumor pseudo-capsule, whereasMT1-MMPwas seen only within the tumors. The estimated mRNA levels ofEMMPRINandMMP-2covariated significantly. Overall, the highest expression was found in the MFH tumors and the lowest levels in the BF tumors.Discussion:These findings suggest that the MMP-inducerEMMPRINand the extracellular matrix degrading system involving the metalloproteinasesMMP-2andMT1-MMPis frequently activated in mesenchymal tumors. The covariation betweenEMMPRINandMMP-2support previous findings that EMMPRIN may be an inducer of MMP-2. The high levels ofMMP-2mRNA in MFH indicate a relationship between the proteolytic activity ofMMP-2and the tumor aggressiveness.
|
|
| 10. |
- Girnita, L., et al.
(författare)
-
Increased expression of insulin-like growth factor I receptor in malignant cells expressing aberrant p53 : Functional impact
- 2000
-
Ingår i: Cancer Research. - 0008-5472 .- 1538-7445. ; 60:18, s. 5278-5283
-
Tidskriftsartikel (refereegranskat)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.
|
|
