SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:0007 0920 OR L773:1532 1827 ;srt2:(2000-2004)"

Sökning: L773:0007 0920 OR L773:1532 1827 > (2000-2004)

  • Resultat 31-40 av 143
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
31.
  • Dabrosin, Charlotta, 1961-, et al. (författare)
  • Oestradiol enhances tumour regression induced by B7-I/IL-2 adenoviral gene transfer in a murine model of breast cancer
  • 2003
  • Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 89:2, s. 385-390
  • Tidskriftsartikel (refereegranskat)abstract
    • The majority of breast cancers are oestrogen dependent and although current treatment strategies have improved, approximately 50% of the patients will develop metastasis. New treatments that result in long-term systemic immunity are therefore being developed. We have previously shown that adenoviral gene transfer of B7-I/IL-2 to murine breast cancer induces a high rate of complete turnout regression and systemic immunity. Since oestrogens not only affect breast cancer but also have been shown to modulate immune function and secretion of immune-regulatory cytokines, we explored whether administration of oestradiol altered the immune response induced by an adenoviral vector expressing B7-I/IL-2. An oestrogen-dependent murine breast cancer tumour was used in ovariectomised mice, supplemented either oestradiol or placebo. We report the somewhat unexpected finding that intratumoral injection of adenovirus expressing B7-I/IL-2 induces complete turnout regression in 76% of oestradiol-supplemented mice, while only 18% of the tumours regressed in the oestrogen-depleted group. Cured mice in both groups exhibited a similar CTL response against the tumour antigen. However, intratumoral IFN-? levels, 2 days after B7-I/IL-2 injection, were significantly higher in mice treated with oestradiol compared to placebo. This may be one mechanism explaining the higher response rate of tumours in oestradiol-replenished mice.
  •  
32.
  • Dalen, Helge, et al. (författare)
  • a-tocopheryl succinate sensitises a T lymphoma cell line to TRAIL-induced apoptosis by suppressing NF-?B activation
  • 2003
  • Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 88:1, s. 153-158
  • Tidskriftsartikel (refereegranskat)abstract
    • Activation of nuclear factor-?B (NF-?B) can interfere with induction of apoptosis triggered by the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL, Apo2L). Therefore, agents that suppress NF-?B activation may sensitise cells to TRAIL-dependent apoptosis. Exposure of Jurkat cells to TRAIL resulted in massive and saturable apoptosis induction, following an initial lag time. This lag was abolished by pretreatment of the cells with subapoptotic doses of a-tocopheryl succinate (a-TOS) or the proteasome inhibitor MGI32. Exposure of the cells to TRAIL led to a rapid, transient activation of NF-?B, a process that was suppressed by cell pretreatment with a-TOS or MGI32. Activation of NF-?B by TNF-a prior to TRAIL exposure increased resistance of the cells to TRAIL-mediated apoptosis. We conclude that a-TOS sensitises cells to TRAIL killing, at least in some cases, through inhibition of NF-?B activation. This further supports the possibility that this semisynthetic analogue of vitamin E is a potential adjuvant in cancer treatment, such as in the case of TRAIL-mediated inhibition of cancer.
  •  
33.
  •  
34.
  • Dryver, ET, et al. (författare)
  • Follow-up of patients with Hodgkin's disease following curative treatment: the routine CT scan is of little value
  • 2003
  • Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 1532-1827 .- 0007-0920. ; 89:3, s. 482-486
  • Tidskriftsartikel (refereegranskat)abstract
    • A total of 10-40% of patients with Hodgkin's disease relapse following initial curative therapy. Intensive follow-up is resource intensive and may identify false relapses. We performed a retrospective review of all patients with Hodgkin's disease treated at our centre between 1990 and 1999 to evaluate the utility of the components of follow-up. A total of 107 patients met the inclusion and exclusion criteria. The median age was 33 years and the median duration of follow-up 38 months. The total number of follow-up visits was 1209 and total number of CT scans 283. There were 109 suspected relapses of which 22 proved to be true relapses. Of the latter, 14 were identified clinically, six radiologically and two via lab testing. The routine CT scan detected only two relapses (9%), yet accounted for 29% of the total follow-up costs. Based on data from our centre, the cost per true relapse was $6000 US, 49% incurred by radiological tests. The majority of the cost of follow-up was incurred by routine follow-up (84%) as opposed to the investigation of suspected relapses (16%). We conclude that most true relapses are clinically symptomatic and that the routine CT is an expensive and inefficient mode of routine follow-up.
  •  
35.
  •  
36.
  •  
37.
  • Erba, E, et al. (författare)
  • Effect of Aplidin in acute lymphoblastic leukaemia cells.
  • 2003
  • Ingår i: British journal of cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 89:4, s. 763-73
  • Tidskriftsartikel (refereegranskat)abstract
    • The cytotoxic effect of Aplidin was investigated on fresh leukaemia cells derived from children with B-cell-precursor (BCP) acute lymphoblastic leukaemia (ALL) by using stromal-layer culture system and on four cell lines, ALL-PO, Reh, ALL/MIK and TOM-1, derived from patients with ALL with different molecular genetic abnormalities. In ALL cell lines Aplidin was cytotoxic at nanomolar concentrations. In the ALL cell lines the drug-induced cell death was clearly related to the induction of apoptosis and appeared to be p53-independent. Only in ALL-PO 20 nM Aplidin treatment caused a block of vascular endothelial growth factor (VEGF) secretion and downregulation of VEGF-mRNA, but Aplidin cytotoxicity does not seem to be related to VEGF inhibition since the sensitivity of ALL-PO cells to Aplidin is comparable to that observed for the other cells used. Aplidin induced a G(1) and a G(2) M block in ALL cell lines. In patient-derived leukaemia cells, Aplidin induced a strong cytotoxicity evidenced in a stroma-supported immunocytometric assay. Cells from children with genetic abnormalities such as t(9;22) and t(4;11) translocations, associated with an inferior treatment outcome, were sensitive to Aplidin to the same extent as that observed in other BCP-ALL cases. Aplidin exerted a strong cell killing effect (>88%) against primary culture cells from five relapsed ALL cases, at concentrations much lower than those reported to be achieved in plasma of patients receiving Aplidin at recommended doses. Taken together these data suggest that Aplidin could be a new anticancer drug to be investigated in ALL patients resistant to available therapy.
  •  
38.
  •  
39.
  •  
40.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 31-40 av 143
Typ av publikation
tidskriftsartikel (142)
forskningsöversikt (1)
Typ av innehåll
refereegranskat (135)
övrigt vetenskapligt/konstnärligt (8)
Författare/redaktör
Ekbom, A (9)
Nyren, O (8)
Adami, HO (6)
Weiderpass, E (5)
Kogner, P (5)
Li, X. (4)
visa fler...
Landberg, Göran (4)
Dillner, J (4)
Ye, W. (4)
Martinsson, Tommy, 1 ... (4)
Hansson, J. (4)
Wolk, A (4)
Olsson, Håkan (3)
Blomqvist, Carl (3)
Lehtinen, M (3)
Glimelius, Bengt (3)
Boffetta, P (3)
Abel, Frida, 1974 (3)
Krona, Cecilia, 1976 (3)
Dong, C. (3)
Ahlman, Håkan, 1947 (3)
Adolfsson, J. (3)
Trichopoulos, D (3)
Rydh, B. (3)
Lund, E. (2)
Nyberg, F (2)
Larsson, O (2)
Henriksson, R (2)
Olsson, H. (2)
Pukkala, E (2)
Lagergren, J (2)
Holmberg, Lars (2)
Rosenquist, R. (2)
Bengtsson, Nils-Olof (2)
Kogner, Per (2)
Sjöberg, Rose-Marie, ... (2)
Ejeskär, Katarina, 1 ... (2)
Magnusson, C (2)
Hall, P (2)
Wängberg, Bo, 1953 (2)
Nilsson, Ola, 1957 (2)
Larsson, P (2)
Engeland, A (2)
Adami, H-O (2)
Dillner, Joakim (2)
Wolk, Alicja (2)
HSIEH, CC (2)
Granath, F. (2)
Lundqvist, A (2)
Kiessling, R (2)
visa färre...
Lärosäte
Karolinska Institutet (89)
Lunds universitet (24)
Göteborgs universitet (14)
Linköpings universitet (14)
Uppsala universitet (12)
Umeå universitet (9)
visa fler...
Örebro universitet (3)
Chalmers tekniska högskola (3)
Mälardalens universitet (2)
visa färre...
Språk
Engelska (142)
Odefinierat språk (1)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (42)
Naturvetenskap (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy