SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:0250 7005 OR L773:1791 7530 ;srt2:(2000-2004);lar1:(uu)"

Sökning: L773:0250 7005 OR L773:1791 7530 > (2000-2004) > Uppsala universitet

  • Resultat 1-10 av 23
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Carlsson, Maria, 1958-, et al. (författare)
  • Treatment modality affects long-term quality of life in gynaecological cancer.
  • 2000
  • Ingår i: Anticancer Research. - : The International Institute of Anticancer Research. - 0250-7005 .- 1791-7530. ; 20:1B, s. 563-568
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to survey the side effects after cancer treatment, quality of life data were collected from females in clinical remission. MATERIALS AND METHODS The study was cross-sectional; every patient that visited the outpatient clinic during a period of three months was asked to anonymously complete the EORTC QLQ-C30 questionnaire and five additional specific questions related to gynaecological cancer. RESULTS In total, 235 patients (90%) returned the questionnaire. In general, both the levels of functioning and symptomatology were time-dependent. Patients with short treatment-free intervals reported more problems than the others. When using treatment modality as an independent variable in the statistical calculations, a treatment-related effect on functioning and symptomatology was demonstrated (p < 0.05 to p < 0.001). Patients previously treated with chemotherapy had poorer role- and cognitive functioning and more problems with fatigue, nausea, vomiting, dyspnoea, constipation and financial problems, compared with those not treated with chemotherapy (p < 0.05 to p < 0.01). Those patients who had been treated with external radiotherapy and/or brachytherapy had significantly more problems with flatulence and diarrhoea (p < 0.05 to p < 0.001). In conclusion, patients who underwent treatment for gynaecological cancer reported long-term side effects also many years after finishing treatment. The problems where related to treatment modality which should be considered, especially when planning adjuvant treatment.
  •  
2.
  • Li, Li, et al. (författare)
  • Induction of apoptosis and G2/M arrest by 2-methoxyestradiol in human cervical cancer HeLaS3 cells.
  • 2004
  • Ingår i: Anticancer Res. - Athens : International institute for anticancer research. - 0250-7005 .- 1791-7530. ; 24:2B, s. 873-80
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: It has been demonstrated that 2-Methoxyestradiol (2-ME), one of the estrogen metabolites, induces apoptosis in many different tumor cell lines. In the present study, the effects of 2-ME on human cervical cancer HeLaS3 cells and on normal cervical epithelial cells were evaluated. MATERIALS AND METHODS: Acridine orange staining, DNA fragmentation arrays and flow cytometry were used to measure the apoptosis and cell cycle progression. In addition, the effect of 2-ME on expression of iNOS was measured by Western blot. RESULTS: 2-ME inhibited the growth of HeLaS3 cells. This growth inhibition was accompanied by apoptosis and G2/M cell cycle arrest. 2-ME increased the expression of iNOS in parallel with apoptosis. Moreover, apoptosis was prevented by the iNOS inhibitor 1400W. 2-ME treatment resulted in a slight increase of the G2/M population, but no apoptosis, in normal cervical epithelial cells. There was no synergetic effect between E2 and 2-ME. CONCLUSION: 2-ME induced apoptosis via the iNOS pathway and caused G2/M cell cycle arrest in human cervical cancer HeLaS3 cells, but showed only slight effects on normal cervical epithelial cells. These data suggest that 2-ME might be an adjuvant agent in the treatment of cervical cancer.
  •  
3.
  • Li, Li, et al. (författare)
  • Induction of apoptosis or necrosis in human endometrial cancer cells by 2-Methoxyestradiol
  • 2004
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 24:6, s. 3983-3990
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:We investigated the effects of 2methoxyestradiol (2-ME), an endogenous estrogenic metabolite, on human endometrial cancer HEC-1-A and RL-95-2 cell lines.MATERIALS AND METHODS:After exposure of HEC-1-A and RL-95-2 cells to 2-ME, the morphological changes were evaluated by acridine orange staining and transmission electron microscopy. Cell cycle progress, apoptosis and necrosis were assessed by flow cytometry, DNA fragmentation and Western blot.RESULTS:2-ME inhibited cell growth by blocking the S- and G2/M-phase in both cell lines, by inducing apoptosis in HEC-1-A cells and by causing necrosis in RL-95-2 cells. Apoptosis, on HEC-1-A cells, was accompanied by an increased expression of iNOS and STAT1. This apoptotic effect was prevented by the iNOS inhibitor 1400W and eliminated by the caspase inhibitor Z-VAD-FMK. Necrosis, on RL-95-2 cells, was due to a severe disruption of the mitochondrial membrane potential. 2-ME had no significant effect on normal human endometrial cells.CONCLUSION:The data suggest that 2-ME has an antitumor effect on human endometrial carcinoma cells (HEC-1-A and RL-95-2) and may contribute as a new therapeutic agent for endometrial cancer patients.
  •  
4.
  • Lindström, Annika, 1953-, et al. (författare)
  • Correlations between serum progesterone and smoking, and the growth fraction of cervical squamous cell carcinoma
  • 2000
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 20, s. 1-
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Possible correlations between growth fraction of squamous cervical carcinomas and serum progesterone (se-P) concentrations, smoking habits and DNA ploidy were studied. MATERIALS AND METHODS: The DNA S-phase fraction (SPF), measured by flow cytometry was used as a marker of tumour growth in 103 cases of squamous cervical cancer stage IB-IV. DNA-ploidy (peridiploidy vs. aneuploidy), Se-P, se-Estradiol, smoking habits, parity, menopausal status, clinical stage and histopathological grading were compared to SPF < 14% vs. SPF > or = 14%. RESULTS: Aneuploidy, (odds ratio (OR) 10.0), se-P > or = 2.6 nmol/l (OR 7.5) and smoking (OR 3.0) were significantly associated with SPF > or = 14%, after adjustments for all factors included in the study. The association with se-P and smoking was attributed to an increased risk for the premenopausal women in the study. DISCUSSION: In this study an increased tumour growth was associated with increased leves of se-P, smoking and aneuploidy in women with invasive squamous cervical carcinoma. This study seems to experimentally confirm epidemiological studies, where smoking and long-term use of oral contraceptives have been linked to cervical neoplasms.
  •  
5.
  • Nilsson, A, et al. (författare)
  • Levels of angiogenic peptides in sera from patients with carcinoid tumours during alpha-interferon treatment
  • 2001
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 21:6A, s. 4087-4090
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Alpha-interferon, a known inhibitor of angiogenesis and cell proliferation, is used in the standard treatment of patients with carcinoid tumors. We studied the levels of two angiogenic peptides (bFGF and VEGF) in sera from patients with carcinoid tumours before and during treatment with alpha-interferon. The aim was to investigate if the antitumoral effect of alpha-interferon in these patients could be at least in part explained by a reduction in the measured angiogenetic peptides. PATIENTS AND METHODS: Sera from 29 patients with carcinoid tumours were collected before and during alpha-interferon treatment and analyzed using commercially available ELISA-kits. RESULTS: Interferon alpha treatment did not cause reduction of bFGF and VEGF levels in serum from patients with carcinoid tumours. In fact there was no correlation between changes in bFGF or VEGF levels and treatment effect. CONCLUSION: The action of alpha-interferon does not seem to be mediated by bFGF or VEGF in patients with carcinoid tumours. If alpha-interferon has an anti-angiogenic effect in this patient group, it is probably mediated by angiogenic peptides other than bFGF and VEGF.
  •  
6.
  • Orlova, Anna, et al. (författare)
  • Targeting against epidermal growth factor receptors : Cellular processing of astatinated EGF after binding to cultured carcinoma cells
  • 2004
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 24:6, s. 4035-4042
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:The alpha-emitting nuclide 211At is of great interest for radionuclide therapy when coupled to a tumor-targeting biomolecule, e.g. epidermal growth factor (EGF) the receptors of which are overexpressed in many malignancies. However, almost no information concerning the cellular processing of astatinated targeting agents is available.MATERIALS AND METHODS:We indirectly astatinated EGF ([211At]-benzoate-EGF) and studied its cellular processing in A-431 carcinoma cells in comparison with data concerning [125I]-benzoate-EGF.RESULTS: The biological half-life of astatine (3.5 h) was longer than the half-life of the iodine label (1.5 h). The increase of the half-life was due to longer retention of the internalised astatine radioactivity. The maximum accumulation for the astatine label occurred later (4-6h) than that for the iodine label (2-4h), indicating a slower excretion of astatine that was confirmed in experiment with 211At/1251-benzoate-EGF.CONCLUSION:The long retention of astatine might be advantageous for radionuclide therapy.
  •  
7.
  • Sand, Lars, et al. (författare)
  • Effects of long-term administration of cancer-promoting substances on oral subepithelial mast cells in the rat
  • 2002
  • Ingår i: Anticancer Research. - Athens : Hellenic Anticancer Institute. - 0250-7005 .- 1791-7530. ; 22, s. 2623-
  • Tidskriftsartikel (refereegranskat)abstract
    • The role of oral subepithelial mast cells in the defence against tumours is a matter of controversy. The effect of established and suggested carcinogens, such as the carcinogen 4-nitroquinoline-N-oxide (4-NQO) and Herpes simplex virus type 1 (HSV-1), in combination with oral snuff on lower lip subepithelial mast cells (MC) was studied in rats. The rats were exposed to prolonged use of oral snuff. The test substances were administered in a surgically created canal in the lower lip of the rats. There were 15 rats in each test group and 10 rats in the control group. The amount of countable subepithelial mast cells decreased significantly when the rat oral mucosa was exposed to the oral carcinogen 4-NQO but the effect of oral snuff and HSV-1 infection was weak. Our findings suggest that mast cells play a role in immunological cell defence against chemical carcinogens. Further studies are needed to clarify the mechanisms.
  •  
8.
  • Simonsen, Lena E., et al. (författare)
  • Haematological toxicity following different dosing schedules of 5-fluorouracil and epirubicin in rats
  • 2000
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 20:3A, s. 1519-1525
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM To study the effects of single and fractionated doses of 5-fluorouracil and epirubicin on the leukocyte counts in rats. METHODS Six different dosing patterns of each drug were injected within one day. The leukocytes were followed for 11-15 days. Pharmacokinetic models were developed using NONMEM. Quantitative and qualitative pharmacokinetic-pharmacodynamic relationships were investigated. RESULTS A one-compartment model with non-linear elimination described 5-fluorouracil pharmacokinetics and a three-compartment model described epirubicin concentration data. Sigmoidal or basic Emax-models quantified the relationships between individual AUCs and decreases in leukocytes, for both drugs. Similar relationships between AUC and toxicity were found, regardless of whether the drugs were given as single or fractionated doses. CONCLUSION Quantitative relationships between AUC and the effect on leukocytes were established for 5-fluorouracil and epirubicin. However, no schedule dependence was indicated for the schedules used in the study.
  •  
9.
  • Wymenga, Feng, et al. (författare)
  • Uptake of 14C- and 11C-labeled glutamate, glutamine and aspirtate in vitro and in vivo
  • 2000
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 20:1A, s. 251-256
  • Tidskriftsartikel (refereegranskat)abstract
    • To explore their potential use as in vivo tracers, the uptake of the amino acids glutamine, glutamate and aspartate, labeled with 11C or 14C, was evaluated in tumor cell aggregates, in vivo in rats and a few pilot studies with positron emission tomography (PET) in patients. The uptake in aggregates increased linearly with time, and was competitively inhibited by the same amino acids. The uptake of 14C-glutamate in carcinoid cells (BON) was inhibited by cystine but not by aspartate, contrary to the result in neuroblastoma (LAN). 6-Diazo-oxy-L-norleucine (a glutamine analogue) and Substance P had different effect on the uptake of glutamate in different cells. The metabolic fate of 14C-glutamate was evaluated with protein separation and with HPLC. The in vivo distribution in rats showed the highest uptake of 11C-glutamine and 11C-glutamate in pancreas and kidney, and of 11C-aspartate in the lung. In the human studies with PET, pancreas had the highest uptake followed by kidney with 11C-glutamate, and followed by spleen with 11C-aspartate. A primary pancreas tumour and metastases in liver were difficult to identify except in one case.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 23

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