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71.
  • Einhorn, N, et al. (författare)
  • A systematic overview of radiation therapy effects in uterine cancer (corpus uteri)
  • 2003
  • Ingår i: Acta Oncologica. - Taylor & Francis. - 1651-226X. ; 42:5-6, s. 557-561
  • Tidskriftsartikel (refereegranskat)abstract
    • A systematic review of radiation therapy trials in several tumour types was performed by The Swedish Council of Technology Assessment in Health Care (SBU). The procedures for evaluation of the scientific literature are described separately (Acta Oncol 2003; 42: 357-365). This synthesis of the literature on radiation therapy for uterine cancer is based on data from one randomized study Moreover, data from two prospective studies and seven retrospective studies were used. In total, 10 scientific articles are included, involving 3446 patients. The results were compared with those of a similar overview from 1996 including 13597 patients. The conclusions reached can be summarized as: There is fairly good evidence that there is no need for adjuvant radiotherapy in patients with good risk uterine cancer. There is fairly good evidence that adjuvant radiotherapy reduces the relapse rate in high-risk patients but has no impact on survival. There is substantial documentation showing that medically inoperable patients and patients with locally recurrent uterine cancer can be treated with radiotherapy alone with curative effect.
72.
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73.
  • Elmroth, Kerstin, 1970-, et al. (författare)
  • Chromatin- and temperature-dependent modulation of radiation-induced double-strand breaks
  • 2003
  • Ingår i: Int J Radiat Biol. - 0955-3002 (Print). ; 79:10, s. 809-16
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: To investigate the influence of chromatin organization and scavenging capacity in relation to irradiation temperature on the induction of double-strand breaks (DSB) in structures derived from human diploid fibroblasts. MATERIALS AND METHODS: Agarose plugs with different chromatin structures (intact cells+/-wortmannin, permeabilized cells with condensed chromatin, nucleoids and DNA) were prepared and irradiated with X-rays at 2 or 37 degrees C and lysed using two different lysis protocols (new ice-cold lysis or standard lysis at 37 degrees C). Induction of DSB was determined by constant-field gel electrophoresis. RESULTS: The dose-modifying factor (DMF(temp)) for irradiation at 37 compared with 2 degrees C was 0.92 in intact cells (i.e. more DSB induced at 2 degrees C), but gradually increased to 1.5 in permeabilized cells, 2.2 in nucleoids and 2.6 in naked DNA, suggesting a role of chromatin organization for temperature modulation of DNA damage. In addition, DMF(temp) was influenced by the presence of 0.1 M DMSO or 30 mM glutathione, but not by post-irradiation temperature. CONCLUSION: The protective effect of low temperature was correlated to the indirect effects of ionizing radiation and was not dependent on post-irradiation temperature. Reasons for a dose modifying factor <1 in intact cells are discussed.
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74.
  • Elmroth, Kerstin, 1970-, et al. (författare)
  • Cleavage of cellular DNA by calicheamicin gamma1.
  • 2003
  • Ingår i: DNA repair. - 1568-7864. ; 2:4, s. 363-74
  • Tidskriftsartikel (refereegranskat)abstract
    • It is assumed that the efficient antitumor activity of calicheamicin gamma1 is mediated by its ability to introduce DNA double-strand breaks in cellular DNA. To test this assumption we have compared calicheamicin gamma1-mediated cleavage of cellular DNA and purified plasmid DNA. Cleavage of purified plasmid DNA was not inhibited by excess tRNA or protein indicating that calicheamicin gamma1 specifically targets DNA. Cleavage of plasmid DNA was not affected by incubation temperature. In contrast, cleavage of cellular DNA was 45-fold less efficient at 0 degrees C as compared to 37 degrees due to poor cell permeability at low temperatures. The ratio of DNA double-strand breaks (DSB) to single-stranded breaks (SSB) in cellular DNA was 1:3, close to the 1:2 ratio observed when calicheamicin gamma1 cleaved purified plasmid DNA. DNA strand breaks introduced by calicheamicin gamma1 were evenly distributed in the cell population as measured by the comet assay. Calicheamicin gamma1-induced DSBs were repaired slowly but completely and resulted in high levels of H2AX phosphorylation and efficient cell cycle arrest. In addition, the DSB-repair deficient cell line Mo59J was hyper sensitive to calicheamicin gamma. The data indicate that DSBs is the crucial damage after calicheamicin gamma1 and that calicheamicin gamma1-induced DSBs are recognized normally. The high DSB:SSB ratio, specificity for DNA and the even damage distribution makes calicheamicin gamma1 a superior drug for studies of the DSB-response and emphasizes its usefulness in treatment of malignant disease.
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75.
  • Ericson, K, et al. (författare)
  • Defective mismatch-repair in patients with multiple primary tumours including colorectal cancer
  • 2003
  • Ingår i: European Journal of Cancer. - Elsevier. - 1879-0852. ; 39:2, s. 8-240
  • Tidskriftsartikel (refereegranskat)abstract
    • Individuals with an inherited predisposition to cancer development are at an increased risk of developing multiple tumours. Hereditary non-polyposis colorectal cancer (HNPCC) is one of the most common hereditary cancer syndromes and is estimated to account for approximately 2% of colorectal cancers. However, HNPCC individuals are at an increased risk of developing other tumour types such as cancers of the endometrium, urothelium and small intestine. We have utilised a population-based regional cancer registry to identify all patients with double primary colorectal cancers and at least one additional malignancy and characterised the tumour spectrum in this patient group. We subsequently selected those 47 individuals who had developed at least four malignancies, including two colorectal cancers, for studies of the tumour characteristics associated with HNPCC. In total, these individuals developed 209 tumours, 156 of which were successfully retrieved. Microsatellite instability (MSI), a phenomenon caused by defective mismatch-repair (MMR), was identified in 63/154 (41%) evaluable tumours with a MSI-high pattern in 59 and a MSI-low pattern in four tumours. All tumours were immunohistochemically stained for the MMR proteins MLH1 and MSH2, with loss of expression in 55/63 (87%) MSI tumours and in 2/89 (2%) microsatellite stable (MSS) tumours. This loss affected MLH1 in 24 tumours and MSH2 in 33 tumours. A concordant loss of expression for the same MMR protein in several tumours from the same individual, a pattern that strongly suggests an underlying germline MMR gene mutation, was found in 17/45 (38%) patients and affected MLH1 in 8 patients and MSH2 in 9 patients. We conclude that the development of multiple primary tumours, including synchronous or metachronous colorectal cancers, is associated with an increased frequency of MSI and loss of immunohistochemical expression of MLH1 and MSH2.
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76.
  • Ericsson, Peter, et al. (författare)
  • ECL Cell Histamine Mobilization Studied byGastric Submucosal Microdialysis in Awake Rats:Methodological Considerations.
  • 2003
  • Ingår i: Pharmacology and Toxicology. - Wiley-Blackwell. - 1600-0773. ; 93:2, s. 57-65
  • Tidskriftsartikel (refereegranskat)abstract
    • The ECL cells are endocrine/paracrine cells in the acid-producing part of the stomach. They secrete histamine in response to circulating gastrin. Gastric submucosal microdialysis has been used to study ECL-cell histamine mobilization in awake rats. In the present study we assess the usefulness and limitations of the technique. Microdialysis probes were implanted in the gastric submucosa. Histological analysis of the stomach wall around the probe revealed a moderate, local inflammatory reaction 1-2 days after implantation; the inflammation persisted for at least 10 days. Experiments were conducted 3 days after the implantation. The "true" submucosal histamine concentration was determined by perfusing at different rates (the zero flow method) or with different concentrations of histamine at a constant rate (the no-net-flux method): in fasted rats it was calculated to be 87±5 (means±S.E.M.) nmol/l and 76±9 nmol/l, respectively. The corresponding histamine concentrations in fed rats were 93±5 and 102±8 nmol/l, respectively. With a perfusion rate of 74 mul/hr the recovery of submucosal histamine was 49%, at 34 mul/hr the recovery increased to 83%. At a perfusion rate below 20 mul/hr the microdialysate histamine concentration was close to the actual concentration in the submucosa. The ECL-cell histamine mobilization was independent of the concentrations of Ca2+ in the perfusion medium (0-3.4 mmol/l Ca2+). In one experiment, histamine mobilization in response to gastrin (10 nmol/kg/hr subcutaneously) was monitored in rats pretreated with prednisolone (60 mg/kg) or indomethacin (15 mg/kg). The two antiinflammatory agents failed to affect the concentration of histamine in the microdialysate either before or during the gastrin challenge, which was in accord with the observation that the inflammatory reaction was modest and that inflammatory cells were relatively few around the probe and in the wall of the probe. In another experiment, rats were given aminoguanidine (10 mg/kg) or metoprine (10 mg/kg) 4 hr before the start of gastrin infusion (5 nmol/kg/hr intravenously). Metoprine (inhibitor of histamine N-methyl transferase) did not affect the microdialysate histamine concentration, while aminoguanidine (inhibitor of diamine oxidase) raised both basal and gastrin-stimulated histamine concentrations. We conclude that microdialysis can be used to monitor changes in the concentration of histamine in the submucosa of the stomach, and that the inflammatory reaction to the probe is moderate and does not affect the submucosal histamine mobilization.
77.
  • Fagman, Henrik, 1975-, et al. (författare)
  • Nuclear accumulation of full-length and truncated adenomatous polyposis coli protein in tumor cells depends on proliferation.
  • 2003
  • Ingår i: Oncogene. - 0950-9232. ; 22:38, s. 6013-22
  • Tidskriftsartikel (refereegranskat)abstract
    • The adenomatous polyposis coli (APC) tumor suppressor is a nucleocytoplasmic protein. The nuclear accumulation of APC was recently found to vary depending on cell density, suggesting that putative APC function(s) in the nucleus is controlled by the establishment of cell contacts. We report here that the density-dependent redistribution of APC between nucleus and cytoplasm prevails in 6/6 thyroid and colorectal carcinoma cell lines. Moreover, mutated APC lacking known nuclear localization sequences had the similar distribution pattern as the full-length protein. APC invariably accumulated in the nuclei of Ki-67 expressing cells, but was largely cytoplasmic when cell cycle exit was induced by serum starvation or at high cell density. APC colocalized with beta-catenin in the nucleus only in one cell line (SW480). Also, APC maintained a predominantly nuclear position in early confluent states when cytoplasmic beta-catenin was recruited to newly formed adherens-like junctions. The results indicate that nuclear targeting of APC is driven by cell cycle entry rather than altered cell-cell contact. The ability of C-terminally truncated APC to accumulate in the nucleus suggests that nuclear import signals other than NLS1(APC) and NLS2(APC) are functionally important. Residual function(s) of N-terminal APC fragments in tumor cells carrying APC mutations might be beneficial to tumor growth and survival.
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78.
  • Falkmer, U, et al. (författare)
  • A systematic overview of radiation therapy effects in skeletal metastases
  • 2003
  • Ingår i: Acta Oncologica. - Taylor & Francis. - 1651-226X. ; 42:5-6, s. 620-633
  • Tidskriftsartikel (refereegranskat)abstract
    • A systematic review of radiation therapy trials in several tumour types was performed by The Swedish Council of Technology Assessment in Health Care (SBU). The procedures for evaluation of the scientific literature are described separately (Acta Oncol 2003; 42: 357-365). This synthesis of the literature on radiation therapy for skeletal metastases is based on data from 16 randomized trials. Moreover, data from 20 prospective studies, 5 retrospective studies and 22 other articles were used. A total of 63 scientific articles are included, involving 8051 patients. The results were compared with those of a similar overview from 1996 including 13054 patients. The conclusions reached can be summarized as follows: Irradiation of skeletal metastases is, with few exceptions, a palliative treatment. There is strong evidence that radiotherapy of skeletal metastases gives an overall (complete and partial pain relief) in more than 80% of patients. There is strong evidence that the duration of pain relief in at least 50% of patients lasts for greater than or equal to6 months. There is convincing evidence that pain relief, in terms of degree and duration, does not depend on the fractionation schedules applied. Irrespective of the fractionation schedule used at irradiation, the number of later complications, such as spinal cord compression or pathological fractures, at the index fields are low. There are some data showing that the difference in cost between single and multifraction treatment is small. However, these data do not permit any firm conclusions to be drawn. Several reports indicate that early diagnosis and early therapy of spinal cord compression are the two most important predictors of a favourable clinical outcome after radiotherapy. However, no controlled studies have been undertaken. When the diagnosis of spinal cord compression is late, a favourable outcome might depend on the radio-responsiveness of the tumour. The documentation is weak and no conclusions can be drawn. There is some evidence that a small proportion of totally paralytic patients can regain walking function after radiotherapy. There is strong evidence that the radionuclides Sr-89 and Sm-153 are efficient when they are used as a systemic treatment of generalized bone pain due to metastasis from carcinomas of the prostate and breast. Overall bone pain relief occurs in about 60-80% of patients with a median response duration of 2-4 months. There is strong evidence that intravenous treatment with bisphosphonates in patients with myeloma and osteolytic bone metastasis due to carcinoma of the breast significantly decreases the number of skeleton-related events and bone pain.
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79.
  • Fernebro, Eva (författare)
  • Rectal Cancer - Tumor Biology and Prognostic Markers
  • 2003
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Popular Abstract in Swedish Cancer i tjock- och ändtarm drabbar årligen drygt 5000 svenskar. En rad faktorer har satts i samband med tumöruppkomst i tarmen, bl a ärftlighet, inflammatorisk tarmsjukdom, kost och motion, men det är till stor del okänt hur dessa faktorer orsakar cancerutveckling. Genetiska förändringar styr tumörutvecklingen Tumörerna utvecklas oftast från ett godartat förstadium, ett adenom eller polyp. Tumöruppkomst sker genom att skador eller mutationer i olika tumörassocierade gener ansamlas. Dessa skador drabbar tre huvudtyper av gener; onkogener, tumör suppressorgener och DNA-reparationsgener. Ett stort antal gener av betydelse i denna process har identifierats och tumörutveckling i tjock- och ändtarm utgör en modell för hur förändringar i tumörassocierade gener leder till cancer. En tredjedel av tjocktarmens tumörer uppstår i ändtarmen, som utgör de nedersta 15 cm av tarmen. Ändtarmscancer skiljer sig delvis från övrig tjocktarmscancer, bl avseende symptom, behandling och tumörbiologi. Under de senaste decennierna har återfallen i ändtarmscancer minskat och överlevnaden har ökat, men trots detta avlider fortfarande omkring 40 % av patienterna i sjukdomen. Förbättrad prognos Idag är mikroskopisk undersökning av tumören med bestämning av dess stadium det viktigaste instrumentet för att förutse patientens prognos, men är ändå ett grovt mått på risken för sjukdomsåterfall. En förbättrad prognostik, där varje tumörs specifika egenskaper studeras för att förutse risken för återfall, skulle vara av stort värde. Härigenom skulle patienter med hög risk för återfall redan tidigt kunna erbjudas tilläggsbehandling, tex i form av cellhämmande medel. Målsättning De frågeställningar som behandlas i avhandlingen omfattar: § Mätning av proteiner i urokinas-plasminogenaktiverings och metalloproteinas systemen i blodprover från patienter med ändtarmscancer. Kan halterna av dessa ämnen användas för att förutse patientens prognos? (arbetena I-II)? § En ny metod, vävnadsmikroarray, har nyligen utvecklats. Metoden bygger på att 0.6 mm i diameter stora cylindrar tas från en paraffin-inbäddad tumör. Upp till 500 olika cylindrar placeras därefter i en ny paraffinkloss som kan snittas och färgas. Därigenom kan många tumörer studeras på ett enda glas. Är denna metod användbar för immunhistokemiska studier av ändtarmscancer (arbete III)? Kan metoden användas för att hitta proteiner vars färgningsmönster samvarierar med prognos (arbete IV)? § Cirka 5% av ändtarmscancer uppkommer hos patienter yngre än 50 år. Orsakas dessa tumörer av samma genetiska förändringar som övriga ändtarmscancrar? I vilken omfattning uppkommer dessa tumörer pga ärftlighet (arbete V)? Proteaser Proteaser är enzymer som deltar i nybildning och nedbrytning av vävnader. Proteaserna finns normalt i mätbara nivåer. Tumörceller och/eller stödjeceller i tumörerna utsöndrar förhöjda nivåer. Mängden proteaser kan mätas i tumörvävnad, vilket kräver tillgång till färskt tumörmaterial. Metoder för analys av dessa faktorer i blodprover har utarbetats, vilket möjliggör analys av nivåerna redan innan operationen. Urokinas plasminogen aktivator systemet och matrix metalloproteinaserna är viktiga för vävnadsnedbrytning. I arbete I mättes halterna av faktorn suPAR, som är den lösliga receptorn i urokinas plasminogen aktivator systemet, i blodprover från 173 patienter med ändtarmscancer. Höga suPAR värden visades medföra sämre överlevnad. I arbete II mättes halten av faktorn TIMP-1, som är en naturligt förekommande hämmare av metalloproteinas, i blodprover från 352 patienter. Även TIMP-1 visades samvariera med prognos; en större andel av patienterna med höga värden avled. Sammanfattningsvis har dessa studier konfirmerat dessa faktorers prognostiska värde i ändtarmscancer. Möjligheten att mäta halterna i ett blodprov taget före behandling skulle kunna användas för att erbjuda patienter med höga nivåer tilläggsbehandling, men ytterligare studier krävs innan bestämning av dessa faktorer kan komma till nytta för patienten. Vävnadsmikroarray I arbete III användes vävnadsmikrorray metoden för immunhistokemisk färgning av proteiner i tumörcellerna och resultaten jämfördes med traditionell teknik där hela snitt av tumören färgas. Vävnadsmikroarray är tids- och vävnadsbesparande för analys av flera faktorer i stora tumörmaterial. Metoden gav goda färgningsresultat, vilka överensstämde väl med resultaten från helvävnadssnitt. I arbete IV togs vävnadscylindrar från 269 ändtarmscancrar och snitt från dessa vävnadsmikroarrayer färgades med immunhistokemisk teknik för flera markörer (Ki-67, p53, Bcl-2, EGFR, ß-catenin, E-cadherin, MLH1 och MSH2), vilka speglar olika företeelser i cellen som celltillväxt, onkogenuttryck, tumör suppressor- genuttryck och DNA-reparation. Uttrycken av dessa faktorer analyserades gentemot tumörens förmåga till spridning (metastas). Förändrade uttryck av markörerna ß-catenin och E-cadherin, som normalt reglerar cellernas sammanhållning, samvarierade med risken för metastas, medan de övriga markörerna inte kunde användas för att förutse metastasrisken. Ändtarmscancer hos unga patienter I arbete V undersöktes ändtarmscancrar från 30 patienter, som utvecklat sjukdomen innan 50 års ålder. Tumörerna studerades med immunhistokemisk färgning och med molekylärgenetiska tekniker i syfte att kartlägga vilka genetiska förändringar som lett till tumöruppkomst. Studien visade att ärftlighet fanns hos 8 av patienterna och att tumörerna hos 3 fall sannolikt uppkommit pga av det ärftliga syndromet hereditär nonpolyposis colorektal cancer (HNPCC). Sammanfattning Sammanfattningsvis har vi i dessa studier funnit att: § Halterna av faktorerna suPAR och TIMP-1 i blodprov från patienter med ändtarmscancer ger prognostisk information. Patienter med höga halter hade kortare överlevnad. § Vänadsmikroarraymetoden kan användas för immunhistokemisk färgning vid ändtarmscancer. Analys av flera olika faktorer i en stor serie av ändtarmscancrar visade att förändrade uttryck av dessa proteiner är vanligt förekommande. Förändrade uttryck av proteinerna ß-catenin och E-cadherin samvarierade med risken för metastas. § Ändtarmcancer hos unga utvecklas liksom tumörerna hos äldre genom en ansamling av genetiska skador. Endast ca 1/10 ändtarmscancrar hos unga tycks bero på det ärftliga syndromet HNPCC.
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80.
  • Ford, Caroline, et al. (författare)
  • Mouse mammary tumor virus-like gene sequences in breast tumors of Australian and Vietnamese women
  • 2003
  • Ingår i: Clinical Cancer Research. - American Association for Cancer Research. - 1078-0432. ; 9:3, s. 1118-1120
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: There is considerable evidence that the presence of mouse mammary tumor virus (MMTV)-like gene sequences in human breast cancer is highly associated with human breast carcinoma. Previous studies have found MMTV-like gene sequences in 38% of breast cancer tissue from United States women. The prevalence of these sequences in Australian and Vietnamese women has never been reported. EXPERIMENTAL DESIGN: Using PCR and primers that amplify MMTV-like gene sequences, we tested cancerous and benign breast tissue from Caucasian-Australian, Vietnamese-Australian, and Vietnamese women. RESULTS: MMTV-like gene sequences were amplified in 19 of 45 (42.2%) archival breast cancer biopsy tissues from Caucasian-Australian women, but only 1 of 120 (0.8%) and 0 of 41 breast cancer biopsy tissues from Vietnamese and Vietnamese-Australian women, respectively. The same sequences were found in only 2 of 111 (1.8%) and 0 of 60 normal (benign) breast tissue samples from Australian and Vietnamese women, respectively. CONCLUSIONS: MMTV-like gene sequences are found in only some human populations and are rarely found in normal human breast tissue from all populations, suggesting they are not present in the normal human genome and have been acquired.
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