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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) srt2:(1995-1999);lar1:(umu)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) > (1995-1999) > Umeå universitet

  • Resultat 1-10 av 17
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1.
  • Eklund, Johan (författare)
  • Searching for genetical cancer risks using a database of familial cancer : part I
  • 1999
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • A method to estimate cancer risks, when a recessive genetic defect is assumed to influence the risk to develop cancer, is presented. The proportion of the recessive defect is also estimated. The method uses cancer diagnosis data from a large sample of biological families. A family is here parents and two children. The information used is the frequencies of cancer diagnoses among siblings. Estimations are performed with the method of moments. The work is methodological, meaning that no specific type of cancer is considered.
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2.
  • Pålsson, Maj-Britt, 1936- (författare)
  • Support for women with breast cancer, and for the district and hospital nurses involved : an intervention study
  • 1995
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The purpose of this study was to investigate breast cancer patients’ experiences of their illness and of traditional nursing care (TNC) or supportive nursing care (SNC) respectively, as well as nurses' experiences of support and of caring for cancer patients. An intervention including extended co-operation between the surgical ward and primary health care, shorter waiting times, and changed routines concerning the information about the diagnosis, as well as training and systematic clinical supervision for the nurses, was implemented. Newly diagnosed breast cancer patients (n=47) from two county councils in the south-east of Sweden were interviewed (IV, V). Thirty-four of them completed scales about well-being, burnout, hopelessness, anxiety and depression (VII). The women who had TNC reported lack of professional support during the initial phase of the disease and suggested changes in the care similar to those implemented in the SNC. In the SNC group the women expressed feelings of safety and security after the professional support and the organizational changes in the care. There were significantly more single women and women who had had breast conserving surgery in the SNC group than in the TNC (VII). The hopelessness scores in the SNC group were significantly higher than in the TNC group.Thirty-nine district nurses (DNs) were interviewed at baseline (I), and thirty-three of them completed scales about burnout, empathy, and sense of coherence (SOC) before and after systematic clinical supervision (VI). Twenty-three of the 39 DNs, as well as 9 hospital nurses (HNs) who participated in the clinical supervision, were interviewed about their experiences of this intervention (III). Twenty-nine tape-recorded supervision sessions in three groups of DNs (n=23) were analysed (II). Baseline interviews and analyses of the content of the supervisory sessions strongly emphasized that DNs experienced problems in the home care of seriously ill cancer patients. Deep human contacts were a source of both strain and enrichment. The clinical supervision was said to provide relief from undesirable thoughts and feelings, confirmation of themselves both as individuals and in their professional role, a broader and deeper knowledge and increased self-confidence. There were no significant differences in the burnout, empathy, and SOC scores between the supervisory group (n=21) and a comparison group (n=12) at the first and second measures, nor over time within the groups. There were some correlations between these phenomena and the Karolinska scales of personality, as well as cor­relations between burnout, empathy and SOC.The groups of women were not entirely similar as regards demographic and medical characteristics, and the sample size of patients and nurses was small. It is obvious that patients in the TNC missed those factors that were implemented in the SNC, at the same time the latter women expressed hopelessness more often than those who had received TNC. This result may be due to the fact that support from nurses had made the women more prepared to express their feelings, that support had not been provided to an adequate extent or in the right way, or that the applied scales were not appropriate. The finding that the nurses experienced the clinical supervision as very positive but that, despite this, there were no significant differences in attitudes measured by scales within or between the groups, can be interpreted in a similar way. Consequently, further research is needed to judge the effects of intervention. The study has, above all, produced qualitative descriptions of patients' experiences of the nursing care after discharge from hospital, and of DNs’ experiences of the care of cancer patients in their homes, and of systematic clinical supervision.
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3.
  • Wiklund, Fredrik, et al. (författare)
  • Prediction of cancer incidence
  • 1998
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • In this paper a method for predicting future number of cancer diagnoses is derived. The method is based on estimation of the cumulative hazard of cancer diagnosis and cumulative hazard of population mortality. The estimation of cancer hazard is done non-parametrically, while the population death hazard is assumed to follow the Gompertz-Makeham distribution. The prediction is based on the assumption that cancer incidence and population mortality in the prediction intervals are derived. Also, prediction intervals, based on non-parametric bootstrap, are presented. The method is applied to predict number of colon cancer diagnoses among females in the northern part of Sweden. It has shown to detect and adjust for changes in population age structure, and to provide good predictions in situation where the cancer incidence and population mortality are stable during the prediction period.
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4.
  • Johansson, Mikael, et al. (författare)
  • Tumor blood flow and the cytotoxic effects of estramustine and its constituents in a rat glioma model
  • 1997
  • Ingår i: Neurosurgery. - : Oxford University Press. - 0148-396X .- 1524-4040. ; 41:1, s. 237-244
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Estramustine (EaM) is a conjugate of nor-nitrogen mustard (NNM) and 17 beta-estradiol (E2) that has cytotoxic and radiosensitizing effects on experimental malignant glioma. Its mechanism of action is only partly understood. To further investigate the mechanism in vivo, the effects on tumor blood flow (TBF) and tumor growth were analyzed.METHODS: TBF was measured by radioactive microspheres, and tumor growth was measured by weight. Apoptosis was evaluated by in situ end labeling and gel electrophoresis. The effects of the constituents NNM and E2 were also evaluated.RESULTS: EaM increased TBF to 153.8 ml/100 g/min after 3 days and to 153.9 ml/100 g/min after 10 days of treatment, compared with 94.0 ml/100 g/min in untreated controls. Cerebral blood flow did not change after EaM treatment. NNM increased TBF but also showed a tendency to increase cerebral blood flow. E2 increased TBF, whereas cerebral blood flow was unchanged. EaM resulted in a rapid reduction in tumor weight from 230 mg in untreated animals to 146 mg after 3 days of treatment. EaM induced an early transient fragmentation of deoxyribonucleic acid in glioma but not in the normal brain. Neither NNM nor E2 affected tumor weight.CONCLUSION: EaM increases TBF in the BT4C rat glioma model with a concomitant rapid antitumoral effect. The increase in TBF could partially be induced by an estrogen-like action of EaM, but the rapid cytotoxic effect of the drug is obviously attributed to the intact EaM compound. This cytotoxic effect might be attributable to the induction of programmed cell death.
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5.
  • Eriksson, Björn, et al. (författare)
  • Establishment and characterization of a mouse strain (TLL) that spontaneously develops T-cell lymphomas/leukemia
  • 1999
  • Ingår i: Experimental Hematology. - 0301-472X .- 1873-2399. ; 27:4, s. 682-688
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study, a mouse strain (TLL) that spontaneously develops T-cell lymphomas/leukemia with an early onset and high incidence was established and characterized. All tumors analyzed were found to express the alpha,beta T-cell receptor, and the majority of them had a mature, CD3+CD4+CD8- immunophenotype. In a few cases, tumors with a more immature CD3+CD4+CD8+ phenotype were isolated. Expanded phenotyping using a broad panel of lymphocyte differentiation markers confirmed the mature T-cell phenotype of the tumors. Histologic and cell cycle analysis of the tumors revealed an aggressive lymphoblastic malignancy with a very high proliferation rate and widespread engagement of bone marrow and lymphoid as well as nonlymphoid organs. Thus, the TLL mouse strain represents a unique model for the analysis of the oncogenesis and progression of mature T-cell tumors and for the development of therapeutic measures to combat such tumors.
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6.
  • Yeung, Moorix Mo-Wai (författare)
  • Specific and nonspecific immune mechanisms in human gut : a comparative study of normal and ulcerative colitis intestine
  • 1996
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The intestine, with its large mucosal surface area, digests and absorbs food nutrients and maintains a beneficial microbial flora in the colon. Local protective immune responses against intestinal pathogens ensure the survival of the individual. These immune reactions are both specific and non-specific in nature. The intestinal epithelium is single-layered and constantly renewed with differentiating epithelial cells moving from the crypt to the luminal surface. Intraepithelial lymphocytes (IEL) are interspersed between the epithelial cells. Ulcerative colitis (UC) is a life-threatening chronic inflammation affecting colon.In this study three molecules belonging to the carcinoembryonic antigen (CEA) family, namely CEA proper, nonspecific cross-reacting antigen 50/90 (NCA 50/90) and biliary glycoprotein (BGP), were found to be specifically localized to the apical surface of colonic epithelial cells. Full expression of these molecules occurs when the cells reach the upper 1/3 of the crypts and are maintained on the mature cells at the luminal surface. Ultrastructurally, CEA, NCA50/90 and BGP are localized to microvesicles and microfilaments of the fuzzy coat/glycocalyx as well as to the microvilli of the epithelial cells. Their unique localization and documented bacterial binding capacities suggest that they have a role in innate immunity.Functional analysis of IEL in normal jejunum, ileum and colon revealed that IEL are in vivo activated T-lymphocytes expressing mRNA for the cytokines IL-1β, IL-2, IL-8, IFNγ and TNFα and that jejunal IEL have T-cell receptor (TCR)/CD3 dependent cytolytic capacity. As many as 10% of IEL actively produce IFNγ. CD4+TCRαβ+IEL, CD8+TCRαβ+IEL and CD4-CD8-TCRαβ+IEL all had a TH1/cytotoxic cytokine profile. IEL could be further stimulated in vitro to express IL-10, TNFβ and TGFβ1, to proliferate and to secrete IFNγ. Thus, active protection and/or regulation of the epithelium via cell-mediated immune reactions are prominent in the gut.UC colon was characterized by a marked lymphocyte infiltration in the lamina propria, 10-50 times the normal level. Most lymphocytes were present in follicle-like cell aggregates containing both T- and B-cells. An unexpected finding was that γδT-cells constituted about 15% of the cells in the aggregates. Such cells are only found intraepithelially in normal gut. γδT-cells of both the intestinal- (TCR-Vδ1/Vγ8) and blood type (TCR-Vδ2/Vγ9) were seen. T-cells in UC colon were activated but nonproliferating and had a down-regulated TCR/CD3 complex. RT-PCR and quantitative immunohistochemistry for cytokine mRNA (n=11) and protein respectively, revealed that the T-cells in UC colon did not produce IL-2, in marked contrast to T-cells in normal colon and to ileal T-cells from UC patients. This was a selective defect since TNFα, IFNγ, IL-1β, IL-8 and TGFβ1 were similarly expressed in normal colon. No TH2 cytokines were seen. Lamina propria leukocytes in UC colon expressed IL-6, a cytokine not found in normal colon. The epithelial cells of UC colon were activated expressing MHC class II antigens, heat shock proteins and the co-stimulatory molecule B7.1/CD80.Our study demonstrates that UC is an immunological disease. The immunopathological picture seen in UC colon probably reflects an inappropriate down-regulation of local immune responses perhaps due to a selective loss of the key cytokine IL-2 in a situation of extreme antigenic stress.
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7.
  • Grönberg, Henrik, 1961- (författare)
  • Prostate cancer : epidemiological studies
  • 1995
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Prostate cancer is a large and increasing medical problem both in Sweden and in the rest of the developed world, with about 300.000 new cases diagnosed world wide annually. Despite the high incidence of this disease, little is known about the aetiology of prostate cancer. The aim of this study was to try to understand more about the natural history and to find possible a etiological risk factors for this tumour.In a population based study of prostate cancer cases in northern Sweden it was found that the large increase in prostate cancer during the last two decades was mainly caused by well (Gl) and moderately (G2) differentiated tumours. However, the incidence of poorly differentiated (G3) tumours remained unchanged. The introduction of new diagnostic methods is the most plausible explanation for the increase of these low grade tumours.The relative survival in prostate cancer was found to be independent of patient age at diagnosis, indicating that tumour proliferation and the aggressiveness of this disease is equal in all ages. However, due to the increasing occurrence of concurrent diseases with growing age the number of lost years caused by prostate cancer decreases dramatically in older age groups. The overall cause specific mortality for prostate cancer was found to be around 50%. In accordance with most other cancer tumours, the annual mortality rate decreased with longer survival also for prostate cancer patients.In a study from the Swedish Twin Register it was found that the proband concordance rates for prostate cancer were 4,5 time greater among monozygotic compared to dizygotic twins. In a large nation-wide cohort study of men who had a father with prostate cancer, the overall standardised incidence ratio (SIR) was 1.70 for prostate cancer. Younger age at diagnosis among the fathers were associated with an increased risk among sons. This cohort study and the twin study indicates that both inherited and familial factors are of importance in a subgroup of prostate cancer patients.In a prospective case-control study, both a high body mass index (BMI) and a high food intake were found to be independent risk factors for prostate cancer. Both BMI and a high food intake might be indicators of a high fat diet, which so far is the most consistent exogenous risk factor for prostate cancer. The use of tobacco or alcoholic beverages were not associated with prostate cancer risk.
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8.
  • Lenner, Per, et al. (författare)
  • Excess Mortality from Breast Cancer in Relation to Mammograpy Screening in Northern Sweden
  • 1997
  • Ingår i: Journal of Medical Screening. - : Sage Publications. - 0969-1413 .- 1475-5793. ; 4:1, s. 6-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives—Previous randomised studies of mammography screening have shown a significant effect on breast cancer mortality, particularly in women aged 50–Q69 at randomisation. Breast cancer mortality has traditionally been studied by judgments on causes of death, either from cause of death registers or from medical records. In this study an alternative method was used, estimating the excess mortality associated with breast cancer.Setting—In 1990 two counties of northern Sweden started population based mammography screening of women aged 40–74. The unscreened population in the two other counties of the same region were selected as controls.Results—Excess mortality associated with breast cancer was lower in the screened population, and was discernible three to four years after the start of screening. The relative risk estimate, based on the cumulative excess number of deaths from breast cancer during 1990–95 in the screened versus the control population aged 40–74 (at diagnosis of breast cancer), was 0.72 (95% confidence interval (CI) 0.53 to 0.99). For women aged 50–69 it was 0.67 (95% CI 0.46 to 0.99). In the 50–69 age group the estimated excess number of deaths from breast cancer during 1995 was 17.0 per 100 000 women (95% CI 5.0 to 29.0) in the screened counties and 51.1 per 100 000 (95% CI 30.2 to 71.9) in the unscreened counties.Conclusions—Population based routine screening has substantial effects on breast cancer mortality in women aged 50–69. Estimation of excess mortality can be used in future studies to evaluate the effects of mammography screening on breast cancer mortality.
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9.
  • Schildt, Elsy-Britt, 1955- (författare)
  • Etiology of oral cancer
  • 1998
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)
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10.
  • Franck-Lissbrant, I, et al. (författare)
  • Testosterone stimulates angiogenesis and vascular regrowth in the ventral prostate in castrated adult rats.
  • 1998
  • Ingår i: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 139:2, s. 451-6
  • Tidskriftsartikel (refereegranskat)abstract
    • The castration-induced regression and testosterone stimulated regrowth of the vasculature in the rat ventral prostate lobe were studied using stereological techniques. Seven days after castration, the endothelial cell proliferation rate (bromodeoxyuridine labeling index); the total weights of blood vessel walls, blood vessel lumina, endothelial cells, glandular epithelial cells; and total organ weight were all decreased. Within 2 days after sc treatment with testosterone, the total weights of blood vessel walls, endothelial cells, and vascular lumina, as well as the endothelial cell proliferation rate, were all normalized. In contrast to the rapid response of the vasculature, the total weight of glandular epithelium and total organ weight were not normalized during the 4 days of testosterone treatment. Growth of the vasculature apparently precedes growth of the glandular epithelium. The testosterone- dependent factors stimulating the vasculature are unknown, but factors derived from epithelial cells, mast cells (which accumulate in the prostate during the first day of testosterone treatment), and tissue macrophages could all be involved. Castration-induced regression and testosterone-stimulated regrowth of the prostatic vasculature can be used as an experimental model to study factors regulating angiogenesis and organ growth in the prostate.
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