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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) srt2:(2010-2014);srt2:(2010);lar1:(umu)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) > (2010-2014) > (2010) > Umeå universitet

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1.
  • Lövgren, Malin, et al. (författare)
  • Clock time and embodied time experienced by patients with inoperable lung cancer
  • 2010
  • Ingår i: Cancer Nursing. - Philadelphia : Lippincott Williams & Wilkins. - 0162-220X .- 1538-9804. ; 14, s. S45-S45
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study, we explore how patients with inoperable lung cancer (LC) discuss their experiences of time, based on content analysis of open interviews with 35 patients 1 year after diagnosis, using Davies' distinction between "clock time" and "embodied time" as sensitizing concepts. Two interrelated themes were derived: (1) aspects related to the healthcare system, with 3 subthemes: waiting times in the healthcare system, limited time for patient-professional contact, and limited time for coordination of services, and (2) existential aspects, with subthemes: the future with LC and managing an uncertain and finite life with LC. Time could be experienced as problematic for these patients, when limited or lacking or through long periods of waiting, especially when these periods occurred without adequate preparation or information. This contributed to exacerbation of these patients' existing sense of uncertainty, their perception of care as impersonal and insecure, and their need to remain alert and act on their own behalf. Awareness of the seriousness of their disease and the prospect of a limited lifetime was described as increasing uncertainty about dying and fear of certain death. People also described efforts to constructively deal with their situation by reprioritizing their remaining time, having increased appreciation of some aspects of daily life, and living consciously in the present. This analysis suggests a collision between clock time, which steers the healthcare system, and embodied time, as experienced by individuals. Greater attention to psychosocial needs is suggested as one means of positively affecting patients' experiences of time and uncertainty.
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2.
  • Antoniou, A. C., et al. (författare)
  • Common breast cancer susceptibility alleles and the risk of breast cancer for BRCA1 and BRCA2 mutation carriers : Implications for risk prediction
  • 2010
  • Ingår i: Cancer Research. - : American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 70:23, s. 9742-9754
  • Tidskriftsartikel (refereegranskat)abstract
    • The known breast cancer susceptibility polymorphisms in FGFR2, TNRC9/TOX3, MAP3K1, LSP1, and 2q35 confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. We evaluated the associations of 3 additional single nucleotide polymorphisms (SNPs), rs4973768 in SLC4A7/NEK10, rs6504950 in STXBP4/COX11, and rs10941679 at 5p12, and reanalyzed the previous associations using additional carriers in a sample of 12,525 BRCA1 and 7,409 BRCA2 carriers. Additionally, we investigated potential interactions between SNPs and assessed the implications for risk prediction. The minor alleles of rs4973768 and rs10941679 were associated with increased breast cancer risk for BRCA2 carriers (per-allele HR = 1.10, 95% CI: 1.03-1.18, P = 0.006 and HR = 1.09, 95% CI: 1.01-1.19, P = 0.03, respectively). Neither SNP was associated with breast cancer risk for BRCA1 carriers, and rs6504950 was not associated with breast cancer for either BRCA1 or BRCA2 carriers. Of the 9 polymorphisms investigated, 7 were associated with breast cancer for BRCA2 carriers (FGFR2, TOX3, MAP3K1, LSP1, 2q35, SLC4A7, 5p12, P = 7 × 10-11 - 0.03), but only TOX3 and 2q35 were associated with the risk for BRCA1 carriers (P = 0.0049, 0.03, respectively). All risk-associated polymorphisms appear to interact multiplicatively on breast cancer risk for mutation carriers. Based on the joint genotype distribution of the 7 risk-associated SNPs in BRCA2 mutation carriers, the 5% of BRCA2 carriers at highest risk (i.e., between 95th and 100th percentiles) were predicted to have a probability between 80% and 96% of developing breast cancer by age 80, compared with 42% to 50% for the 5% of carriers at lowest risk. Our findings indicated that these risk differences might be sufficient to influence the clinical management of mutation carriers.
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3.
  • Ehrsson, Ylva Tiblom, et al. (författare)
  • Explorative study on the predictive value of systematic inflammatory and metabolic markers on weight loss in head and neck cancer patients undergoing radiotherapy
  • 2010
  • Ingår i: Supportive Care in Cancer. - : Springer Science and Business Media LLC. - 0941-4355 .- 1433-7339. ; 18:11, s. 1385-1391
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose This study aimed to explore the predictive value of systematic inflammatory and metabolic markers in head and neck (H&N) cancer patients during radiotherapy (RT). Methods Twenty-seven patients were evaluated. The protocol included serial blood tests [highly sensitive C-reactive protein (hsCRP), albumin, insulin-like growth factor 1 (IGF-1), IGF binding protein 1 (IGFBP-1) and ghrelin], measurements of body weight and assessment of oral mucositis. Results The mean nadir of weight loss was observed at the end of RT. At the time of diagnosis, mean hsCRP was 5.2 +/- 1.0 mg/L. HsCRP significantly increased during RT and decreased during the post-RT period. Mean maximum hsCRP was 35.8 +/- 8.5 mg/L, with seven patients reaching >40 mg/L. A numerical decrease of albumin (by 18.2%) and only small changes in IGF-1, IGFBP-1 and ghrelin levels were observed. None of the metabolic parameters was significantly associated with weight loss. Conclusions HsCRP increased in response to RT for H&N cancer as a sign of irradiation-induced inflammation. Weight loss was not preceded by changes of the metabolic parameters, indicating that assessment of the blood markers used in this study is of little value. Regular body weight measurement and assessment of oral mucositis are feasible, cheap and important procedures to control the metabolic homeostasis during RT.
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4.
  • Försti, Asta, et al. (författare)
  • Polymorphisms in the transforming growth factor beta 1 pathway in relation to colorectal cancer progression
  • 2010
  • Ingår i: Genes, Chromosomes and Cancer. - New York : Liss. - 1045-2257 .- 1098-2264. ; 49:3, s. 270-281
  • Tidskriftsartikel (refereegranskat)abstract
    • Transforming growth factor beta1 (TGFB1) acts as a growth inhibitor of normal colonic epithelial cells, however, as a tumor promoter of colorectal cancer (CRC) cells. To explore the association between genetic polymorphisms in the TGFB1 pathway and CRC susceptibility and clinical outcome, we carried out a case-control study on a Swedish population of 308 CRC cases and 585 age- and gender-matched controls. The cases were sampled prospectively and had up to 16 years follow-up, making the study material particularly suitable for survival analysis. On the basis of their reported or predicted functional effect, nine single-nucleotide polymorphisms (TGFB1: Leu10Pro; TGFBR1: 9A/6A and IVS7G+24A; FURIN: C-229T; THBS1: T+42C; LTBP1L: C-256G; LTBP4: T-893G and Thr750Ala; BAMBI: T-779A) were selected for genotyping. We evaluated the associations between genotypes and CRC and Dukes' stage. Survival probabilities were compared between different subgroups. The observed statistically significant associations included a decreased CRC risk for TGFBR1 IVS7G+24A minor allele carriers (odds ratio (OR): 0.72, 95% confidence interval (CI): 0.53-0.97), less aggressive tumors with Dukes' stage A+B for carriers of LTBP4 Thr750Ala and BAMBI T-779A minor alleles (OR: 0.58, 95%CI: 0.36-0.93 and OR: 0.51, 95%CI: 0.29-0.89, respectively) and worse survival for FURIN C-229T heterozygotes (hazard ratio: 1.63, 95%CI: 1.08-2.46). As this is the first study about the influence of the polymorphisms in the TGFB1 pathway on CRC progression, further studies in large independent cohorts are warranted.
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5.
  • Hayat Roshanai, Afsaneh, et al. (författare)
  • Disclosing cancer genetic information within families : perspectives of counselees and their at-risk relatives
  • 2010
  • Ingår i: Familial Cancer. - : Springer Science and Business Media LLC. - 1389-9600 .- 1573-7292. ; 9:4, s. 669-679
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: The aim of the present descriptive study was to investigate the experience of sharing genetic information among cancer genetic counselees and their at-risk relatives. Methods: In total, 147 cancer genetic counselees and 81 of their at-risk relatives answered to a study specific questionnaire and/or were interviewed. Counselees' communication of genetic information to at-risk relatives was assessed with regard to who they informed, how they felt, and how they perceived their relatives' reactions. In addition, at-risk relatives' experiences of receiving genetic information were studied. Results: Most of the counselees had shared the genetic information received at the counseling session personally with their at-risk relatives. The majority of the counselees (68%) reported positive or neutral feelings about sharing the genetic information with their relatives while 9% stated negative feelings. Counselees mostly interpreted the relatives' reactions to the information as positive or neutral (62% of responses), and in few cases as negative (14% of responses). About half of relatives reported positive or neutral reactions (54%) to the received information, while about one-fifth reported negative reactions (22%). Nevertheless, most relatives were satisfied with the received information and half of the relatives intended to seek genetic counseling themselves. Conclusion: Sharing genetic information to at-risk relatives appears to be accomplished without any major difficulties or negative feelings. However, more assistance may be needed to optimize the communication of the genetic information within at-risk families.
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6.
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7.
  • Nilsson, Lena Maria, 1965-, et al. (författare)
  • Consumption of filtered and boiled coffee and the risk of incident cancer : a prospective cohort study
  • 2010
  • Ingår i: Cancer Causes and Control. - : Springer Netherlands. - 0957-5243 .- 1573-7225. ; 21:10, s. 1533-1544
  • Tidskriftsartikel (refereegranskat)abstract
    • Background  Despite potentially relevant chemical differences between filtered and boiled coffee, this study is the first to investigate consumption in relation to the risk of incident cancer.Methods  Subjects were from the Västerbotten Intervention Project (64,603 participants, including 3,034 cases), with up to 15 years of follow-up. Hazard ratios (HR) were calculated by multivariate Cox regression.Results  No associations were found for all cancer sites combined, or for prostate or colorectal cancer. For breast cancer, boiled coffee ≥4 versus <1 occasions/day was associated with a reduced risk (HR = 0.52, CI = 0.30–0.88, p trend = 0.247). An increased risk of premenopausal and a reduced risk of postmenopausal breast cancer were found for both total (HRpremenopausal = 1.69, CI = 0.96–2.98, p trend = 0.015, HRpostmenopausal = 0.60, CI = 0.39–0.93, p trend = 0.006) and filtered coffee (HRpremenopausal = 1.76, CI = 1.04–3.00, p trend = 0.045, HRpostmenopausal = 0.52, CI = 0.30–0.88, p trend = 0.045). Boiled coffee was positively associated with the risk of respiratory tract cancer (HR = 1.81, CI = 1.06–3.08, p trend = 0.084), a finding limited to men. Main results for less common cancer types included total coffee in renal cell cancer (HR = 0.30, CI = 0.11–0.79, p trend = 0.009) and boiled coffee in pancreas cancer (HR = 2.51 CI = 1.15–5.50, p trend = 0.006).Conclusion  These findings demonstrate, for the first time, the potential relevance of brewing method in investigations of coffee consumption and cancer risk, but they must be confirmed in future studies.
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8.
  • Högberg, Thomas, et al. (författare)
  • Sequential adjuvant chemotherapy and radiotherapy in endometrial cancer-Results from two randomised studies.
  • 2010
  • Ingår i: European Journal of Cancer. - : Elsevier. - 0959-8049 .- 1879-0852. ; 46:13, s. 2422-2431
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: Endometrial cancer patients with high grade tumours, deep myometrial invasion or advanced stage disease have a poor prognosis. Randomised studies have demonstrated the prevention of loco-regional relapses with radiotherapy (RT) with no effect on overall survival (OS). The possible additive effect of chemotherapy (CT) remains unclear. Two randomised clinical trials (NSGO-EC-9501/EORTC-55991 and MaNGO ILIADE-III) were undertaken to clarify if sequential combination of chemotherapy and radiotherapy improves progression-free survival (PFS) in high-risk endometrial cancer. The two studies were pooled. METHODS: Patients (n=540; 534 evaluable) with operated endometrial cancer International Federation of Obstetrics and Gynaecology (FIGO) stage I-III with no residual tumour and prognostic factors implying high-risk were randomly allocated to adjuvant radiotherapy with or without sequential chemotherapy. RESULTS: In the NSGO/EORTC study, the combined modality treatment was associated with 36% reduction in the risk for relapse or death (hazard ratio (HR) 0.64, 95%confidence interval (CI) 0.41-0.99; P=0.04); two-sided tests were used. The result from the Gynaecologic Oncology group at the Mario Negri Institute (MaNGO)-study pointed in the same direction (HR 0.61), but was not significant. In the combined analysis, the estimate of risk for relapse or death was similar but with narrower confidence limits (HR 0.63, CI 0.44-0.89; P=0.009). Neither study showed significant differences in the overall survival. In the combined analysis, overall survival approached statistical significance (HR 0.69, CI 0.46-1.03; P=0.07) and cancer-specific survival (CSS) was significant (HR 0.55, CI 0.35-0.88; P=0.01). CONCLUSION: Addition of adjuvant chemotherapy to radiation improves progression-free survival in operated endometrial cancer patients with no residual tumour and a high-risk profile. A remaining question for future studies is if addition of radiotherapy to chemotherapy improves the results.
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9.
  • Hemmingsson, Oskar, 1975-, et al. (författare)
  • ASNA-1 activity modulates sensitivity to cisplatin
  • 2010
  • Ingår i: Cancer Research. - : American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 70:24, s. 10321-10328
  • Tidskriftsartikel (refereegranskat)abstract
    • Cancer can be cured by platinum based chemotherapy but resistance is a major cause of treatment failure. Here we present the nematode Caenorhabditis elegans as a model to study interactions between the platinum drug cisplatin and signaling pathways in vivo. Null mutations in a single gene, asna-1, makes worms hypersensitive to cisplatin. The metalloregulated ATPase ASNA-1 promotes insulin secretion and membrane insertion of tail-anchored proteins. Using structural data from ASNA-1 homologs, we identify specific ASNA-1 mutants that are sensitive to cisplatin while still able to promote insulin signaling. Mutational analysis reveals that hypersensitivity of ASNA-1 mutants to cisplatin remains in absence of CEP-1/p53 or apoptosis. Human ASNA1 can substitute for the worm gene, indicating a conserved function. Cisplatin sensitivity is not affected by decreased insulin signaling in wild type nematodes or restored insulin signaling in asna-1 mutants. These findings provide a functional insight into ASNA-1, demonstrate that C. elegans can be used to characterize cisplatin resistance mechanisms and propose that rationally designed drugs against ASNA-1 can sensitize cancer cells to cisplatin.
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10.
  • Johansson, Ann-Sofie, et al. (författare)
  • Fish oil delays lymphoma progression in the TLL mouse
  • 2010
  • Ingår i: Leukemia and Lymphoma. - : Informa UK Limited. - 1042-8194 .- 1029-2403. ; 51:11, s. 2092-2097
  • Tidskriftsartikel (refereegranskat)abstract
    • The objective was to investigate the effects of omega-3 fatty acids, known for their anti-inflammatory effects, on time to lymphoma progression and survival in the TLL mouse, a strain genetically prone to developing aggressive T-cell lymphoma. Compared to mice fed a standard diet, TLL mice fed omega-3 (menhaden fish oil) experienced a significant delay in disease progression and were more likely to remain alive and symptom free during the first 8 months of the study. In contrast, omega-6 supplementation (corn oil) did not significantly affect lymphoma progression. Irrespective of diet, all mice eventually progressed, and 1-year survival was not different between the groups. Immunological analysis demonstrated a significantly altered B-cell compartment and fewer NK cells in healthy C57Black6 mice fed omega-3, compared to controls. In conclusion, a diet rich in omega-3 fatty acids delays lymphoma development in the TLL mouse possibly by mechanisms that include complex effects on immune function.
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