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421.
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422.
  • Pastor, Susana, et al. (författare)
  • Levels of DNA damage (Micronuclei) in patients suffering from chronic kidney disease. Role of GST polymorphisms
  • 2018
  • Ingår i: Mutation Research - Genetic Toxicology and Environmental Mutagenesis. - Elsevier. - 1383-5718. ; 836, s. 41-46
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic kidney disease (CKD) patients are characterized by the presence of high levels of DNA damage, and a poor response to ionizing radiation. In this study, we proposed that variants in GST genes could explain this fact. One-hundred twenty seven CKD patients and one-hundred forty five controls constituted the studied groups. Micronuclei (MN) frequency was determined in peripheral blood lymphocytes at both basal level, and after challenging the cells with 0.5 Gy of ionizing radiation. The following polymorphisms: GSTP1 (rs749174), GSTO1 (rs2164624), and GSTO2 (rs156697) were evaluated in the two groups. Results indicate that gene variants were distributed differentially between CKD patients and controls. Although GSTO1 and GSTO2 variants were associated with lower levels of MN, this was observed in both CKD patients and controls. When net MN values were determined after irradiation, GSTO1 and GSTO2 variants were also associated with lower MN-frequencies. On the contrary, individuals with the GSTP1 variant showed higher values of induced MN. In conclusion, we have demonstrate that the selected GST polymorphism play a role in the incidence of CKD, and affects the levels of MN. Interestingly, the modulating effects observed on both, the basal and induced levels of DNA damage, are characteristic of the overall population, not only of the CKD patients.
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423.
  • Pearce, Neil E, et al. (författare)
  • IARC Monographs 40 Years of Evaluating Carcinogenic Hazards to Humans
  • 2015
  • Ingår i: Journal of Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 123:6, s. 507-514
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: Recently the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also the approach used to perform these evaluations. Some critics have claimed that IARC Working Groups' failures to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans.</p><p>OBJECTIVES: The authors of this paper are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We have examined here criticisms of the IARC classification process to determine the validity of these concerns. We review the history of IARC evaluations and describe how the IARC evaluations are performed.</p><p>DISCUSSION: We conclude that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various discipline and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.</p><p>CONCLUSIONS<strong>:</strong> The IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.</p>
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424.
  • Pertesi, Maroulio, et al. (författare)
  • Genetic predisposition for multiple myeloma
  • ????
  • Ingår i: Leukemia. - Nature Publishing Group. - 0887-6924.
  • Forskningsöversikt (refereegranskat)abstract
    • Multiple myeloma (MM) is the second most common blood malignancy. Epidemiological family studies going back to the 1920s have provided evidence for familial aggregation, suggesting a subset of cases have an inherited genetic background. Recently, studies aimed at explaining this phenomenon have begun to provide direct evidence for genetic predisposition to MM. Genome-wide association studies have identified common risk alleles at 24 independent loci. Sequencing studies of familial cases and kindreds have begun to identify promising candidate genes where variants with strong effects on MM risk might reside. Finally, functional studies are starting to give insight into how identified risk alleles promote the development of MM. Here, we review recent findings in MM predisposition field, and highlight open questions and future directions.
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425.
  • Prasad, Rashmi B, et al. (författare)
  • Verification of the susceptibility loci on 7p12.2, 10q21.2, and 14q11.2 in precursor B-cell acute lymphoblastic leukemia of childhood
  • 2010
  • Ingår i: Blood. - American Society of Hematology. - 1528-0020. ; 115:9, s. 7-1765
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent genome-wide association data have implicated genetic variation at 7p12.2 (IKZF1), 10q21.2 (ARIDB5), and 14q11.2 (CEBPE) in the etiology of B-cell childhood acute lymphoblastic leukemia (ALL). To verify and further examine the relationship between these variants and ALL risk, we genotyped 1384 cases of precursor B-cell childhood ALL and 1877 controls from Germany and the United Kingdom. The combined data provided statistically significant support for an association between genotype at each of these loci and ALL risk; odds ratios (OR), 1.69 (P = 7.51 x10(-22)), 1.80 (P = 5.90 x 10(-28)), and 1.27 (P = 4.90 x 10(-6)), respectively. Furthermore, the risk of ALL increases with an increasing numbers of variant alleles for the 3 loci (OR(per-allele) = 1.53, 95% confidence interval, 1.44-1.62; P(trend) = 3.49 x 10(-42)), consistent with a polygenic model of disease susceptibility. These data provide unambiguous evidence for the role of these variants in defining ALL risk underscoring approximately 64% of cases.
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426.
  • Rachakonda, P. Sivaramakrishna, et al. (författare)
  • Somatic Mutations in Exocrine Pancreatic Tumors: Association with Patient Survival
  • 2013
  • Ingår i: PLoS ONE. - Public Library of Science. - 1932-6203. ; 8:4
  • Tidskriftsartikel (refereegranskat)abstract
    • KRAS mutations are major factors involved in initiation and maintenance of pancreatic tumors. The impact of different mutations on patient survival has not been clearly defined. We screened tumors from 171 pancreatic cancer patients for mutations in KRAS and CDKN2A genes. Mutations in KRAS were detected in 134 tumors, with 131 in codon 12 and only 3 in codon 61. The GGT>GAT (G12D) was the most frequent mutation and was present in 60% (80/134). Deletions and mutations in CDKN2A were detected in 43 tumors. Analysis showed that KRAS mutations were associated with reduced patient survival in both malignant exocrine and ductal adenocarcinomas (PDAC). Patients with PDACs that had KRAS mutations showed a median survival of 17 months compared to 30 months for those without mutations (log-rank P = 0.07) with a multivariate hazard ratio (HR) of 2.19 (95% CI 1.09-4.42). The patients with G12D mutation showed a median survival of 16 months (log-rank-test P = 0.03) and an associated multivariate HR 2.42 (95% CI 1.14-2.67). Although, the association of survival in PDAC patients with CDKN2A aberrations in tumors was not statistically significant, the sub-group of patients with concomitant KRAS mutations and CDKN2A alterations in tumors were associated with a median survival of 13.5 months compared to 22 months without mutation (log-rank-test P = 0.02) and a corresponding HR of 3.07 (95% CI 1.33-7.10). Our results are indicative of an association between mutational status and survival in PDAC patients, which if confirmed in subsequent studies can have potential clinical application.
427.
  • Rasche, Leo, et al. (författare)
  • Low expression of hexokinase-2 is associated with false-negative FDG–positron emission tomography in multiple myeloma
  • 2017
  • Ingår i: Blood. - American Society of Hematology. - 0006-4971. ; 130:1, s. 30-34
  • Tidskriftsartikel (refereegranskat)abstract
    • 18F-Fluorodeoxyglucose (FDG)–positron emission tomography (PET) and diffusion-weighted magnetic resonance imaging with background signal suppression (DWIBS) are 2 powerful functional imaging modalities in the evaluation of malignant plasma cell (PC) disease multiple myeloma (MM). Preliminary observations have suggested that MM patients with extensive disease according to DWIBS may be reported as being disease-free on FDG-PET (“PET false-negative”). The aim of this study was to describe the proportion of PET false-negativity in a representative set of 227 newly diagnosed MM patients with simultaneous assessment of FDG-PET and DWIBS, and to identify tumor-intrinsic features associated with this pattern. We found the incidence of PET false-negativity to be 11%. Neither tumor load–associated parameters, such as degree of bone marrow PC infiltration, nor the PC proliferation rate were associated with this subset. However, the gene coding for hexokinase-2, which catalyzes the first step of glycolysis, was significantly lower expressed in PET false-negative cases (5.3-fold change, P < .001) which provides a mechanistic explanation for this feature. In conclusion, we demonstrate a relevant number of patients with FDG-PET false-negative MM and a strong association between hexokinase-2 expression and this negativity: a finding which may also be relevant for clinical imaging of other hematological cancers.
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428.
  • Riihimaeki, M., et al. (författare)
  • Death causes in breast cancer patients
  • 2012
  • Ingår i: Annals of Oncology. - Oxford University Press. - 1569-8041. ; 23:3, s. 604-604
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Due to improved outcomes in breast cancer (BCa), the proportion of affected women dying of other causes has increased. Thus, a better survival of BCa requires knowledge of other causes of death. Materials and methods: Data on the population, cancers, and causes of death were gathered from the nationwide Swedish Family-Cancer Database, enrolling similar to 3.68 million Swedish women. A Cox regression model, comparing BCa patients against all other women, was applied. Cause-of-death-specific hazard ratios (HRs) were calculated for both underlying and multiple causes of death. Results: Among 641 000 deaths from 1987 to 2006, 48 000 were BCa patients. For underlying causes except BCa, the highest cause-specific HRs were found for diseases of pulmonary circulation {1.51 [95% confidence interval (CI) 1.36-1.68]}, suicide [1.39 (1.19-1.63)], and heart failure [1.29 (1.22-1.37)]. For specific multiple causes, the highest ratios were found for external causes [1.86 (1.80-1.91)] and gastrointestinal disease [1.68 (1.62-1.74)]. Conclusions: Diagnosis of BCa is associated with increased risks of dying of various causes, including external causes, heart failure, diseases of pulmonary circulation, and gastrointestinal disease. The study fulfills the gap in knowledge of death causes in BCa patients and suggests to draw more attention to comorbidities.
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429.
  • Riihimaeki, Matias, et al. (författare)
  • What Do Prostate Cancer Patients Die Of?
  • 2011
  • Ingår i: Oncologist. - AlphaMed Press. - 1083-7159. ; 16:2, s. 175-181
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. A recent rise in the incidence of prostate cancer and a more favorable outcome have increased the proportions of other causes of death in affected men. Extending the survival of prostate cancer patients thus requires knowledge of all causes of death. Methods. Data on the population, cancers, and causes of death were gathered from the nationwide Swedish Family-Cancer Database. A Cox regression model, comparing prostate cancer patients with all other men, was applied. Hazard ratios (HR) were calculated both for the underlying cause and for dying with a specific cause listed among multiple causes of death. Findings. Among 686,500 observed deaths, 62,500 were prostate cancer patients. For underlying causes other than prostate cancer, the highest cause-specific HRs were found for external causes (HR, 1.24; 95% confidence interval [CI], 1.16-1.31), diseases of the pulmonary circulation (HR, 1.22; 95% CI, 1.09-1.37), and heart failure (HR, 1.18; 95% CI, 1.11-1.24). For specific multiple causes, the highest HRs were found for anemia (HR, 2.28; 95% CI, 2.14-2.42), diseases of the pulmonary circulation (HR, 1.61; 95% CI, 1.55-1.68), and urinary system disease (HR, 1.90; 95% CI, 1.84-1.96). Interpretations. Prostate cancer patients have a higher risk for dying from various causes other than prostate cancer, including external causes and heart failure. Mechanisms have been proposed linking these elevated risks to both cancer and treatment. More attention should be paid to comorbidities in men with prostate cancer. The present study fulfills a gap in the knowledge of death causes in prostate cancer patients. The Oncologist 2011; 16: 175-181
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430.
  • Riihimäki, Matias, et al. (författare)
  • Clinical landscape of cancer metastases
  • 2018
  • Ingår i: Cancer Medicine. - Wiley-Blackwell. - 2045-7634. ; 7:11, s. 5534-5542
  • Tidskriftsartikel (refereegranskat)abstract
    • Population-based data on metastatic patterns are lacking because cancer registries seldom record metastases. This study uses a novel population-based approach to identify metastases and describes metastatic pathways from 14 common primary cancers to 12 specific metastatic sites. A total of 179 581 patients with metastatic cancer were identified from the Swedish Cancer Registry and metastatic sites were identified using the Cause of Death Register and the National Patient Register. Patterns of metastatic spread were described across age and sex. In men, colorectal cancer was the main source of lung, peritoneal, and liver metastases. Lung cancer was the main origin of pleural and nervous system metastases. Prostate cancer dominated bone metastases but had minor contribution to other metastatic sites. Among women, breast cancer was the dominant origin of most metastatic sites, with the exception of peritoneum which was ruled by metastases from the ovary. As other exceptions, for nervous system metastases, lung cancer was the origin of metastases somewhat more frequently than breast cancer and for liver metastases, colorectal cancer was the main origin instead of breast cancer. The present achievement was to implement the first nationwide description of clinical landscape of cancer metastases, with an aim to serve as a reliable source for clinicians and researchers.
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