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  • 1. Balassiano, Karen
    et al.
    Lima, Sheila
    Jenab, Mazda
    Overvad, Kim
    Tjonneland, Anne
    Boutron-Ruault, Marie Christine
    Clavel-Chapelon, Francoise
    Canzian, Federico
    Kaaks, Rudolf
    Boeing, Heiner
    Meidtner, Karina
    Trichopoulou, Antonia
    Laglou, Pagona
    Vineis, Paolo
    Panico, Salvatore
    Palli, Domenico
    Grioni, Sara
    Tumino, Rosario
    Lund, Eiliv
    Bueno-de-Mesquita, H. Bas
    Numans, Mattjis E.
    Peeters, Petra H. M.
    Ramon Quiros, J.
    Sanchez, Maria-Jose
    Navarro, Carmen
    Ardanaz, Eva
    Dorronsoro, Miren
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Stenling, Roger
    Umeå University, Faculty of Medicine, Department of Medical Biosciences.
    Ehrnstrom, Roy
    Regner, Sara
    Allen, Naomi E.
    Travis, Ruth C.
    Khaw, Kay-Tee
    Offerhaus, G. Johan A.
    Sala, Nuria
    Riboli, Elio
    Hainaut, Pierre
    Scoazec, Jean-Yves
    Sylla, Bakary S.
    Gonzalez, Carlos A.
    Herceg, Zdenko
    Aberrant DNA methylation of cancer-associated genes in gastric cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST)2011In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 311, no 1, p. 85-95Article in journal (Refereed)
    Abstract [en]

    Epigenetic events have emerged as key mechanisms in the regulation of critical biological processes and in the development of a wide variety of human malignancies, including gastric cancer (GC), however precise gene targets of aberrant DNA methylation in GC remain largely unknown. Here, we have combined pyrosequencing-based quantitative analysis of DNA methylation in 98 GC cases and 64 controls nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort and in cancer tissue and non-tumorigenic adjacent tissue of an independent series of GC samples. A panel of 10 cancer-associated genes (CHRNA3, DOK1, MGMT, RASSF1A, p14ARF, CDH1, MLH1, ALDH2, GNMT and MTHFR) and LINE-1 repetitive elements were included in the analysis and their association with clinicopathological characteristics (sex, age at diagnosis, anatomical sub-site, histological sub-type) was examined. Three out of the 10 genes analyzed exhibited a marked hypermethylation, whereas two genes (ALDH2 and MTHFR) showed significant hypomethylation, in gastric tumors. Among differentially methylated genes, we identified new genes (CHRNA3 and DOK1) as targets of aberrant hypermethylation in GC, suggesting that epigenetic deregulation of these genes and their corresponding cellular pathways may promote the development and progression of GC. We also found that global demethylation of tumor cell genomes occurs in GC, consistent with the notion that abnormal hypermethylation of specific genes occurs concomitantly with genome-wide hypomethylation. Age and gender had no significant influence on methylation states, but an association was observed between LINE-1 and MLH1 methylation levels with histological subtype and anatomical sub-site. This study identifies aberrant methylation patters in specific genes in GC thus providing information that could be exploited as novel biomarkers in clinics and molecular epidemiology of GC.

  • 2. Bethke, Lara
    et al.
    Sullivan, Kate
    Webb, Emily
    Murray, Anne
    Schoemaker, Minouk
    Auvinen, Anssi
    Kiuru, Anne
    Salminen, Tiina
    Johansen, Christoffer
    Collatz Christensen, Helle
    Muir, Kenneth
    McKinney, Patricia
    Hepworth, Sarah
    Dimitropoulou, Polyxeni
    Lophatananon, Artitaya
    Feychting, Maria
    Lönn, Stefan
    Ahlbom, Anders
    Malmer, Beatrice
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Henriksson, Roger
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Swerdlow, Anthony
    Houlston, Richard
    CASP8 D302H and meningioma risk: an analysis of five case-control series2009In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 273, no 2, p. 312-315Article in journal (Refereed)
    Abstract [en]

    Caspase 8 (CASP8) is a key regulator of apoptosis or programmed cell death, and hence a defence against cancer. The CASP8 polymorphism D302H has recently been shown to influence the risk of breast cancer. We tested the hypothesis that the CASP8 polymorphism D302H may influence risk of meningioma through analysis of five independent series of case patients and controls (n=631 and 637, respectively). Carrier status for 302H was not associated with a statistically significantly increased risk (OR=1.16; 95% CI: 0.87-1.53; P=0.31) making it unlikely that this variant contributes to the inherited risk of meningioma.

  • 3.
    Gu, Xiaolian
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Coates, Philip J
    Boldrup, Linda
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Nylander, Karin
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    p63 contributes to cell invasion and migration in squamous cell carcinoma of the head and neck2008In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 263, no 1, p. 26-34Article in journal (Refereed)
  • 4.
    Johansson, David
    et al.
    Umeå University, Faculty of Medicine, Medical Biosciences, Clinical chemistry.
    Johansson, Anders
    Umeå University, Faculty of Medicine, Odontology.
    Behnam-Motlagh, Parviz
    Umeå University, Faculty of Medicine, Medical Biosciences, Clinical chemistry.
    alpha-Toxin of Staphylococcus aureus overcomes acquired cisplatin-resistance in malignant mesothelioma cells.2008In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 265, no 1, p. 67-75Article in journal (Refereed)
    Abstract [en]

    alpha-Toxin (alpha-hemolysin) of Staphylococcus aureus is a pore-forming bacterial toxin which after caveolin-1-dependent assembly induces apoptosis in eukaryotic cells. We investigated if a sub-toxic concentration of staphylococcal alpha-toxin could enhance cisplatin-induced apoptosis and overcome acquired cisplatin-resistance in cultured malignant pleural mesothelioma (MPM) cells. MPM cells (P31wt) and a cisplatin-resistant sub-line (P31res) was incubated with alpha-toxin and/or cisplatin followed by determination of cell viability, apoptosis, and signaling pathways. P31res cells were more sensitive to alpha-toxin than P31 wt cells due to induction of apoptosis. A low-toxic concentration of alpha-toxin re-sensitized cisplatin P31res cytotoxicity by apoptosis-induced through the mitochondrial pathway without detectable activation of common up-stream apoptosis signaling proteins. The toxin/drug combination should be tested for cisplatin-resistant mesothelioma treatment.

  • 5. Lohr, Miriam
    et al.
    Edlund, Karolina
    Botling, Johan
    Hammad, Seddik
    Hellwig, Birte
    Othman, Amnah
    Berglund, Anders
    Lambe, Mats
    Holmberg, Lars
    Ekman, Simon
    Bergqvist, Michael
    Pontén, Fredrik
    Cadenas, Cristina
    Marchan, Rosemarie
    Hengstler, Jan G
    Rahnenführer, Jörg
    Micke, Patrick
    The prognostic relevance of tumour-infiltrating plasma cells and immunoglobulin kappa C indicates an important role of the humoral immune response in non-small cell lung cancer.2013In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 333, no 2Article in journal (Refereed)
    Abstract [en]

    A prognostic impact of immunoglobulin kappa C (IGKC) expression has been described in cancer. We analysed the influence of B-cell and plasma cell markers, as well as IGKC expression, in non-small lung cancer (NSCLC) using immunohistochemistry on a tissue microarray. IGKC protein expression was independently associated with longer survival, with particular impact in the adenocarcinoma subgroup. Moreover, a correlation was seen with CD138+ cells, but not with CD20. CD138 expression revealed a comparable association with survival. In conclusion, IGKC expression in stroma-infiltrating plasma cells is a prognostic marker in NSCLC, supporting emerging treatment concepts that exploit the humoral immune response.

  • 6. Søreide, Kjetil
    et al.
    Sund, Malin
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Epidemiological-molecular evidence of metabolic reprogramming on proliferation, autophagy and cell signaling in pancreas cancer2015In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 356, no 2, p. 281-288Article in journal (Refereed)
    Abstract [en]

    Pancreatic cancer remains one of the deadliest human cancers with little progress made in survival over the past decades, and 5-year survival usually below 5%. Despite this dismal scenario, progresses have been made in understanding of the underlying tumor biology through among other definition of precursor lesions, delineation of molecular pathways, and advances in genome-wide technology. Further, exploring the relationship between epidemiological risk factors involving metabolic features to that of an altered cancer metabolism may provide the foundation for new therapies. Here we explore how nutrients and caloric intake may influence the KRAS-driven ductal carcinogenesis through mediators of metabolic stress, including autophagy in presence of TP53, advanced glycation end products (AGE) and the receptors (RAGE) and ligands (HMGB1), as well as glutamine pathways, among others. Effective understanding the cancer metabolism mechanisms in pancreatic cancer may propose new ways of prevention and treatment.

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