L C Andersson

University of Helsinki, Helsinki, Uusimaa, Finland

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Publications (328)1676.89 Total impact

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    ABSTRACT: Effects of triclosan (5-chloro-2′-(2,4-dichlorophenoxy)phenol) on mammalian cells were investigated using human peripheral blood mono nuclear cells (PBMC), keratinocytes (HaCaT), porcine spermatozoa and kidney tubular epithelial cells (PK-15), murine pancreatic islets (MIN-6) and neuroblastoma cells (MNA) as targets. We show that triclosan (1–10 μg ml−1) depolarised the mitochondria, upshifted the rate of glucose consumption in PMBC, HaCaT, PK-15 and MNA, and subsequently induced metabolic acidosis. Triclosan induced a regression of insulin producing pancreatic islets into tiny pycnotic cells and necrotic death. Short exposure to low concentrations of triclosan (30 min, ≤ 1 μg/ml) paralysed the high amplitude tail beating and progressive motility of spermatozoa, within 30 min exposure, depolarized the spermatozoan mitochondria and hyperpolarised the acrosome region of the sperm head and the flagellar fibrous sheath (distal part of the flagellum). Experiments with isolated rat liver mitochondria showed that triclosan impaired oxidative phosphorylation, downshifted ATP synthesis, uncoupled respiration and provoked excessive oxygen uptake. These exposure concentrations are 100 - 1000 fold lower that those permitted in consumer goods. The mitochondriotoxic mechanism of triclosan differs from that of valinomycin, cereulide and the enniatins by not involving potassium ionophoric activity.
    Toxicology Reports 04/2015; 46. DOI:10.1016/j.toxrep.2015.03.012
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    ABSTRACT: Amylosin, a heat-stable channel-forming non-ribosomally synthesized peptide toxin produced by strains of Bacillus amyloliquefaciens isolated from moisture-damaged buildings, is shown in this paper to have immunotoxic and cytotoxic effects on human cells as well as antagonistic effects on microbes. Human macrophages exposed to 50 ng of amylosin ml(-1) secreted high levels of cytokines IL-1β and IL-18 within two hours, indicating activation of the NLRP3 inflammasome, an integral part of the innate immune system. At the same exposure level, expression of IL-1β and IL-18 mRNA increased. Amylosin caused dose-dependent potassium ion efflux from all tested mammalian cells (human monocytes and keratinocytes and porcine sperm cells) at 1 to 2 μM exposure. Amylosin also inhibited the motility of porcine sperm cells and depolarized the mitochondria of human keratinocytes. Amylosin may thus trigger the activation of the NLRP3 inflammasome and subsequently cytokine release by causing potassium efflux from the exposed cells. The results of this study indicate that exposure to amylosin activates the innate immune system which could offer an explanation for the inflammatory symptoms experienced by occupants of moisture-damaged buildings. In addition, the amylosin-producing B. amyloliquefaciens inhibited the growth of both prokaryotic and eukaryotic indoor microbes and purified amylosin also had an antimicrobial effect. These antimicrobial effects could make amylosin-producers dominant and therefore significant causal agents of health problems in some moisture-damaged sites. Copyright © 2015, American Society for Microbiology. All Rights Reserved.
    Applied and Environmental Microbiology 02/2015; 81(8). DOI:10.1128/AEM.03430-14 · 3.95 Impact Factor
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    ABSTRACT: We investigated statistical association between gingival inflammation and cancer in a group of patients followed up for 26 years with the hypothesis that gingival inflammation affects carcinogenesis. Altogether, 1676 30- to 40-year-old subjects from Stockholm were clinically examined in 1985. In 2011, we compared the baseline oral examination and follow-up data with cancer diagnoses sourced from the Swedish national hospital register databases. Of 1676 individuals, 89 (55 women, 34 men) had got cancer by the year 2011. Women were found to be at higher risk for cancer than men. Smoking (expressed in pack-years) had been more prevalent in the cancer group than in those with no cancer diagnosis. Gingival index, marker of gingival inflammation, was higher in the cancer group than in subjects with no cancer. There were no significant differences between the groups regarding age, education, dental plaque and calculus index scores, or in the number of missing teeth. In multiple logistic regression analysis with cancer as the dependent variable and several independent variables, pack-years of smoking appeared to be a principal independent predictor with odds ratio (OR) 1.32 while gingival inflammation showed OR 1.29. Hence, our present findings showed that together with smoking, gingival inflammation indeed associated with the incidence of cancer in this cohort. © 2014 The Author(s) Published by the Royal Society. All rights reserved.
    Philosophical Transactions of The Royal Society B Biological Sciences 02/2015; 370(1661). DOI:10.1098/rstb.2014.0041 · 6.31 Impact Factor
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    ABSTRACT: Colorectal cancer (CRC) is one of the world's three most common cancers and its incidence is rising. To identify patients who benefit from adjuvant therapy requires novel biomarkers. The regenerating islet-derived gene (REG) 4 belongs to a group of small secretory proteins involved in cell proliferation and regeneration. Its up-regulated expression occurs in inflammatory bowel diseases also in gastrointestinal cancers. Reports on the association of REG4 expression with CRC prognosis have been mixed. Our aim was to investigate tumor REG4 expression in CRC patients and its coexpression with other intestinal markers.
    PLoS ONE 10/2014; 9(10):e109600. DOI:10.1371/journal.pone.0109600 · 3.53 Impact Factor
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    ABSTRACT: Objectives: The current treatment for celiac disease is strict gluten-free diet. Technical processing may render gluten-containing foods safe for consumption by celiac patients, but so far in vivo safety testing can only be performed on patients. We modified a celiac disease mouse model to test antigenicity and inflammatory effects of germinated rye sourdough, a food product characterized by extensive prolamin hydrolysis. Methods: Lymphopenic Rag1-/- or nude mice were injected with splenic CD4+CD62L-CD44high memory T cells from gliadin- or secalin-immunized wildtype donor mice. Results: 1) Rag1-/- recipients challenged with wheat or rye gluten lost more body weight and developed more severe histological duodenitis than mice on gluten-free diet. This correlated with increased secretion of IFNγ, IL-2 and IL-17 by secalin-restimulated splenocytes. 2) In vitro gluten testing using competitive R5 ELISA demonstrated extensive degradation of the gluten R5 epitope in germinated rye sourdough. 3) However, in nude recipients challenged with germinated rye sourdough (vs. native rye sourdough), serum anti-secalin IgG/Th1-associated IgG2c titers were only reduced, but not eliminated. In addition, there were no reductions in body weight loss, histological duodenitis or T cell cytokine secretion in Rag1-/- recipients challenged accordingly. Conclusions: 1) Prolamin-primed CD4+CD62L-CD44high memory T cells induce gluten-sensitive enteropathy in Rag1-/- mice. 2) Hydrolysis of secalins in germinated-rye sourdough remains incomplete. Secalin peptides retain B and T cell stimulatory capacity, and remain harmful to the intestinal mucosa in this celiac disease model. 3) Current antibody-based prolamin detection methods may fail to detect antigenic gluten fragments in processed cereal food products.
    AJP Gastrointestinal and Liver Physiology 01/2014; 306(6). DOI:10.1152/ajpgi.00136.2013 · 3.74 Impact Factor
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    ABSTRACT: Background: Infections of teeth are highly prevalent, often leading to tooth extractions. Missing teeth can thus be considered as proxy for chronic dental infections, caries or periodontitis. We followed-up a cohort for 24 years investigating the association between missing teeth and the incidence of cancer with the hypothesis that dental chronic inflammation links to cancer. Methods: WHO ICD-7-9-10 malignant diagnoses were recorded from the Swedish Cancer Registry from 1985 to 2009 in 1 390 individuals who had underwent clinical oral examination in 1985. The subjects appeared periodontally healthy and thus the probable reason for tooth extractions was deep caries. Using Fisher's exact t-test and multiple logistic regression analysis the results were analysed for the association between cancer incidence and baseline oral health parameters and a number of other explanatory factors. Results: Of the 1 390 subjects 71 had got cancer by year 2009. The results of the multiple regression analysis showed that between any type of cancer as a dependent variable, and several independent explanatory variables, missing second molar in the right mandible and age appeared as the principle independent predictors significantly associating with cancer, with an odds ratio (95% confidence interval) of 2.62 (1.18-5.78) and 1.91 (1.06-3.43), respectively. Conclusions: In periodontally healthy subjects extracted molars, proxy for past dental infections, seemed to predict cancer risk in the studied age group - hence supporting a role of chronic dental infection/inflammation in carcinogenesis.
    01/2014; 5(2):79-85. DOI:10.7150/jca.7402
  • Cancer Research 08/2013; 73(8 Supplement):626-626. DOI:10.1158/1538-7445.AM2013-626 · 9.28 Impact Factor
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    ABSTRACT: We investigated statistical association between long-term periodontal disease and cancer in a group of patients followed-up for 24 years with the hypothesis that chronic infection affects carcinogenesis. We made a prospective study of 1676 30-40-year old subjects in Stockholm, clinically examined in 1985. The data were combined with Swedish Cancer Registry in 2009. All cancer types were registered according to WHO International Classification of Diseases. Associations between cancer and dental parameters were studied using multiple logistic regression analysis with background variables and known risk factors for cancer. Age, gender, dental visits, education, income, socioeconomic status, working history, smoking, dental plaque, calculus, gingival bleeding, periodontal disease indicated by extracted or extruded molars were the independent variables. 286 subjects had periodontal disease in 1985. Of these, 18 subjects (6.3%) got cancer by 2009. In women breast cancer dominated (50%) while in men the types of malignancies were scattered. Logistic regression analysis showed that if a subject had periodontitis with extruded/extracted first molar tooth (d. 46) of the mandible in 1985, the risk of cancer increased with odds ratio (OR) 8.43, if the second molar (d. 47) was missing, OR for cancer was 6.11. To conclude chronic periodontal disease indicated by extracted or extruded molars associated statistically with elevated incidence of cancer.
    International Journal of Cancer Research 04/2013; 47:2051-784.
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    ABSTRACT: We induced upregulation of stanniocalcin-1 (STC-1) by various mild and long lasting stresses and assayed its influence on mitochondrial membrane potential (MMP) in the neural crest-derived cell line Paju. The obtained data showed that starvation (24-96h), exposure to 10nM TPA, and low concentrations (0.05-1μM) of As2O3 significantly (3-5 times) upregulated Paju cell STC-1 RNA and stabilized the mitochondrial membrane potential (MMP). However, high concentrations of As2O3 (2.5-5.0μM) increased intracellular ROS and free calcium levels and, consequently, suppressed STC-1 and MMP. The results show that cells preconditioned by various mild stresses expressed more STC-1 and their MMP were more resistant to a secondary exposure to As2O3 (2.5-5μM, 96h) demonstrating mitohormesis. We suggest that MMP deviation from control levels, to an extent innocuous to cell viability, is a general signal for STC-1-induction and MMP-protection. Our findings of Paju cell MMP-regulation may be of great importance for inventing new ways to prevent neurodegenerative diseases and unravel the mechanisms behind drug resistance.
    Journal of the neurological sciences 04/2013; DOI:10.1016/j.jns.2013.03.011 · 2.26 Impact Factor
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    ABSTRACT: Bacillus cereus, aseptically isolated from potato tubers, were screened for cereulide production and for toxicity on human and other mammalian cells. The cereulide producing isolates grew slowly, the colonies remained small (∼1 mm), tested negative for starch hydrolysis, and varied in productivity from 1 to 100 ng of cereulide mg(-1) wet wt (∼ 0.01 to 1 ng per 10(5) CFU). By DNA-fingerprint analysis the isolates matched B. cereus F5881/94, connected to human foodborne illness, but were distinct from cereulide producing endophytes of spruce tree (Picea abies). Exposure to cell extracts (1 to 10 μg bacterial biomass ml(-1)) and to purified cereulide ( 0.4 to 7 ng ml(-1)) from the potato isolates caused mitochondrial depolarization (loss of ΔΨm) in human peripheral blood mononuclear cells (PBMC) and keratinocytes (HaCaT), porcine spermatozoa and kidney tubular epithelial cells (PK-15), murine fibroblasts (L-929) and pancreatic insulin producing cells (MIN-6). Cereulide (10 - 20 ng ml(-1)) exposed pancreatic islets (MIN-6) disintegrated into small pyknotic cells followed by necrotic death. Necrotic death in other test cells was observed only after 2 logs higher exposure. Exposure to 30 - 60 ng ml(-1) of cereulide induced K(+) translocation in intact, live PBMC, keratinocytes and sperm cells within seconds of exposure, depleting 2 to 10% of the cellular K(+) stores in 10 minutes. The ability of cereulide to transfer K(+) ions across biological membranes may benefit the producer bacterium in K(+) deficient environments such as extracellular spaces inside plant tissue, but is a pathogenic trait when in contact with mammalian cells.
    Applied and Environmental Microbiology 03/2013; DOI:10.1128/AEM.00201-13 · 3.95 Impact Factor
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    ABSTRACT: Objectives: Bacteria may play a role in oncogenesis (Chang & Parsonnet, Clin Microbiol Rev 2010;23:837). Infections of teeth are highly prevalent, often leading to tooth extractions. Missing teeth can thus be considered as proxy for chronic dental infections. We followed-up a cohort for 24 years investigating the association between missing teeth and the incidence of cancer with the hypothesis that chronic inflammation links with cancer (Meurman & Bascones-Martinez, Oral Dis 2011;17:779). Methods: WHO ICD-7-9-10 malignant diagnoses were recorded from the Swedish Cancer Registry from 1985 to 2009 in a cohort of 1390 individuals who had underwent clinical oral examination in 1985. The subjects appeared periodontally healthy and thus the probable reason for tooth extractions was deep caries. Using Fisher’s exact t-test and multiple logistic regression analysis the results were analysed for the association between cancer incidence and baseline oral health, and a number of explanatory factors such as age, gender, socio-economic status, smoking, and oral health parameters. Results: Of the 1390 subjects 71 had got cancer by the year 2009. The results of the multiple regression analysis showed that between any type of cancer as a dependent variable, and several independent explanatory variables, second molar in the right mandible (OR 2.62) and age (OR 1.91) appeared as the principle independent predictors significantly associating with cancer (p = 0.017 and p= 0.031, respectively). Conclusions: A missing molar in the mandible, proxy for long lasting dental infection, seemed to predict cancer risk – hence supporting the role of chronic inflammation in carcinogenesis.
    IADR/AADR/CADR General Session and Exhibition 2013; 03/2013
  • Kukka Heiskala, Leif C Andersson
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    ABSTRACT: Reg IV is a 17kD secreted C-type lectin physiologically found in selected enteroendocrine cells (EEC). It is thought be involved in the regulation of normal and pathological intestinal and/or neuroendocrine differentiation and proliferation but its ultimate functional role(s) is still unclear. We used immunostaining and compared the cellular expression of Reg IV with a panel of neuroendocrine markers in human GI-tract tissue samples. Reg IV showed cellular co-distribution with serotonin and chromogranin A in all parts of GI-tract. Co-localization of Reg IV with somatostatin was seen in colon and with substance P in ileum. Subpopulations of cells expressing Reg IV overlapped with EECs containing GLP-1, GLP-2, secretin, PYY, and ghrelin, depending on the anatomical localization of the samples. The results further underscore the high degree of diversity among EECs and suggest that Reg IV may be involved in the finetuning of functions exerted by the neuroendocrine cells in the GI-tract.
    Regulatory Peptides 03/2013; DOI:10.1016/j.regpep.2013.03.007 · 2.01 Impact Factor
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    ABSTRACT: Breast cancer can recur even decades after the primary therapy. Markers are needed to predict cancer progression and the risk of late recurrence. The estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor-2 (HER2), proliferation marker Ki-67, and cytokeratin CK5 were studied to find out whether their expression or occurrence in subgroups of breast cancers correlated with the time of recurrence. The expression of HER2, ER, PR, Ki-67, and CK5 was studied by IHC in 72 primary breast cancers and their corresponding recurrent/metastatic lesions. The patients were divided into three groups according to the time of the recurrence/metastasis: before two years, after 5 years, and after 10 years. Based on their IHC profiles, the tumors were divided into surrogates of the genetically defined subgroups of breast cancers and the subtype definitions were as follows: luminal A (ER or PR+HER2-), luminal B (ER or PR+HER2+), HER2 overexpressing (ER-PR-HER2+), triple-negative (ER-PR-HER2-), basal-like (ER-PR-HER2-CK5+), non-classified (ER-PR-HER2-CK5-) and luminobasal (ER or PR+CK5+). In multivariate analysis, tumor size and HER2 positivity were a significant risk of early cancer relapse. The metastases showed a significantly lower CK5 expression. CK5 positivity distinguished triple negative tumors into rapidly and slowly recurring cancers. The IHC subtype ER or PR+HER2- luminal A presented a significantly lower risk of early tumor recurrence. Ki-67 expression denoted early-relapsing tumors and correlated linearly with tumor progression, since Ki-67 positivity declined gradually from early-relapsing toward late-recurring cancers.
    Breast cancer 01/2013; 7:23-34. DOI:10.4137/BCBCR.S10701
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    ABSTRACT: Stanniocalcin 1 (STC1), originally described as an antihypercalcemic hormone in fish, is highly expressed in differentiated mammalian neurons. Mild hypoxic treatment and focal cerebral ischemia induce upregulation of STC1 in the brain. These findings prompted us to investigate whether STC1 contributes to neuroprotection after ischemia and whether STC1 is required for development of ischemic tolerance. We induced 60 minutes of temporary middle cerebral artery occlusion in wild type (WT) and STC1-deficient mice (STC1(-/-)) with or without prior hypoxic preconditioning (HPC, 8% oxygen for 6 hours followed by reoxygenation for 24 hours). Infarct sizes, neurological scores, and Stc1, Stc2, and Il-6 mRNA brain levels were measured 24 hours after ischemia. Additionally, we examined blood-brain barrier (BBB) integrity (Evans Blue fluorescence) under normal conditions and 0 and 24 hours after hypoxia. STC1(-/-) and WT mice developed brain infarcts of similar size. In both strains, HPC triggered ischemic tolerance with similar reduction in infarct size. However, STC1(-/-) mice had worse neurological scores in both scenarios. HPC induced upregulation of STC1 and STC2 in WT mice and of STC2 in STC1(-/-) mice. Ischemic STC1(-/-) mice showed significantly lower Il-6 mRNA expression than ischemic WT mice. Evans Blue fluorescence levels showed no difference in between WT and STC1(-/-) mice under evaluated conditions, thus BBB integrity is preserved despite STC1 deficiency. STC1 was not crucial for the development of ischemic tolerance triggered by HPC or for preserving BBB integrity but may be involved in functional recovery after stroke.
    Neuroscience 11/2012; 229. DOI:10.1016/j.neuroscience.2012.10.062 · 3.33 Impact Factor
  • B. SDER, M. YAKOB, J.H. MEURMAN, L.C. ANDERSSON, P. SDER
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    ABSTRACT: Objectives: To study whether the amount of dental plaque, which indicates poor oral hygiene and is potential source of oral infections, associates with premature death in the chronic infection – carcinogenesis paradigm. Methods: In a prospective cohort study, 1390 randomly selected healthy young Swedes followed up from 1985 to 2009. All subjects underwent oral clinical examination and answered a questionnaire assessing background variables such as socio-economic status and smoking. Causes of death recorded from national statistics and classified according to the WHO International Classification of Diseases. Unpaired t-test, chi-square tests, and multiple logistic regressions were used. Results: Of the 1390 participants, 4.2% had died during follow-up. Women had died at a mean age of 61.0 (±2.6 SD) years and men at the age of 60.2 (±2.9 SD) years. The amount of dental plaque (PLI) between those who had died was 0.91 ± (0.61SD) versus survived 0.70 ± (0.48SD) was statistically significant (p<0.001). In multiple logistic regression analysis, dental plaque appeared a significant independent predictor associated with 1.79 times the odds ratio (OR) of death (p<0.05). Age increased the risk by OR 1.98 (p<0.05) and gender (male) by OR 1.91 (p<0.05). The malignancies were more widely scattered in men, whilst breast cancer was the most frequent cause of death in women. Conclusions: Our study hypothesis was confirmed by showing that poor oral hygiene, as reflected in the amount of dental plaque, appeared to pose an increased cancer-mortality risk.
    PER/IADR Congress 2012; 09/2012
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    ABSTRACT: Prostate and seminal vesicle are two similar hormone responsive human organs that differ dramatically in their cancer incidence. DNA damage response (DDR) is required for maintenance of genomic integrity. In this study we investigated the DDR and cell cycle checkpoint activation of these organs using orthotopic cultures of human surgery-derived tissues and primary cultures of isolated prostate and seminal vesicle cells. We find that the activation of ATM signaling pathway by ionizing radiation (IR) was comparable in both tissues. Previously, we have shown that the prostate secretory cells express low levels of histone variant H2AX and phosphorylated H2AX (γH2AX) after IR. Here we demonstrate that H2AX levels are low also in the secretory seminal vesicle cells suggesting that this is a common phenotype of postmitotic cells. We consequently established primary epithelial cell cultures from both organs to compare their DDR. Interestingly, contrary to human prostate epithelial cells (HPEC), primary seminal vesicle epithelial cells (HSVEC) displayed effective cell cycle checkpoints after IR and expressed higher levels of Wee1A checkpoint kinase. Furthermore, HSVEC but not HPEC cells were able to activate p53 and to induce p21 cell cycle inhibitor. Our results show that during replication, the checkpoint enforcement is more proficient in the seminal vesicle than in the prostate epithelium cells. This indicates a more stringent enforcement of DDR in replicating seminal vesicle epithelial cells, and suggests that epithelial regeneration combined with sub-optimal checkpoint responses may contribute to high frequency of genetic lesions in the prostate epithelium.
    The Prostate 07/2012; 72(10):1060-70. DOI:10.1002/pros.21509 · 3.57 Impact Factor
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    ABSTRACT: Bmx (Bone marrow kinase in chromosome X), also known as Etk, is a member of the Tec family of nonreceptor tyrosine kinases. Bmx is expressed mainly in arterial endothelia and in myeloid hematopoietic cells. Bmx regulates ischemia-mediated arteriogenesis and lymphangiogenesis, but its role in tumor angiogenesis is not known. In this study, we characterized the function of Bmx in tumor growth using both Bmx knockout and transgenic mice. Isogenic colon, lung, and melanoma tumor xenotransplants showed reductions in growth and tumor angiogenesis in Bmx gene-deleted ((-/-)) mice, whereas developmental angiogenesis was not affected. In addition, growth of transgenic pancreatic islet carcinomas and intestinal adenomas was also slower in Bmx(-/-) mice. Knockout mice showed high levels of Bmx expression in endothelial cells of tumor-associated and peritumoral arteries. Moreover, endothelial cells lacking Bmx showed impaired phosphorylation of extracellular signal-regulated kinase (Erk) upon VEGF stimulation, indicating that Bmx contributes to the transduction of vascular endothelial growth factor signals. In transgenic mice overexpressing Bmx in epidermal keratinocytes, tumors induced by a two-stage chemical skin carcinogenesis treatment showed increased growth and angiogenesis. Our findings therefore indicate that Bmx activity contributes to tumor angiogenesis and growth.
    Cancer Research 05/2012; 72(14):3512-21. DOI:10.1158/0008-5472.CAN-11-1070 · 9.28 Impact Factor
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    ABSTRACT: To study whether the amount of dental plaque, which indicates poor oral hygiene and is potential source of oral infections, associates with premature death from cancer. Prospective cohort study. 1390 randomly selected healthy young Swedes followed up from 1985 to 2009. All subjects underwent oral clinical examination and answered a questionnaire assessing background variables such as socioeconomic status and smoking. Causes of death were recorded from national statistics and classified according to the WHO International Classification of Diseases. Unpaired t test, χ(2) tests and multiple logistic regressions were used. Of the 1390 participants, 4.2% had died during the follow-up. Women had died at a mean age of 61.0 (±2.6 SD) years and men at the age of 60.2 (±2.9 SD) years. The amount of dental plaque between those who had died versus survived was statistically significant (p<0.001). In multiple logistic regression analysis, dental plaque appeared to be a significant independent predictor associated with 1.79 times the OR of death (p<0.05). Age increased the risk with an OR of 1.98 (p<0.05) and gender (men) with an OR of 1.91 (p<0.05). The malignancies were more widely scattered in men, while breast cancer was the most frequent cause of death in women. This study hypothesis was confirmed by showing that poor oral hygiene, as reflected in the amount of dental plaque, was associated with increased cancer mortality.
    BMJ Open 05/2012; 2(3). DOI:10.1136/bmjopen-2012-001083 · 2.06 Impact Factor
  • Ji Jiang, Johan A Westberg, Leif C Andersson
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    ABSTRACT: Stanniocalcin 2 (STC2) is a homolog of stanniocalcin 1, a 56kD glycoprotein hormone that originally was found to confer calcitonin-like activity in fish. Human STC2 is expressed in various tissues such as kidney, spleen, heart, and pancreas. STC2 has been demonstrated to be induced by different kinds of stress and display cytoprotective activity, but the molecular mechanism is poorly understood. Heme oxygenase 1 (HO1) degrades heme to biliverdin, carbon monoxide and free iron, and is a stress-responsive protein. Using yeast two-hybrid screening we identified HO1 as a binding partner of STC2. The interaction was validated by in vivo co-immunoprecipitation and immunofluorescence. The binding site for HO1 was located to amino acids 181-200 of STC2. We also found that STC2 binds hemin via a consensus heme regulatory motif. Moreover, STC2 expression was induced by heat shock in HEK293 cells. Taken together, our findings point to three novel functions of STC2, and suggest that STC2 interacts with HO1 to form a eukaryotic 'stressosome' involved in the degradation of heme.
    Biochemical and Biophysical Research Communications 04/2012; 421(2):274-9. DOI:10.1016/j.bbrc.2012.03.151 · 2.28 Impact Factor

Publication Stats

10k Citations
1,676.89 Total Impact Points

Institutions

  • 1972–2015
    • University of Helsinki
      • • Department of Pathology
      • • Department of Psychiatry
      • • Department of Medical Genetics
      • • Department of Neurology
      • • Transplantation Laboratory
      • • Department of Bacteriology and Immunology
      Helsinki, Uusimaa, Finland
  • 1973–2010
    • Helsinki University Central Hospital
      • • Department of Pathology
      • • Department of Oncology
      • • Department of Obstetrics and Gynaecology
      • • Department of Medicine
      • • Department of Surgery
      Helsinki, Uusimaa, Finland
  • 2004
    • Institute of Theoretical and Experimental Biophysics
      Pushchino-na-Oke, Moskovskaya, Russia
  • 1998
    • Armed Forces Institute of Pathology
      Ralalpindi, Punjab, Pakistan
  • 1996
    • Karolinska University Hospital
      Tukholma, Stockholm, Sweden
  • 1995
    • The University of Tokyo
      • Division of Internal Medicine
      Tokyo, Tokyo-to, Japan
  • 1991
    • Åbo Akademi University
      Turku, Province of Western Finland, Finland
  • 1987
    • University of Oulu
      • Department of Surgery
      Uleoborg, Northern Ostrobothnia, Finland
    • University of Kuopio
      Kuopio, Eastern Finland Province, Finland
  • 1981
    • Uppsala University
      Uppsala, Uppsala, Sweden