Database : MEDLINE
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[PMID]: 29486982
[Au] Autor:Zahedi H; Djalalinia S; Sadeghi O; Asayesh H; Noroozi M; Gorabi AM; Mohammadi R; Qorbani M
[Ad] Address:Department of Clinical Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Title:Dietary Inflammatory Potential Score and Risk of Breast Cancer: Systematic Review and Meta-analysis.
[So] Source:Clin Breast Cancer;, 2018 Feb 07.
[Is] ISSN:1938-0666
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Several studies have been conducted on the relationship between dietary inflammatory potential (DIP) and breast cancer. However, the findings are conflicting. This systematic review and meta-analysis summarizes the findings on the association between DIP and the risk of breast cancer. We used relevant keywords and searched online international electronic databases, including PubMed and NLM Gateway (for Medline), Institute for Scientific Information (ISI), and Scopus for articles published through February 2017. All cross-sectional, case-control, and cohort studies were included in this meta-analysis. Meta-analysis was performed using the random effects meta-analysis method to address heterogeneity among studies. Findings were analyzed statistically. Nine studies were included in the present systematic review and meta-analysis. The total sample size of these studies was 296,102, and the number of participants varied from 1453 to 122,788. The random effects meta-analysis showed a positive and significant association between DIP and the risk of breast cancer (pooled odds ratio, 1.14; 95% confidence interval, 1.01-1.27). The pooled effect size was not statistically significant because of the type of studies, including cohort (pooled relative risk, 1.04; 95% confidence interval, 0.98-1.10) and case-control (pooled odds ratio, 1.63; 95% confidence interval, 0.89-2.37) studies. We found a significant and positive association between higher DIP score and risk of breast cancer. Modifying inflammatory characteristics of diet can substantially reduce the risk of breast cancer.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

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[PMID]: 28453756
[Au] Autor:Hovde Ø; Høivik ML; Henriksen M; Solberg IC; Småstuen MC; Moum BA
[Ad] Address:Department of Gastroenterology, Innlandet Hospital Trust, Gjøvik, Norway.
[Ti] Title:Malignancies in Patients with Inflammatory Bowel Disease: Results from 20 Years of Follow-up in the IBSEN Study.
[So] Source:J Crohns Colitis;11(5):571-577, 2017 May 01.
[Is] ISSN:1876-4479
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background and Aims: Whether patients with inflammatory bowel diseases [IBDs] have increased risk of developing cancer has been debated. The aims of the study were to determine the prevalence of intestinal/extraintestinal cancers in an IBD cohort 20 years after diagnosis and to assess whether these patients had an increased cancer-specific risk compared with a matched control population. Methods: Patients with ulcerative colitis [UC] and Crohn's disease [CD] diagnosed 1990-1993 have been prospectively followed up for 20 years. Follow-up visits were carried out 1, 5, 10, and 20 years after inclusion. Data on all cancer cases, deaths, and causes of death were collected from the Cancer Registry of Norway and from the Norwegian Cause of Death Registry. Results: In all, 756 patients [519 UC and 237 CD] were diagnosed with IBD. Increased risk of cancer was seen in UC patients (hazard ratio [HR] = 1.40, 95% confidence interval [CI] 1.08-1.81, p < 0.01), but not in CD patients [HR = 1.23, 95% CI 0.80-2.03, p = 0.30]. Stratified by gender, our data revealed a statistically increased risk for all cancers only in male UC patients compared with the controls [HR = 1.51, 95% CI 1.08-2.11, p = 0.017]. In both groups breast cancer was seen more often than expected. Conclusions: Male UC patients display an increased risk of development of colorectal cancer and, also all cancers combined, compared with the controls. In both UC and CD, standardized incidence ratio for breast cancer was increased.
[Mh] MeSH terms primary: Inflammatory Bowel Diseases/complications
Intestinal Neoplasms/epidemiology
Neoplasms/epidemiology
[Mh] MeSH terms secundary: Adolescent
Adult
Aged
Aged, 80 and over
Cause of Death
Child
Child, Preschool
Colitis, Ulcerative/complications
Crohn Disease/complications
Female
Follow-Up Studies
Humans
Intestinal Neoplasms/etiology
Male
Middle Aged
Neoplasms/etiology
Neoplasms/mortality
Norway/epidemiology
Registries
Risk Factors
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw193

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[PMID]: 29510614
[Au] Autor:Lee M; Song IH; Heo SH; Kim YA; Park IA; Bang WS; Park HS; Gong G; Lee HJ
[Ad] Address:Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
[Ti] Title:Expression of Immunoproteasome Subunit LMP7 in Breast Cancer and Its Association with Immune-Related Markers.
[So] Source:Cancer Res Treat;, 2018 Feb 26.
[Is] ISSN:2005-9256
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Purpose: In the presence of interferon, proteasome subunits are replaced by their inducible counterparts to form an immunoproteasome (IP) plays a key role in generation of antigenic peptides presented by MHC class I molecules, leading to elicitation of a T cell‒mediated immune response. Although the roles of IP in other cancers, and inflammatory diseases have been extensively studied, its significance in breast cancer is unclear. Materials and Methods: We investigated the expression of LMP7, an IP subunit, and its relationship with immune system components in two breast cancer cohorts. Results: In 668 consecutive breast cancer cohort, 40% of tumors showed high level of LMP7 expression, and tumors with high expression of LMP7 had more tumor-infiltrating lymphocytes (TILs) in each subtype of breast cancer. In another cohort of 681 triple-negative breast cancer patients cohort, the expression of LMP7 in tumor cells was significantly correlated with the amount of TILs and the expression of interferon-associated molecules (MxA [p < 0.001] and PKR [p < 0.001]), endoplasmic reticulum stress-associated molecules (PERK [p=0.012], p-eIF2a [p=0.001], and XBP1 [p < 0.001]), and damage-associated molecular patterns (HMGN1 [p < 0.001] and HMGB1 [p < 0.001]). Patients with higher LMP7 expression had better disease-free survival outcomes than those with no or low expression in the positive lymph node metastasis group (p=0.041). Conclusion: Close association between the TIL levels and LMP7 expression in breast cancer indicates that better antigen presentation through greater LMP7 expression might be associated with more TILs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.4143/crt.2017.500

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[PMID]: 28464803
[Au] Autor:Mu J; Zhu D; Shen Z; Ning S; Liu Y; Chen J; Li Y; Li Z
[Ad] Address:Department of Nutrition and Food Hygiene, The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, 211100, China.
[Ti] Title:The repressive effect of miR-148a on Wnt/ß-catenin signaling involved in Glabridin-induced anti-angiogenesis in human breast cancer cells.
[So] Source:BMC Cancer;17(1):307, 2017 May 02.
[Is] ISSN:1471-2407
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Glabridin (GLA), a major component extracted from licorice root, has anti-inflammatory and antioxidant activities, but few studies report its mechanism of inhibition of angiogenesis. This study was an extension of our previous work, which demonstrated that GLA suppressed angiogenesis in human breast cancer (MDA-MB-231 and Hs-578T) cells. Breast cancer is one of the most common malignant diseases in females worldwide, and the major cause of mortality is metastasis that is primarily attributed to angiogenesis. Thus, anti-angiogenesis has become a strategy for the treatment of breast cancer. METHODS: Cell viability of different concentration treatment groups were detected by Cell Counting Kit-8 assay. The expression of several related genes in the Wnt1 signaling pathway in MDA-MB-231 and Hs-578T cells treated with GLA were measured at both the transcription and translation levels using quantitative real-time PCR analyses and western blotting. Immunofluorescence assay analyzed the nuclear translocation of ß-catenin. The microRNA-inhibitor was used to knockdown microRNA-148a (miR-148a) expression. Angiogenic potentials of breast cancer cells were analyzed by enzyme-linked immunosorbent assay (ELISA) and tube formation in vitro. RESULTS: GLA attenuated angiogenesis by the suppression of miR-148a-mediated Wnt/ß-catenin signaling pathway in two human breast cancer cell lines (MDA-MB-231 and Hs-578T). GLA also upregulated the expression of miR-148a in a dose-dependent manner, miR-148a, which could directly target Wnt-3'-untranslated regions (UTRs), and decreased the expression of Wnt1, leading to ß-catenin accumulation in the membranes from the cytoplasm and nucleus. Downregulation of miR-148a contributed to the reduction of GLA-induced suppression of the Wnt/ß-catenin signaling pathway, the angiogenesis and vascular endothelial grow factor (VEGF) secretion. CONCLUSIONS: Our study identified a molecular mechanism of the GLA inhibition of angiogenesis through the Wnt/ß-catenin signaling pathway via miR-148a, suggesting that GLA could serve as an adjuvant chemotherapeutic agent for breast cancer.
[Mh] MeSH terms primary: Antineoplastic Agents/pharmacology
Breast Neoplasms/metabolism
Isoflavones/pharmacology
MicroRNAs/genetics
Neovascularization, Pathologic/metabolism
Phenols/pharmacology
Wnt Signaling Pathway/genetics
[Mh] MeSH terms secundary: Cell Line, Tumor
Female
Human Umbilical Vein Endothelial Cells
Humans
MicroRNAs/metabolism
Signal Transduction/genetics
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Isoflavones); 0 (MIRN148 microRNA, human); 0 (MicroRNAs); 0 (Phenols); HOC5567T41 (glabridin)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3298-1

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[PMID]: 28460441
[Au] Autor:Arora J; Sauer SJ; Tarpley M; Vermeulen P; Rypens C; Van Laere S; Williams KP; Devi GR; Dewhirst MW
[Ad] Address:Duke Cancer Institute, Duke University, Durham, NC, USA.
[Ti] Title:Inflammatory breast cancer tumor emboli express high levels of anti-apoptotic proteins: use of a quantitative high content and high-throughput 3D IBC spheroid assay to identify targeting strategies.
[So] Source:Oncotarget;8(16):25848-25863, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Inflammatory breast cancer (IBC) is one of the most lethal breast cancer variants; with existing therapy, 5-yr survival rate is only 35%. Current barriers to successful treatment of IBC include frequent infiltration and the presence of tumor cell clusters, termed tumor emboli, within the breast parenchyma and lymphatics. Prior studies have identified the role of anti-apoptotic signaling, in particular hyperactivation of NFκB and its target genes, in IBC pathobiology and therapeutic resistance. The objectives of this study were to: (1) determine if IBC tumor emboli express anti-apoptotic proteins and (2) develop a high content, multiparametric assay to assess the morphology of the IBC 3D spheroids and to optimize a high throughput format to screen for compounds that can inhibit the formation of the IBC tumor clusters/embolic structures. Immunohistochemical analysis of IBC patient tumor samples with documented tumor emboli revealed high NFκB (p65) staining along with expression of XIAP, a potent anti-apoptotic protein known to interact with NFκB signaling in enhancing survival of malignant cells. Subsequently, the high content assay developed allowed for simultaneous imaging and morphometric analysis, including count and viability of spheroids derived from SUM149, rSUM149 and SUM190 cells and its application to evaluate XIAP and NFκB inhibitory agents. We demonstrate the efficacy of the off-patent drug disulfiram when chelated with copper, which we had previously reported to inhibit NFκB signaling, was highly effective in disrupting both IBC spheroids and emboli grown in vitro. Taken together, these results identify a high-throughput approach to target tumor spheroid formation for drug discovery. Finally, disulfiram is a safe and approved drug for management of alcohol abuse, warranting its evaluation for repurposing in IBC therapy.
[Mh] MeSH terms primary: Apoptosis Regulatory Proteins/genetics
Inflammatory Breast Neoplasms/genetics
Inflammatory Breast Neoplasms/pathology
Neoplastic Cells, Circulating/metabolism
[Mh] MeSH terms secundary: Apoptosis Regulatory Proteins/metabolism
Biomarkers, Tumor
Cell Culture Techniques
Cell Survival/genetics
Copper/pharmacology
Disulfiram/pharmacology
Female
Gene Expression
High-Throughput Screening Assays
Humans
Inflammatory Breast Neoplasms/metabolism
Mitochondria/metabolism
NF-kappa B/genetics
NF-kappa B/metabolism
Spheroids, Cellular
Tumor Cells, Cultured
X-Linked Inhibitor of Apoptosis Protein/genetics
X-Linked Inhibitor of Apoptosis Protein/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Apoptosis Regulatory Proteins); 0 (Biomarkers, Tumor); 0 (NF-kappa B); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 789U1901C5 (Copper); TR3MLJ1UAI (Disulfiram)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15667

  6 / 5395 MEDLINE  
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[PMID]: 29289266
[Au] Autor:Trop-Steinberg S; Azar Y
[Ad] Address:Faculty of Life and Health Sciences (ST-S), JCT Lev Academic Institute, Jerusalem, Israel. Electronic address: shivtia@g.jct.ac.il.
[Ti] Title:Is Myc an Important Biomarker? Myc Expression in Immune Disorders and Cancer.
[So] Source:Am J Med Sci;355(1):67-75, 2018 Jan.
[Is] ISSN:1538-2990
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The proto-oncogene Myc serves as a paradigm for understanding the dynamics of transcriptional regulation. Myc protein has been linked to immune dysfunction, cancer development and neoplastic transformation. We review recent research regarding functions of Myc as an important modulator in immune disorders, postallogeneic hematopoietic stem cell transplantation (HSCT) and several cancers. Myc overexpression has been repeatedly linked to immune disorders and specific cancers, such as myasthenia gravis, psoriasis, pemphigus vulgaris, atherosclerosis, long-term allogeneic survival among HSCT patients, (primary) inflammatory breast cancer, (primary) ovarian carcinoma and hematological malignancies: acute myeloid leukemia, chronic myelogenous leukemia, Hodgkin's lymphoma and diffuse large B-cell lymphoma. However, decreased expression of Myc has been observed in HSCT patients who did not survive. Understanding impaired or inappropriate expression of Myc may present a path for the discovery of new targets for therapeutic applications.
[Mh] MeSH terms primary: Biomarkers, Tumor/biosynthesis
Gene Expression Regulation, Neoplastic
Immune System Diseases/metabolism
Neoplasms/metabolism
Proto-Oncogene Proteins c-myc/biosynthesis
[Mh] MeSH terms secundary: Allografts
Disease-Free Survival
Hematopoietic Stem Cell Transplantation
Humans
Immune System Diseases/pathology
Immune System Diseases/therapy
Neoplasms/pathology
Neoplasms/therapy
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Biomarkers, Tumor); 0 (MYC protein, human); 0 (Proto-Oncogene Proteins c-myc)
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180101
[St] Status:MEDLINE

  7 / 5395 MEDLINE  
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[PMID]: 28460643
[Au] Autor:Clarke CA; Canchola AJ; Moy LM; Neuhausen SL; Chung NT; Lacey JV; Bernstein L
[Ad] Address:Cancer Prevention Institute of California, 2201 Walnut Ave. Suite 300, Fremont, CA, 94538, USA.
[Ti] Title:Regular and low-dose aspirin, other non-steroidal anti-inflammatory medications and prospective risk of HER2-defined breast cancer: the California Teachers Study.
[So] Source:Breast Cancer Res;19(1):52, 2017 May 01.
[Is] ISSN:1465-542X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Regular users of aspirin may have reduced risk of breast cancer. Few studies have addressed whether risk reduction pertains to specific breast cancer subtypes defined jointly by hormone receptor (estrogen and progesterone receptor) and human epidermal growth factor receptor 2 (HER2) expression. This study assessed the prospective risk of breast cancer (overall and by subtype) according to use of aspirin and other non-steroidal anti-inflammatory medications (NSAIDs) in a cohort of female public school professionals in California. METHODS: In 1995 - 1996, participants in the California Teachers Study completed a baseline questionnaire on family history of cancer and other conditions, use of NSAIDs, menstrual and reproductive history, self-reported weight and height, living environment, diet, alcohol use, and physical activity. In 2005-2006, 57,164 participants provided some updated information, including use of NSAIDs and 1457 of these participants developed invasive breast cancer before January 2013. Multivariable Cox proportional hazards regression models provided hazard rate ratios (HRR) for the association between NSAID use and risk of invasive breast cancer as well as hormone receptor- and HER2-defined subtypes. RESULTS: Developing breast cancer was associated inversely with taking three or more tablets of low-dose aspirin per week (23% of participants). Among women reporting this exposure, the HRR was 0.84 (95% confidence interval (CI) 0.72-0.98) compared to those not taking NSAIDs and this was particularly evident in women with the hormone receptor-positive/HER2-negative subtype (HRR = 0.80, 95% CI 0.66-0.96). Use of three or more tablets of "other" NSAIDs was marginally associated with lower risk of breast cancer (HRR = 0.79, 95% CI 0.62-1.00). Other associations with NSAIDs were generally null. CONCLUSION: Our observation of reduced risk of breast cancer, among participants who took three or more tablets of low-dose aspirin weekly, is consistent with other reports looking at aspirin without differentiation by dose. This is the first report to suggest that the reduction in risk occurs for low-dose aspirin and not for regular-dose aspirin and only among women with the hormone receptor-positive/HER2-negative subtype. This preliminary study builds on previous knowledge and further supports the need for formal cancer chemoprevention studies of low-dose aspirin.
[Mh] MeSH terms primary: Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
Aspirin/therapeutic use
Breast Neoplasms/drug therapy
Receptor, ErbB-2/genetics
[Mh] MeSH terms secundary: Aged
Breast Neoplasms/epidemiology
Breast Neoplasms/pathology
California
Dose-Response Relationship, Drug
Female
Gene Expression Regulation, Neoplastic/drug effects
Humans
Middle Aged
Proportional Hazards Models
Receptors, Estrogen/genetics
Receptors, Progesterone/genetics
Risk Factors
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); R16CO5Y76E (Aspirin)
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s13058-017-0840-7

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[PMID]: 28456993
[Au] Autor:Serna-Marquez N; Diaz-Aragon R; Reyes-Uribe E; Cortes-Reynosa P; Salazar EP
[Ad] Address:Departamento de Biologia Celular, Cinvestav-IPN, Av IPN # 2508, San Pedro Zacatenco, 07360, Ciudad de Mexico, Mexico.
[Ti] Title:Linoleic acid induces migration and invasion through FFAR4- and PI3K-/Akt-dependent pathway in MDA-MB-231 breast cancer cells.
[So] Source:Med Oncol;34(6):111, 2017 Jun.
[Is] ISSN:1559-131X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:An increased risk of developing breast cancer has been associated with high levels of dietary fat intake. Linoleic acid (LA) is an essential fatty acid and the major ω-6 polyunsaturated fatty acid in occidental diets, which is able to induce inappropriate inflammatory responses that contribute to several chronic diseases including cancer. In breast cancer cells, LA induces migration. However, the signal transduction pathways that mediate migration and whether LA induces invasion in MDA-MB-231 breast cancer cells have not been studied in detail. We demonstrate here that LA induces Akt2 activation, invasion, an increase in NFκB-DNA binding activity, miR34a upregulation and miR9 downregulation in MDA-MB-231 cells. Moreover, Akt2 activation requires EGFR and PI3K activity, whereas migration and invasion are dependent on FFAR4, EGFR and PI3K/Akt activity. Our findings demonstrate, for the first time, that LA induces migration and invasion through an EGFR-/PI3K-/Akt-dependent pathway in MDA-MB-231 breast cancer cells.
[Mh] MeSH terms primary: Breast Neoplasms/metabolism
Cell Movement/drug effects
Linoleic Acid/pharmacology
Neoplasm Invasiveness/physiopathology
Phosphatidylinositol 3-Kinases/metabolism
Proto-Oncogene Proteins c-akt/metabolism
Receptors, G-Protein-Coupled/metabolism
[Mh] MeSH terms secundary: Cell Line, Tumor
Female
Humans
Signal Transduction/drug effects
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (O3FAR1 protein, human); 0 (Receptors, G-Protein-Coupled); 9KJL21T0QJ (Linoleic Acid); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[Js] Journal subset:IM
[Da] Date of entry for processing:170501
[St] Status:MEDLINE
[do] DOI:10.1007/s12032-017-0969-3

  9 / 5395 MEDLINE  
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[PMID]: 27776840
[Au] Autor:Lee JY; Ryu S; Cheong E; Sung KC
[Ad] Address:Division of Cardiology, Department of Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University, School of Medicine, Seoul, Republic of Korea.
[Ti] Title:Association of Physical Activity and Inflammation With All-Cause, Cardiovascular-Related, and Cancer-Related Mortality.
[So] Source:Mayo Clin Proc;91(12):1706-1716, 2016 Dec.
[Is] ISSN:1942-5546
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To investigate the association between physical activity (PA) and risk of mortality in a large middle-aged cohort stratified by inflammatory status. PATIENTS AND METHODS: A total of 336,560 individuals (mean age, 39.7 years; 58% male) who underwent comprehensive health screenings were enrolled in this prospective cohort study. They were grouped according to self-reported PA level using a questionnaire: no regular PA with a sedentary lifestyle, regular but insufficient PA (below the guidelines), sufficient PA (concordant with the guidelines), and health-enhancing PA. Inflammation was assessed via high-sensitivity C-reactive protein (hsCRP) level. Study end points were all-cause, cardiovascular-related, and cancer-related mortality. RESULTS: During the 1,976,882 person-years of follow-up (median follow-up duration, 6.17 years), 2062 deaths occurred. Compared with a sedentary lifestyle, the hazard ratios (95% CIs) on the multivariable Cox proportional hazards regression analyses for all-cause mortality by PA level were 0.95 (0.84-1.07), 0.85 (0.72-0.99), and 0.75 (0.60-0.93) (P for trend=.003), and those for cardiovascular- and cancer-related mortality were 0.95, 0.80, and 0.55 (P for trend=.05) and 0.82, 0.83, and 0.78 (P for trend=.01), respectively. Compared with participants with low hsCRP levels and any regular PA, those with high hsCRP levels and no regular PA had a significantly higher risk of mortality (1.59 [1.38-1.84]). CONCLUSION: Higher PA levels were associated with a dose-dependent reduced risk of cardiovascular-related, cancer-related, and all-cause mortality. Individuals with high hsCRP levels and no regular PA had the highest risk of mortality.
[Mh] MeSH terms primary: Cardiovascular Diseases/mortality
Exercise/physiology
Inflammation Mediators/blood
Inflammation/epidemiology
Neoplasms/mortality
[Mh] MeSH terms secundary: Adult
Biomarkers/blood
Breast Neoplasms/metabolism
C-Reactive Protein/metabolism
Cardiovascular Diseases/metabolism
Causality
Cohort Studies
Comorbidity
Female
Humans
Inflammation/metabolism
Male
Middle Aged
Motor Activity/physiology
Neoplasms/metabolism
Prospective Studies
Risk Assessment
United States/epidemiology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers); 0 (Inflammation Mediators); 9007-41-4 (C-Reactive Protein)
[Em] Entry month:1705
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:161026
[St] Status:MEDLINE

  10 / 5395 MEDLINE  
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[PMID]: 29462226
[Au] Autor:Kimball AB; Sundaram M; Cloutier M; Gauthier-Loiselle M; Gagnon-Sanschagrin P; Guérin A; Ganguli A
[Ti] Title:Increased Prevalence of Cancer in Adult Patients With Psoriasis in the United States: A Claims Based Analysis.
[So] Source:J Drugs Dermatol;17(2):180-186, 2018 Feb 01.
[Is] ISSN:1545-9616
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Psoriasis (Ps) is a chronic inflammatory immune-mediated skin disease that has been identified as a risk factor for various conditions including neoplasms. OBJECTIVE: To compare prevalence of cancer between Ps and Ps-free patients. METHODS: Adult patients continuously enrolled for ≥12 months (≥1 month in 2014) were selected from a large United States (US) claims database (Q1:2010-Q4:2014) and classified as Ps patients (≥2 Ps diagnoses; International Classification of Diseases 9th Revision, [ICD-9] code: 696.1x) and Ps-free patients (no Ps diagnosis). Patients were exactly matched (1:1) based on age, gender, state of residence, and insurance plan type. Prevalence of cancer was compared between cohorts over patients' last 12 months of continuous healthcare plan enrollment using logistic-regression models. RESULTS: A total of 179,066 pairs of Ps and Ps-free patients were selected. Median age was 54.0 years, 51.7% were females. Prevalence of cancer was higher among Ps patients for any type of neoplasms (OR [95% confidence interval (CI)]=1.86 [1.83; 1.89]), malignant neoplasms (OR [95% CI]=1.53 [1.49;1.57]), as well as malignant skin neoplasms (OR [95% CI]=1.87 [1.79; 1.95]), lymphatic and hematopoietic tissues (OR [95% CI]=1.70 [1.57;1.84]), genital (OR [95% CI]=1.33 [1.26;1.41]), breast (OR [95% CI]=1.32 [1.24;1.40]), digestive organs and peritoneum (OR [95% CI]=1.24 [1.13;1.35]), urinary organs (OR [95% CI]=1.49 [1.36;1.64]), respiratory and intrathoracic organs (OR [95% CI]=1.30 [1.17;1.44]), and metastatic cancer (OR [95% CI]=1.14 [1.06;1.24]), all P less than 0.01. LIMITATIONS: Impact of Ps severity could not be assessed. CONCLUSION: Ps patients had a higher prevalence of cancer than Ps-free patients. J Drugs Dermatol. 2018;17(2):180-186.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:In-Process


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