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  1. Article: The metabolic syndrome: A high-risk state for cancer?

    Cowey, Stephanie / Hardy, Robert W

    The American journal of pathology

    2006  Volume 169, Issue 5, Page(s) 1505–1522

    Abstract: The metabolic syndrome is composed of cardiovascular risk factors including increased body mass index/waist circumference, blood pressure, plasma glucose, and triglycerides, as well as decreased high-density lipoprotein cholesterol. The essence of the ... ...

    Abstract The metabolic syndrome is composed of cardiovascular risk factors including increased body mass index/waist circumference, blood pressure, plasma glucose, and triglycerides, as well as decreased high-density lipoprotein cholesterol. The essence of the metabolic syndrome lies in the clustering of these risk factors, which are associated with cardiovascular disease. Interestingly, most of the components of the metabolic syndrome have individually been linked in some way to the development of cancer. However, epidemiological studies linking the metabolic syndrome to cancer are scarce. Nevertheless, two such studies indicate that the clustering of metabolic syndrome components significantly increases the risk of colon cancer mortality compared with the individual components. The purpose of this review is to further explore the potential relationship between the metabolic syndrome and cancer risk. Specifically, we examine the hypothesis that individual components of the metabolic syndrome contribute to the development of several processes, including insulin resistance, aromatase activity, adipokine production, angiogenesis, glucose utilization, and oxidative stress/DNA damage, which can work together to increase cancer risk beyond that of the individual components alone. We propose that the metabolic syndrome be considered as a high-risk state for certain types of cancer and that this relationship should be systematically explored across cancer types.
    MeSH term(s) Humans ; Metabolic Syndrome/complications ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/metabolism ; Metabolic Syndrome/pathology ; Neoplasms/complications ; Neoplasms/etiology ; Neoplasms/metabolism ; Risk Factors
    Language English
    Publishing date 2006-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.2353/ajpath.2006.051090
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  2. Article ; Online: Stearate preferentially induces apoptosis in human breast cancer cells.

    Evans, Lynda M / Cowey, Stephanie L / Siegal, Gene P / Hardy, Robert W

    Nutrition and cancer

    2009  Volume 61, Issue 5, Page(s) 746–753

    Abstract: Stearic acid (stearate) is an 18-carbon saturated fatty acid that has been shown to inhibit invasion and proliferation and induce apoptosis in various human cell types. The specificity of stearate-induced apoptosis for cancerous versus noncancerous ... ...

    Abstract Stearic acid (stearate) is an 18-carbon saturated fatty acid that has been shown to inhibit invasion and proliferation and induce apoptosis in various human cell types. The specificity of stearate-induced apoptosis for cancerous versus noncancerous breast cells has not been examined, and the mechanism underlying stearate-induced apoptosis is unknown. Morphological analysis, cell viability, and caspase-3 activity assays demonstrated that stearate activated apoptosis preferentially in cancerous breast cells in a time- and dose-dependent manner. Inhibition of de novo diacylgycerol synthesis or protein kinase C (PKC) blocked stearate-induced caspase-3 activity, indicating the involvement of a novel or classical PKC isozyme. To our knowledge this is the first study showing that stearate induces apoptosis preferentially in breast cancer cells and implicates protein kinase C in the signaling cascade. These results raise the possibility of dietary stearate having a beneficial role in the prevention or treatment of breast cancer.
    MeSH term(s) Antineoplastic Agents/administration & dosage ; Apoptosis ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Caspase 3/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Movement ; Cell Shape ; Cell Survival ; Coenzyme A Ligases/antagonists & inhibitors ; Dietary Fats ; Diglycerides/biosynthesis ; Female ; Humans ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/metabolism ; Stearic Acids/administration & dosage
    Chemical Substances Antineoplastic Agents ; Dietary Fats ; Diglycerides ; Stearic Acids ; Protein Kinase C (EC 2.7.11.13) ; Caspase 3 (EC 3.4.22.-) ; Coenzyme A Ligases (EC 6.2.1.-)
    Language English
    Publishing date 2009-10-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 424433-3
    ISSN 1532-7914 ; 0163-5581
    ISSN (online) 1532-7914
    ISSN 0163-5581
    DOI 10.1080/01635580902825597
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  3. Article: Stearate Preferentially Induces Apoptosis in Human Breast Cancer Cells

    Evans, Lynda M / Cowey, Stephanie L / Siegal, Gene P / Hardy, Robert W

    Nutrition and cancer. 2009 Sept-Oct, v. 61, no. 5

    2009  

    Abstract: Stearic acid (stearate) is an 18-carbon saturated fatty acid that has been shown to inhibit invasion and proliferation and induce apoptosis in various human cell types. The specificity of stearate-induced apoptosis for cancerous versus noncancerous ... ...

    Abstract Stearic acid (stearate) is an 18-carbon saturated fatty acid that has been shown to inhibit invasion and proliferation and induce apoptosis in various human cell types. The specificity of stearate-induced apoptosis for cancerous versus noncancerous breast cells has not been examined, and the mechanism underlying stearate-induced apoptosis is unknown. Morphological analysis, cell viability, and caspase-3 activity assays demonstrated that stearate activated apoptosis preferentially in cancerous breast cells in a time- and dose-dependent manner. Inhibition of de novo diacylgycerol synthesis or protein kinase C (PKC) blocked stearate-induced caspase-3 activity, indicating the involvement of a novel or classical PKC isozyme. To our knowledge this is the first study showing that stearate induces apoptosis preferentially in breast cancer cells and implicates protein kinase C in the signaling cascade. These results raise the possibility of dietary stearate having a beneficial role in the prevention or treatment of breast cancer.
    Keywords human cell lines ; breast neoplasms ; dietary fat ; stearic acid ; saturated fatty acids ; cell culture ; apoptosis ; chemoprevention ; anticarcinogenic activity ; cytotoxins ; cytotoxicity ; cell invasion ; cell motility ; immunoblotting ; protein kinase C ; diacylglycerols ; biochemical pathways ; nutritional intervention ; fat intake
    Language English
    Dates of publication 2009-09
    Size p. 746-753.
    Document type Article
    ZDB-ID 424433-3
    ISSN 0163-5581
    ISSN 0163-5581
    Database NAL-Catalogue (AGRICOLA)

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  4. Article: Abdominal obesity, insulin resistance, and colon carcinogenesis are increased in mutant mice lacking gastrin gene expression.

    Cowey, Stephanie L / Quast, Michael / Belalcazar, Ligia Maria / Wei, Jingwa / Deng, Xiaoling / Given, Randall / Singh, Pomila

    Cancer

    2005  Volume 103, Issue 12, Page(s) 2643–2653

    Abstract: Background: The authors recently reported that gastrin gene knockout (GAS-KO) mice had an increased risk for colon carcinogenesis in response to azoxymethane (AOM) compared with their wild type (WT) littermates. In the current report, the authors ... ...

    Abstract Background: The authors recently reported that gastrin gene knockout (GAS-KO) mice had an increased risk for colon carcinogenesis in response to azoxymethane (AOM) compared with their wild type (WT) littermates. In the current report, the authors discuss the predisposition of GAS-KO mice to develop obesity and metabolic hormonal changes that may contribute to their increased risk of colon carcinogenesis.
    Methods: The weight and deposition of fat was monitored in the mice over a 14 month period, using magnetic resonance imaging and nuclear magnetic resonance techniques. Changes in plasma concentrations of ghrelin, leptin, insulin, and glucose were assessed using radioimmunoassay analysis and enzyme-linked immunosorbent assays. Preneoplastic markers of colon carcinogenesis (aberrant crypt foci [ACFs]), in response to AOM, were measured in a subset of obese versus lean GAS-KO mice and were compared with the markers in WT mice.
    Results: Increases in visceral adiposity were evident by age 2 months in GAS-KO mice, resulting in macroscopic obesity by age 7 months. Hyperinsulinemia and insulin:glucose ratios were increased significantly in GAS-KO mice as young as 1 month and preceded alterations in nonfasting leptin and ghrelin levels. The number of ACFs per mouse colon were increased significantly in the following order: obese GAS-KO mice > lean GAS-KO mice > WT mice. Fasting plasma insulin levels were 0.88 +/- 0.1 ng/mL, 1.45 +/- 0.3, and 2.76 +/- 0.9 ng/mL in the WT, GAS-KO lean, and GAS-KO obese mice, respectively.
    Conclusions: The current results suggest the novel possibility that loss of amidated gastrins may increase adipogenesis, hyperinsulinemia, and colon carcinogenesis in GAS-KO mice. The increase in colon carcinogenesis may be due in part to hyperinsulinemia, increased obesity, and other associated hormone changes that were measured in GAS-KO mice.
    MeSH term(s) Animals ; Azoxymethane/toxicity ; Body Weight ; Carcinogens/toxicity ; Colonic Neoplasms/etiology ; Colonic Neoplasms/pathology ; Gastrins/genetics ; Gastrins/physiology ; Gene Expression/drug effects ; Ghrelin ; Glucose/metabolism ; Hyperinsulinism ; Insulin/metabolism ; Insulin Resistance ; Leptin/metabolism ; Magnetic Resonance Imaging ; Male ; Mice ; Mice, Knockout ; Obesity/etiology ; Peptide Hormones/metabolism ; Precancerous Conditions/chemically induced ; Precancerous Conditions/pathology ; Radioimmunoassay ; Thinness/metabolism
    Chemical Substances Carcinogens ; Gastrins ; Ghrelin ; Insulin ; Leptin ; Peptide Hormones ; Glucose (IY9XDZ35W2) ; Azoxymethane (MO0N1J0SEN)
    Language English
    Publishing date 2005-06-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1429-1
    ISSN 1097-0142 ; 0008-543X ; 1934-662X
    ISSN (online) 1097-0142
    ISSN 0008-543X ; 1934-662X
    DOI 10.1002/cncr.21094
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  5. Article ; Online: Evaluating the value of intrapartum fetal scalp blood sampling to predict adverse neonatal outcomes: A UK multicentre observational study.

    Al Wattar, Bassel H / Lakhiani, Aarti / Sacco, Adalina / Siddharth, Aditi / Bain, Alexandra / Calvia, Alexandra / Kamran, Atiyah / Tiong, Bing / Warwick, Bethan / MacMahon, Caroline / Marcus, Diana / Long, Emma / Coyle, Gillian / Lever, Gillian Elizabeth / Michel, Gina / Gopal, Gomathy / Baig, Hana / Price, Hannah Louise / Badri, Hawra /
    Stevenson, Helen / Hoyte, Helene / Malik, Humaira / Edwards, Jade / Hartley, Jennifer / Hemers, Jennifer / Tamblyn, Jennifer / Dalton, John Alexander William / Frost, Jonathan / Subba, Kamana / Baxter, Kathryn / Sivakumar, Kavitha / Murphy, Kelly / Papadakis, Konstantinos / Bladon, Laura Rachel / Kasaven, Lorraine / Manning, Louisa / Prior, Mathew / Ghosh, Mausumi / Couch, Melanie / Altunel, Melis / Pearce, Melissa / Cocker, Michael / Stephanou, Michael / Jie, Michelle / Mistry, Minesh / Wahby, Mohammed Osama / Saidi, Nabila Shahid / Ramshaw, Nicola Louise / Tempest, Nicola / Parker, Nina / Tan, Phoebe L / Johnson, Racheal Louise / Harris, Rachel / Tildesley, Rachel / Ram, Ramya / Painuly, Ritu / Cuffolo, Romana / Bugeja, Roberta / Ngadze, Rose / Grainger, Rosie / Gurung, Sabitra / Mak, Sammy / Farrell, Sara / Cowey, Sarah / Neary, Sarah / Quinn, Sarah / Nijjar, Simrit Kaur / Kenyon, Sophie / Lamb, Stephanie / Tracey, Susan / Lee, Tara / Kinsella, Therese / Davidson, Trecia / Corr, Trent / Sampson, Uzo / McQueen, Victoria / Smith, William Parry / Castling, Zora

    European journal of obstetrics, gynecology, and reproductive biology

    2019  Volume 240, Page(s) 62–67

    Abstract: Objective: To evaluate the value of fetal scalp blood sampling (FBS) as an adjunct test to cardiotocography, to predict adverse neonatal outcomes.: Study design: A multicentre service evaluation observational study in forty-four maternity units in ... ...

    Abstract Objective: To evaluate the value of fetal scalp blood sampling (FBS) as an adjunct test to cardiotocography, to predict adverse neonatal outcomes.
    Study design: A multicentre service evaluation observational study in forty-four maternity units in the UK. We collected data retrospectively on pregnant women with singleton pregnancy who received FBS in labour using a standardised data collection tool. The primary outcome was prediction of neonatal acidaemia diagnosed as umbilical cord arterial pH < 7.05, the secondary outcomes were the prediction of Apgar scores<7 at 1st and 5th minutes and admission to the neonatal intensive care unit (NICU). We evaluated the correlation between the last FBS blood gas before birth and the umbilical cord blood and adjusted for time intervals. We constructed 2 × 2 tables to calculate the sensitivity, specificity, positive (PPV) and negative predictive value (NPV) and generated receiver operating curves to report on the Area Under the Curve (AUC).
    Results: In total, 1422 samples were included in the analysis; pH values showed no correlation (r = 0.001, p = 0.9) in samples obtained within an hour (n = 314), or within half an hour from birth (n = 115) (r=-0.003, p = 0.9). A suboptimal FBS pH value (<7.25) had a poor sensitivity (22%) and PPV (4.9%) to predict neonatal acidaemia with high specificity (87.3%) and NPV (97.4%). Similar performance was noted to predict Apgar scores <7 at 1st (sensitivity 14.5%, specificity 87.5%, PPV 23.4%, NPV 79.6%) and 5th minute (sensitivity 20.3%, specificity 87.4%, PPV 7.6%, NPV 95.6%), and admission to NICU (sensitivity 20.3%, specificity 87.5%, PPV 13.3%, NPV 92.1%). The AUC for FBS pH to predict neonatal acidaemia was 0.59 (95%CI 0.59-0.68, p = 0.3) with similar performance to predict Apgar scores<7 at 1st minute (AUC 0.55, 95%CI 0.51-0.59, p = 0.004), 5th minute (AUC 0.55, 95%CI 0.48-0.62, p = 0.13), and admission to NICU (AUC 0.58, 95%CI 0.52-0.64, p = 0.002). Forty-one neonates had acidaemia (2.8%, 41/1422) at birth. There was no significant correlation in pH values between the FBS and the umbilical cord blood in this subgroup adjusted for sampling time intervals (r = 0.03, p = 0.83).
    Conclusions: As an adjunct tool to cardiotocography, FBS offered limited value to predict neonatal acidaemia, low Apgar Scores and admission to NICU.
    MeSH term(s) Acidosis/blood ; Acidosis/diagnosis ; Blood Gas Analysis ; Female ; Fetal Blood ; Fetal Distress/blood ; Fetal Distress/diagnosis ; Humans ; Hydrogen-Ion Concentration ; Infant, Newborn ; Labor, Obstetric ; Male ; Pregnancy ; Pregnancy Outcome ; Retrospective Studies ; Scalp ; United Kingdom
    Language English
    Publishing date 2019-06-15
    Publishing country Ireland
    Document type Journal Article ; Multicenter Study ; Observational Study
    ZDB-ID 190605-7
    ISSN 1872-7654 ; 0301-2115 ; 0028-2243
    ISSN (online) 1872-7654
    ISSN 0301-2115 ; 0028-2243
    DOI 10.1016/j.ejogrb.2019.06.012
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