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  • 1
    ISSN: 1434-4475
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    ISSN: 1618-2650
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Keywords: CANCER ; GROWTH ; GROWTH-FACTOR ; BLOOD ; PROSTATE ; RISK ; PROTEIN ; SAMPLE ; SAMPLES ; TIME ; BIOMARKERS ; BINDING ; HEALTH ; AGE ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; FACTOR-I ; BINDING PROTEIN ; cord blood ; IGF-I ; WEIGHT ; biomarker ; USA ; HORMONES ; TESTOSTERONE ; INCREASED RISK ; CANCER-RISK ; BINDING GLOBULIN ; CORD ; BIRTH-WEIGHT ; BONE-MINERAL DENSITY ; AFRICAN-AMERICAN ; ANDROSTANEDIOL GLUCURONIDE ; WHITE MEN ; WELL ; SEX-STEROID-HORMONES ; MOTHER ; AMNIOTIC-FLUID ; SERUM TESTOSTERONE LEVELS
    Abstract: Background: To address whether umbilical cord blood concentrations of sex steroid hormones and the insulin-like growth factor (IGF) axis differ between African-American and White male neonates. Methods: In 2004 and 2005, venous cord blood samples were collected from 75 African-American and 38 White male full-term uncomplicated births along with birth weight, placental weight, mother's age and parity, and time of birth. Testosterone, androstanediol glucuronide, estradiol, and sex hormone binding globulin (SHBG) were measured by immunoassay, and IGF-I, IGF-2, and IGF binding protein (BP)-3 by ELISA. Crude and multivariable-adjusted geometric mean concentrations were computed. Results: Androstanediol glucuronide, estradiol, and SHBG concentrations did not differ by race; however, the molar ratio of testosterone to SHBG was higher in African-American than White male babies after adjustment (P = 0.01). Both before and after adjustment, Whites had higher concentrations of IGF-I (adjusted; White, African-American, 93.1, 71.9 ng/mL), IGF-2 (537.3-474.8 ng/mL), and IGFBP-3 (1,673-1,482 ng/mL) than African-Americans (P 〈 0.05), although the molar ratio of IGF-I plus IGF-2 to IGFBP-3 did not differ by race. Conclusion: The higher cord blood testosterone to SHBG ratio in African-American compared with White male babies after taking into account maternal and birth factors is compatible with the hypothesis that differences in androgen levels in utero contribute to their higher prostate cancer risk, although we would have expected crude differences as well. Lower cord blood IGF-I and IGF-2 levels in African-American compared with White male babies are not consistent with the hypothesis that differences in growth factor levels contribute to their higher prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1484-91)
    Type of Publication: Journal article published
    PubMed ID: 19423525
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  • 4
    Keywords: RECEPTOR ; EXPRESSION ; tumor ; THERAPY ; RISK ; BREAST ; OVARIAN-CANCER ; FACTOR-I ; BINDING PROTEIN-3 ; GENOME-WIDE ASSOCIATION
    Abstract: Background The insulin-like growth factor (IGF) signaling pathway has been implicated in prostate cancer (PCa) initiation, but its role in progression remains unknown. Methods Among 5887 PCa patients (704 PCa deaths) of European ancestry from seven cohorts in the National Cancer Institute Breast and Prostate Cancer Cohort Consortium, we conducted Cox kernel machine pathway analysis to evaluate whether 530 tagging single nucleotide polymorphisms (SNPs) in 26 IGF pathway-related genes were collectively associated with PCa mortality. We also conducted SNP-specific analysis using stratified Cox models adjusting for multiple testing. In 2424 patients (313 PCa deaths), we evaluated the association of prediagnostic circulating IGF1 and IGFBP3 levels and PCa mortality. All statistical tests were two-sided. Results The IGF signaling pathway was associated with PCa mortality (P = .03), and IGF2-AS and SSTR2 were the main contributors (both P = .04). In SNP-specific analysis, 36 SNPs were associated with PCa mortality with P-trend less than .05, but only three SNPs in the IGF2-AS remained statistically significant after gene-based corrections. Two were in linkage disequilibrium (r(2) = 1 for rs1004446 and rs3741211), whereas the third, rs4366464, was independent (r(2) = 0.03). The hazard ratios (HRs) per each additional risk allele were 1.19 (95% confidence interval [CI] = 1.06 to 1.34; P-trend = .003) for rs3741211 and 1.44 (95% CI = 1.20 to 1.73; P-trend 〈 .001) for rs4366464. rs4366464 remained statistically significant after correction for all SNPs (P-trend.corr =.04). Prediagnostic IGF1 (HRhighest vs lowest quartile = 0.71; 95% CI = 0.48 to 1.04) and IGFBP3 (HR = 0.93; 95% CI = 0.65 to 1.34) levels were not associated with PCa mortality. Conclusions The IGF signaling pathway, primarily IGF2-AS and SSTR2 genes, may be important in PCa survival.
    Type of Publication: Journal article published
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  • 5
    Keywords: MODEL ; RISK ; ACTIVATION ; TARGET ; STEM-CELLS ; DIABETES-MELLITUS ; ARREST ; DUCTAL ADENOCARCINOMA ; METAANALYSIS ; TO-MESENCHYMAL TRANSITION
    Abstract: Metformin treatment is associated with a decreased risk and better prognosis of pancreatic cancer (PC) in patients with type 2 diabetes, but the mechanism of metformin's PC growth inhibition in the context of a prediabetic state is unknown. We used a Panc02 pancreatic tumor cell transplant model in diet-induced obese (DIO) C57BL/6 mice to compare the effects of metformin and the direct mammalian target of rapamycin (mTOR) inhibitor rapamycin on PC growth, glucose regulation, mTOR pathway signaling, and candidate microRNA (miR) expression. In DIO/prediabetic mice, metformin and rapamycin significantly reduced pancreatic tumor growth and mTOR-related signaling. The rapamycin effects centered on decreased mTOR-regulated growth and survival signaling, including increased expression of let-7b and cell cycle-regulating miRs. Metformin (but not rapamycin) reduced glucose and insulin levels and expression of miR-34a and its direct targets Notch, Slug, and Snail. Metformin also reduced the number and size of Panc02 tumor spheres in vitro and inhibited the expression of Notch in spheroids. Our results suggest that metformin and rapamycin can both inhibit pancreatic tumor growth in obese, prediabetic mice through shared and distinct mechanisms. Metformin and direct mTOR inhibitors, alone or possibly in combination, represent promising intervention strategies for breaking the diabetes-PC link.
    Type of Publication: Journal article published
    PubMed ID: 25576058
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  • 6
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  31. Wissenschaftliche Jahrestagung der Deutschen Gesellschaft für Phoniatrie und Pädaudiologie (DGPP) zusammen mit dem 5. Pädakustiker-Symposium der Akademie für Hörgeräte-Akustik; 20140918-20140921; Lübeck; DOCP15 /20140902/
    Publication Date: 2014-09-03
    Description: Hintergrund: Nach Cochlea-Implantat (CI)-Versorgung bei Kindern dient die Bestimmung der Aufblähkurve (ABK), sowie des Sprachverstehens als Maß um den Erfolg der CI-Versorgung zu beurteilen. Die Hörleistung kann mit dem jeweiligen Höralter, oder mit Kindern gleichen Lebensalters verglichen werden. In der vorliegenden Studie soll untersucht werden, ob die Schwellen der ABK in der Erstanpassungsphase (audioverbale Therapie/AVT) sich zwischen jüngeren und älteren Kindern unterscheiden.Material und Methoden: Es wurden Gruppen in Abhängigkeit vom Alter zum Zeitpunkt der Ersteinstellung (bis 16. Lebensmonat/30.-60. Lebensmonat) und dem Vorhandensein von Begleitbehinderungen (monosymptomatische cochleäre Schwerhörigkeit/ Schwerhörigkeit mit Begleitbehinderungen) gebildet und die ABK verglichen. Alle Kinder sammelten zuvor mit Hörgeräten Hörerfahrungen.Ergebnisse: Bei den Kindern mit monosymptomatischer Schwerhörigkeit lag die 1. ABK bei den später implantierten Kindern besser als bei den jüngeren. Bei den Kindern mit Begleitbehinderungen unterschied sich die 1. ABK nur wenig in beiden Altersgruppen, die jüngeren schnitten etwas besser ab. Alle Kinder, mit und ohne Begleitbehinderungen, konnten sich während der 1. AVT verbessern, die älteren rascher. Während der 2. AVT verbesserten sich erneut alle Kinder, die jüngeren stärker.Diskussion: Dass die 1. ABK in der 1. AVT bei den älteren Kindern bei geringeren Lautstärken lag, ist auf mehr Hörerfahrungen und das höhere Lebensalter zurückzuführen. Die 1. ABK lagen in dem Lautstärkebereich, in dem normalhörende Neugeborene Hörreaktionen zeigen. Vor allem für die höheren Frequenzen zeigten die später operierten Kinder große Fortschritte. Im Vergleich zu normalhörenden Kindern gleichen Lebensalters lag die ABK am Ende der 1. AVT unabhängig vom Implantationsalter um 30-40 dB schlechter. Vergleicht man die 1. ABK aller Kinder, dann fällt das Ergebnis bei Kindern mit Begleitbehinderungen insbesondere bei den älteren ungünstiger aus. Am Ende der 2. AVT lagen die Kinder mit Begleitbehinderungen ebenfalls etwas schlechter.Fazit: Für die korrekte Bewertung der ABK bei CI-versorgten Kindern sind das Lebensalter, eine Begleitbehinderung und die Zeit seit der Ersteinstellung zu berücksichtigen. Die vorliegenden Daten erlauben eine Einordnung.
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 7
    Abstract: Pharmacoepidemiologic studies provide evidence that use of metformin, a drug commonly prescribed for type II diabetes, is associated with a substantial reduction in cancer risk. Experimental models show that metformin inhibits the growth of certain neoplasms by cell autonomous mechanisms such as activation of AMP kinase with secondary inhibition of protein synthesis or by an indirect mechanism involving reduction in gluconeogenesis leading to a decline in insulin levels and reduced proliferation of insulin-responsive cancers. Here, we show that metformin attenuates paraquat-induced elevations in reactive oxygen species (ROS), and related DNA damage and mutations, but has no effect on similar changes induced by H(2)0(2), indicating a reduction in endogenous ROS production. Importantly, metformin also inhibited Ras-induced ROS production and DNA damage. Our results reveal previously unrecognized inhibitory effects of metformin on ROS production and somatic cell mutation, providing a novel mechanism for the reduction in cancer risk reported to be associated with exposure to this drug.
    Type of Publication: Journal article published
    PubMed ID: 22262811
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  • 8
    Keywords: CANCER ; GROWTH ; GROWTH-FACTOR ; BLOOD ; PROSTATE ; DIAGNOSIS ; INFORMATION ; DISEASE ; RISK ; PROTEIN ; PROTEINS ; SAMPLE ; SAMPLES ; TIME ; PATIENT ; SERA ; INDEX ; ANTIGEN ; BINDING ; ASSOCIATION ; NO ; STAGE ; AGE ; MEN ; smoking ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; RECRUITMENT ; BINDING-PROTEINS ; SELECTION ; ALCOHOL ; PREDICTORS ; body mass index ; HETEROGENEITY ; BINDING PROTEIN ; SERUM ; BODIES ; IGF-I ; GRADE ; EXTRACTION ; prospective studies ; METAANALYSIS ; GROWTH-FACTOR-I ; I IGF-I ; LEVEL ; analysis ; methods ; POWER ; MASS ; PARTICIPANTS ; FACTOR (IGF)-I ; USA ; HORMONES ; prospective ; prospective study ; NOR ; HIGH-GRADE ; CANCER-RISK ; ENGLAND ; SET ; Insulin-Like Growth Factor I ; steroids ; BINDING PROTEINS ; MEDICINE ; FACTOR AXIS ; LOW-GRADE ; androgens ; body mass ; SUBSEQUENT RISK ; synthesis ; RATIO ; BLOOD-LEVELS ; INVESTIGATORS ; COLLECTION ; growth factor ; PSA ERA
    Abstract: Background: Some, but not all, published results have shown an association between circulating blood levels of some insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) and the subsequent risk for prostate cancer. Purpose: To assess the association between levels of IGFs and IGFBPs and the subsequent risk for prostate cancer. Data Sources: Studies identified in PubMed, Web of Science, and CancerLit. Study Selection: The principal investigators of all studies that published data on circulating concentrations of sex steroids, IGFs, or IGFBPs and prostate cancer risk using prospectively collected blood samples were invited to collaborate. Data Extraction: Investigators provided individual participant data on circulating concentrations of IGF-I, IGF-II, IGFBP-II, and IGFBP-III and participant characteristics to a central data set in Oxford, United Kingdom. Data Synthesis: The study included data on 3700 men with prostate cancer and 5200 control participants. On average, case patients were 61.5 years of age at blood collection and received a diagnosis of prostate cancer 5 years after blood collection. The greater the serum IGF-I concentration, the greater the subsequent risk for prostate cancer (odds ratio [OR] in the highest vs. lowest quintile, 1.38 [95% CI, 1.19 to 1.60]; P 〈 0.001 for trend). Neither IGF-II nor IGFBP-II concentrations were associated with prostate cancer risk, but statistical power was limited. Insulin-like growth factor I and IGFBP-III were correlated (r = 0.58), and although IGFBP-III concentration seemed to be associated with prostate cancer risk, this was secondary to its association with IGF-I levels. Insulin-like growth factor I concentrations seemed to be more positively associated with low-grade than high-grade disease; otherwise, the association between IGFs and IGFBPs and prostate cancer risk had no statistically significant heterogeneity related to stage or grade of disease, time between blood collection and diagnosis, age and year of diagnosis, prostate-specific antigen level at recruitment, body mass index, smoking, or alcohol intake. Limitations: Insulin-like growth factor concentrations were measured in only 1 sample for each participant, and the laboratory methods to measure IGFs differed in each study. Not all patients had disease stage or grade information, and the diagnosis of prostate cancer may differ among the studies. Conclusion: High circulating IGF-I concentrations are associated with a moderately increased risk for prostate cancer
    Type of Publication: Journal article published
    PubMed ID: 18838726
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  • 9
    Keywords: GROWTH ; PATHWAY ; MESSENGER-RNA ; STRESS ; CAENORHABDITIS-ELEGANS ; MAMMALIAN-CELLS ; PROTEIN-SYNTHESIS ; ETV6-NTRK3 GENE FUSION ; TUMOR-CELL SURVIVAL ; FACTOR-II
    Abstract: Metabolic adaptation is essential for cell survival during nutrient deprivation. We report that eukaryotic elongation factor 2 kinase (eEF2K), which is activated by AMP-kinase (AMPK), confers cell survival under acute nutrient depletion by blocking translation elongation. Tumor cells exploit this pathway to adapt to nutrient deprivation by reactivating the AMPK-eEF2K axis. Adaptation of transformed cells to nutrient withdrawal is severely compromised in cells lacking eEF2K. Moreover, eEF2K knockdown restored sensitivity to acute nutrient deprivation in highly resistant human tumor cell lines. In vivo, overexpression of eEF2K rendered murine tumors remarkably resistant to caloric restriction. Expression of eEF2K strongly correlated with overall survival in human medulloblastoma and glioblastoma multiforme. Finally, C. elegans strains deficient in efk-1, the eEF2K ortholog, were severely compromised in their response to nutrient depletion. Our data highlight a conserved role for eEF2K in protecting cells from nutrient deprivation and in conferring tumor cell adaptation to metabolic stress. PAPERCLIP:
    Type of Publication: Journal article published
    PubMed ID: 23706743
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  • 10
    Abstract: The role of insulin-like growth factors (IGFs) in prostate cancer development is not fully understood. To investigate the association between circulating concentrations of IGFs (IGF-I, IGF-II, IGFBP-1, IGFBP-2, IGFBP-3) and prostate cancer risk, we pooled individual participant data from 17 prospective and two cross-sectional studies, including up to 10,554 prostate cancer cases and 13,618 control participants. Conditional logistic regression was used to estimate the odds ratios (ORs) for prostate cancer based on the study-specific fifth of each analyte. Overall, IGF-I, IGF-II, IGFBP-2, and IGFBP-3 concentrations were positively associated with prostate cancer risk (Ptrend all {less than or equal to} 0.005), and IGFBP-1 was weakly inversely associated with risk (Ptrend = 0.05). However, heterogeneity between the prospective and cross-sectional studies was evident (Pheterogeneity = 0.03), unless the analyses were restricted to prospective studies (with the exception of IGF-II, Pheterogeneity = 0.02). For prospective studies, the OR for men in the highest versus the lowest fifth of each analyte was 1.29 (95% confidence interval=1.16-1.43) for IGF-I, 0.81 (0.68-0.96) for IGFBP-1, and 1.25 (1.12-1.40) for IGFBP-3. These associations did not differ significantly by time-to-diagnosis or tumor stage or grade. After mutual adjustment for each of the other analytes, only IGF-I remained associated with risk. Our collaborative study represents the largest pooled analysis of the relationship between prostate cancer risk and circulating concentrations of IGF-I, providing strong evidence that IGF-I is highly likely to be involved in prostate cancer development.
    Type of Publication: Journal article published
    PubMed ID: 26921328
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