Circadian pathway genes in relation to glioma risk and outcome

Purpose: There is growing evidence that circadian disruption may alter risk and aggressiveness of cancer. We evaluated common genetic variants in the circadian gene pathway for associations with glioma risk and patient outcome in a US clinic-based case–control study. Methods: Subjects were genotyped...

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Veröffentlicht in:Cancer causes & control 2014-01, Vol.25 (1), p.25-32
Hauptverfasser: Madden, Melissa H., Anic, Gabriella M., Thompson, Reid C., Nabors, L. Burton, Olson, Jeffrey J., Browning, James E., Monteiro, Alvaro N., Egan, Kathleen M.
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container_end_page 32
container_issue 1
container_start_page 25
container_title Cancer causes & control
container_volume 25
creator Madden, Melissa H.
Anic, Gabriella M.
Thompson, Reid C.
Nabors, L. Burton
Olson, Jeffrey J.
Browning, James E.
Monteiro, Alvaro N.
Egan, Kathleen M.
description Purpose: There is growing evidence that circadian disruption may alter risk and aggressiveness of cancer. We evaluated common genetic variants in the circadian gene pathway for associations with glioma risk and patient outcome in a US clinic-based case–control study. Methods: Subjects were genotyped for 17 candidate single nucleotide polymorphisms in ARNTL, CRY1, CRY2, CSNK1E, KLHL30, NPAS2, PER1, PER3, CLOCK, and MYRIP. Unconditional logistic regression was used to estimate age and gender-adjusted odds ratios (OR) and 95 % confidence intervals (CI) for glioma risk under three inheritance models (additive, dominant, and recessive). Proportional hazards regression was used to estimate hazard ratios for glioma-related death among 441 patients with high-grade tumors. Survival associations were validated using The Cancer Genome Atlas (TCGA) dataset. Results: A variant in PER1 (rs2289591) was significantly associated with overall glioma risk (per variant allele OR 0.80; 95 % CI 0.66–0.97; ptrend = 0.027). The variant allele for CLOCK rs11133391 under a recessive model increased risk of oligodendroglioma (OR 2.41; 95 % CI 1.31–4.42; p = 0.005), though not other glioma subtypes (p for heterogeneity = 0.0033). The association remained significant after false discovery rate adjustment (p = 0.008). Differential associations by gender were observed for MYRIP rs6599077 and CSNK1E rs1534891 though differences were not significant after adjustment for multiple testing. No consistent mortality associations were identified. Several of the examined genes exhibited differential expression in glioblastoma multiforme versus normal brain in TCGA data (MYRIP, ARNTL, CRY1, KLHL30, PER1, CLOCK, and PER3), and expression of NPAS2 was significantly associated with a poor patient outcome in TCGA patients. Conclusion: This exploratory analysis provides some evidence supporting a role for circadian genes in the onset of glioma and possibly the outcome of glioma.
doi_str_mv 10.1007/s10552-013-0305-y
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Proportional hazards regression was used to estimate hazard ratios for glioma-related death among 441 patients with high-grade tumors. Survival associations were validated using The Cancer Genome Atlas (TCGA) dataset. Results: A variant in PER1 (rs2289591) was significantly associated with overall glioma risk (per variant allele OR 0.80; 95 % CI 0.66–0.97; ptrend = 0.027). The variant allele for CLOCK rs11133391 under a recessive model increased risk of oligodendroglioma (OR 2.41; 95 % CI 1.31–4.42; p = 0.005), though not other glioma subtypes (p for heterogeneity = 0.0033). The association remained significant after false discovery rate adjustment (p = 0.008). Differential associations by gender were observed for MYRIP rs6599077 and CSNK1E rs1534891 though differences were not significant after adjustment for multiple testing. No consistent mortality associations were identified. Several of the examined genes exhibited differential expression in glioblastoma multiforme versus normal brain in TCGA data (MYRIP, ARNTL, CRY1, KLHL30, PER1, CLOCK, and PER3), and expression of NPAS2 was significantly associated with a poor patient outcome in TCGA patients. 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Burton</au><au>Olson, Jeffrey J.</au><au>Browning, James E.</au><au>Monteiro, Alvaro N.</au><au>Egan, Kathleen M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Circadian pathway genes in relation to glioma risk and outcome</atitle><jtitle>Cancer causes &amp; control</jtitle><stitle>Cancer Causes Control</stitle><addtitle>Cancer Causes Control</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>25</volume><issue>1</issue><spage>25</spage><epage>32</epage><pages>25-32</pages><issn>0957-5243</issn><eissn>1573-7225</eissn><coden>CCCNEN</coden><abstract>Purpose: There is growing evidence that circadian disruption may alter risk and aggressiveness of cancer. We evaluated common genetic variants in the circadian gene pathway for associations with glioma risk and patient outcome in a US clinic-based case–control study. Methods: Subjects were genotyped for 17 candidate single nucleotide polymorphisms in ARNTL, CRY1, CRY2, CSNK1E, KLHL30, NPAS2, PER1, PER3, CLOCK, and MYRIP. Unconditional logistic regression was used to estimate age and gender-adjusted odds ratios (OR) and 95 % confidence intervals (CI) for glioma risk under three inheritance models (additive, dominant, and recessive). Proportional hazards regression was used to estimate hazard ratios for glioma-related death among 441 patients with high-grade tumors. Survival associations were validated using The Cancer Genome Atlas (TCGA) dataset. Results: A variant in PER1 (rs2289591) was significantly associated with overall glioma risk (per variant allele OR 0.80; 95 % CI 0.66–0.97; ptrend = 0.027). The variant allele for CLOCK rs11133391 under a recessive model increased risk of oligodendroglioma (OR 2.41; 95 % CI 1.31–4.42; p = 0.005), though not other glioma subtypes (p for heterogeneity = 0.0033). The association remained significant after false discovery rate adjustment (p = 0.008). Differential associations by gender were observed for MYRIP rs6599077 and CSNK1E rs1534891 though differences were not significant after adjustment for multiple testing. No consistent mortality associations were identified. Several of the examined genes exhibited differential expression in glioblastoma multiforme versus normal brain in TCGA data (MYRIP, ARNTL, CRY1, KLHL30, PER1, CLOCK, and PER3), and expression of NPAS2 was significantly associated with a poor patient outcome in TCGA patients. Conclusion: This exploratory analysis provides some evidence supporting a role for circadian genes in the onset of glioma and possibly the outcome of glioma.</abstract><cop>Dordrecht</cop><pub>Springer</pub><pmid>24135790</pmid><doi>10.1007/s10552-013-0305-y</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Adolescent
Adult
Aged
Aged, 80 and over
Alleles
Apoptosis
Biomedical and Life Sciences
Biomedicine
Brain cancer
Breast cancer
Cancer Research
Case-Control Studies
Cell cycle
Circadian rhythm
Circadian Rhythm - genetics
Clinical outcomes
Epidemiology
Female
Gene expression
Genes
Genomes
Genomics
Genotype
Glioma
Glioma - etiology
Glioma - genetics
Glioma - mortality
Hematology
Humans
Male
Middle Aged
Mortality
Oligodendroglioma
Oncology
Original Paper
Patients
Polymorphism, Single Nucleotide - genetics
Prostate
Proxy reporting
Proxy statements
Public Health
Risk
Tumors
Young Adult
title Circadian pathway genes in relation to glioma risk and outcome
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