TY - JOUR
T1 - Association between an interleukin 1 receptor, type I promoter polymorphism and self-reported attentional function in women with breast cancer
AU - Merriman, John D.
AU - Aouizerat, Bradley E.
AU - Cataldo, Janine K.
AU - Dunn, Laura
AU - Cooper, Bruce A.
AU - West, Claudia
AU - Paul, Steven M.
AU - Baggott, Christina R.
AU - Dhruva, Anand
AU - Kober, Kord
AU - Langford, Dale J.
AU - Leutwyler, Heather
AU - Ritchie, Christine S.
AU - Abrams, Gary
AU - Dodd, Marylin
AU - Elboim, Charles
AU - Hamolsky, Deborah
AU - Melisko, Michelle
AU - Miaskowski, Christine
N1 - Funding Information:
This study was funded by grants from the National Cancer Institute ( CA107091 and CA118658 ). Dr. Merriman was supported by a National Institute of Nursing Research (NINR) F31 National Research Service Award ( NR012604 ); an American Cancer Society (ACS) Doctoral Degree Scholarship in Cancer Nursing ( DSCNR-10-087 ); an Oncology Nursing Society (ONS) Foundation Doctoral Scholarship; and a University of California, San Francisco (UCSF) Nursing Alumni Association Scholarship. He is currently supported as a Postdoctoral Scholar by an NINR T32 NRSA ( NR011972 ). Dr. Aouizerat was funded through a National Institutes of Health (NIH) Roadmap for Medical Research Grant ( KL2 RR624130 ). Dr. Cataldo is partially supported by an ONS Genetic Fellowship Award. Dr. Dunn received funding from the Mount Zion Health Fund. Dr. Baggott is supported by an ACS Mentored Research Scholar Grant ( MRSG-12-01-PCSM ). Dr. Dhruva is funded through an NIH Mentored Patient-Oriented Research Career Development Award ( K23 AT005340 ). Dr. Langford is supported by a Breast Cancer Research Program Department of Defense Postdoctoral Fellowship. Dr. Leutwyler is supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through UCSF-CTSI Grant Number KL2TR000143 . Dr. Ritchie is funded through an NIH Geriatric Academic Leadership Award ( 1K07AG31779 ) and the Harris Fishbon Professorship for Clinical Translational Research in Aging. Dr. Miaskowski is funded by the ACS as a Clinical Research Professor. This project is supported by NIH/NCRR UCSF-CTSI Grant Number UL1 RR024131 . Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.
PY - 2014
Y1 - 2014
N2 - Subgroups of patients with breast cancer may be at greater risk for cytokine-induced changes in cognitive function after diagnosis and during treatment. The purposes of this study were to identify subgroups of patients with distinct trajectories of attentional function and evaluate for phenotypic and genotypic (i.e., cytokine gene polymorphisms) predictors of subgroup membership. Self-reported attentional function was evaluated in 397 patients with breast cancer using the Attentional Function Index before surgery and for six months after surgery (i.e., seven time points). Using growth mixture modeling, three attentional function latent classes were identified: High (41.6%), Moderate (25.4%), and Low-moderate (33.0%). Patients in the Low-moderate class were significantly younger than those in the High class, with more comorbidities and lower functional status than the other two classes. No differences were found among the classes in years of education, race/ethnicity, or other clinical characteristics. DNA was recovered from 302 patients' samples. Eighty-two single nucleotide polymorphisms among 15 candidate genes were included in the genetic association analyses. After controlling for age, comorbidities, functional status, and population stratification due to race/ethnicity, IL1R1 rs949963 remained a significant genotypic predictor of class membership in the multivariable model. Carrying the rare "A" allele (i.e., GA. +. AA) was associated with a twofold increase in the odds of belonging to a lower attentional function class (OR: 1.98; 95% CI: 1.18, 3.30; p=.009). Findings provide evidence of subgroups of women with breast cancer who report distinct trajectories of attentional function and of a genetic association between subgroup membership and an IL1R1 promoter polymorphism.
AB - Subgroups of patients with breast cancer may be at greater risk for cytokine-induced changes in cognitive function after diagnosis and during treatment. The purposes of this study were to identify subgroups of patients with distinct trajectories of attentional function and evaluate for phenotypic and genotypic (i.e., cytokine gene polymorphisms) predictors of subgroup membership. Self-reported attentional function was evaluated in 397 patients with breast cancer using the Attentional Function Index before surgery and for six months after surgery (i.e., seven time points). Using growth mixture modeling, three attentional function latent classes were identified: High (41.6%), Moderate (25.4%), and Low-moderate (33.0%). Patients in the Low-moderate class were significantly younger than those in the High class, with more comorbidities and lower functional status than the other two classes. No differences were found among the classes in years of education, race/ethnicity, or other clinical characteristics. DNA was recovered from 302 patients' samples. Eighty-two single nucleotide polymorphisms among 15 candidate genes were included in the genetic association analyses. After controlling for age, comorbidities, functional status, and population stratification due to race/ethnicity, IL1R1 rs949963 remained a significant genotypic predictor of class membership in the multivariable model. Carrying the rare "A" allele (i.e., GA. +. AA) was associated with a twofold increase in the odds of belonging to a lower attentional function class (OR: 1.98; 95% CI: 1.18, 3.30; p=.009). Findings provide evidence of subgroups of women with breast cancer who report distinct trajectories of attentional function and of a genetic association between subgroup membership and an IL1R1 promoter polymorphism.
KW - Attention
KW - Breast cancer
KW - Cytokine genes
KW - Inflammation
KW - Interleukin 1 receptor, type I
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U2 - 10.1016/j.cyto.2013.11.003
DO - 10.1016/j.cyto.2013.11.003
M3 - Article
C2 - 24315345
AN - SCOPUS:84892476325
SN - 1043-4666
VL - 65
SP - 192
EP - 201
JO - Cytokine
JF - Cytokine
IS - 2
ER -