scholarly journals A Population-Based Study of Childhood Cancer Survivors’ Body Mass Index

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Echo L. Warner ◽  
Mark Fluchel ◽  
Jennifer Wright ◽  
Carol Sweeney ◽  
Kenneth M. Boucher ◽  
...  

Background.Population-based studies are needed to estimate the prevalence of underweight or overweight/obese childhood cancer survivors.Procedure.Adult survivors (diagnosed ≤20 years) were identified from the linked Utah Cancer Registry and Utah Population Database. We included survivors currently aged ≥20 years and ≥5 years from diagnosis(N=1060), and a comparison cohort selected on birth year and sex(N=5410). BMI was calculated from driver license data available from 2000 to 2010. Multivariable generalized linear regression models were used to calculate prevalence relative risks (RR) and 95% confidence intervals (95% CI) of BMI outcomes for survivors and the comparison cohort.Results.Average time since diagnosis was 18.5 years(SD=7.8), and mean age at BMI for both groups was 30.5 (survivorsSD=7.7, comparisonSD=8.0). Considering all diagnoses, survivors were not at higher risk for being underweight or overweight/obese than the comparison. Male central nervous system tumor survivors were overweight (RR=1.12, 95% CI 1.01–1.23) more often than the comparison. Female survivors, who were diagnosed at age 10 and under, had a 10% higher risk of being obese than survivors diagnosed at ages 16–20(P<0.05).Conclusion.While certain groups of childhood cancer survivors are at risk for being overweight/obese, in general they do not differ from population estimates.

Author(s):  
Kelly McCastlain ◽  
Carrie R Howell ◽  
Catherine E Welsh ◽  
Zhaoming Wang ◽  
Carmen L Wilson ◽  
...  

Abstract Background Adult childhood cancer survivors are at risk for frailty, including low muscle mass and weakness (sarcopenia). Using peripheral blood (PB) mitochondrial DNA copy number (mtDNAcn) as a proxy for functional mitochondria, this study describes cross-sectional associations between mtDNAcn and sarcopenia among survivors. Methods Among 1,762 adult childhood cancer survivors (51.6% male; median age = 29.4 [IQR = 23.3-36.8] years), with a median of 20.6 years from diagnosis (IQR = 15.2-28.2), mtDNAcn estimates were derived from whole-genome sequencing. A subset was validated by quantitative polymerase chain reaction and evaluated cross-sectionally using multivariable logistic regression for their association with sarcopenia, defined by race-, age-, and sex-specific low lean muscle mass or weak grip strength. All statistical tests were 2-sided. Results The prevalence of sarcopenia was 27.0%, higher among females than males (31.5% vs. 22.9%; P &lt; 0.001) and associated with age at diagnosis; 51.7% of survivors with sarcopenia were diagnosed ages 4-13 years (p = 0.01). Sarcopenia was most prevalent (39.0%) among central nervous system tumor survivors. Cranial radiation (OR = 1.84; 95% CI = 1.32-2.59) and alkylating agents (OR = 1.34; 95% CI = 1.04-1.72) increased, while glucocorticoids decreased odds (OR = 0.72; 95% CI = 0.56-0.93) of sarcopenia. mtDNAcn decreased with age (β=-0.81; P = 0.002), was higher among females (β = 9.23; P = 0.01) and among survivors with a C allele at mt.204 (β=-17.9; P = 0.02). In adjusted models, every standard deviation decrease in mtDNAcn increased the odds of sarcopenia 20% (OR = 1.20; 95% CI = 1.07-1.34). Conclusions While a growing body of evidence supports PB mtDNAcn as a biomarker for adverse health outcomes, this study is the first to report an association between mtDNAcn and sarcopenia among childhood cancer survivors.


2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 10014-10014
Author(s):  
Melissa A. Richard ◽  
Sogol Mostoufi-Moab ◽  
Nisha Rathore ◽  
Austin L. Brown ◽  
Stephen J. Chanock ◽  
...  

10014 Background: Childhood cancer survivors face increased risk for DM, a polygenic trait also attributable to cancer treatment exposures, particularly abdominal radiation. We aimed to characterize the role of genetic and treatment risk factors for DM among two large cohorts of childhood cancer survivors. Methods: We performed a nested case-control genome-wide association study for DM managed with oral medications in the original CCSS cohort (diagnosed 1970-1986). Logistic regression was conducted in the total sample (N = 5083) and stratified by 1) European ancestry (EA) and 2) abdominal radiation. Replication of suggestive variants (P < 1×10-7) using Fisher’s exact test was performed in independent cohorts: i) CCSS expansion diagnosed 1987-1999 (N = 2588) and ii) SJLIFE diagnosed 1962-2012 (N = 2182). To evaluate the effect of cancer treatment on the background genetic predisposition to DM, we estimated standardized effect sizes (Z’) among EA survivors in each abdominal radiation group for 398 index variants from the largest population-based EA DM study. Radiation group Z’ estimates were compared using linear regression. Results: In the original CCSS cohort we identified nine variants associated with DM and provide further support for four linked variants in the ERCC6L2 locus. Among all survivors, the rs55849673-A allele was associated with increased odds for DM among survivors in the original CCSS cohort (minor allele frequency [MAF]-cases = 0.055; MAF-controls = 0.024; adjusted odds ratio [aOR] = 2.9, 95% CI: 2.0-4.2, P = 3.7×10-8). Allele frequencies were consistent in the CCSS expansion (MAF-cases = 0.075; MAF-controls = 0.028; P = 0.07) and SJLIFE (MAF-cases = 0.036; MAF-controls = 0.027; P = 0.5). Additionally, rs55849673-A estimates were consistent among EA survivors and stronger among survivors not treated with abdominal radiation (MAF-cases = 0.052; MAF-controls = 0.021; aOR = 3.6, P = 1.6×10-6). Notably, in the CCSS expansion all rs55849673-A EA carriers who developed DM did not receive abdominal radiation (MAF-cases = 0.1; MAF-controls = 0.026; P = 0.04). More broadly, the Z’ of population-based DM index variants were 78% lower in survivors treated with abdominal radiation than survivors not treated with abdominal radiation (beta = 0.22; P = 0.01), indicating the background genetic risk for DM may be altered by treatment. Conclusions: We provide evidence for a novel locus of DM in childhood cancer survivors. This locus is a regulatory region associated with expression of ERCC6L2, a gene implicated in an East Asian population-based DM study. Taken together, our findings support the overwhelming effect of abdominal radiation on DM risk in childhood cancer survivors, relative to other risk factors, and provide insight on a genetic locus that may be useful for DM risk prediction in the context of cancer treatment.


In Vivo ◽  
2020 ◽  
Vol 34 (2) ◽  
pp. 929-933 ◽  
Author(s):  
JAESUNG HEO ◽  
HYUN JOO JUNG ◽  
O KYU NOH ◽  
LOGYOUNG KIM ◽  
JUN EUN PARK

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 10564-10564
Author(s):  
Daniel A. Mulrooney ◽  
Kirsten K. Ness ◽  
Sujuan Huang ◽  
Aimee Santucci ◽  
Robert P. Hebbel ◽  
...  

10564 Background: Endothelial dysfunction, as an indicator of vascular disease in childhood cancer survivors (CCS) has not been widely studied. Methods: Markers of vascular inflammation (high sensitivity C-reactive protein [hsCRP]), hemostasis (fibrinogen), activation (endothelial cell expression of vascular cell adhesion molecule [VCAM-1]) and functional testing (large/small artery elasticity [L/SAE], pulse wave velocity [PWV]) were assessed in 200 CCS, ≥10 years from diagnosis, and 192 age/gender matched healthy controls. Exclusion criteria included: inflammatory processes, use of anti-inflammatory or cardiovascular medications, or pregnancy. Differences were assessed by adjusted multivariable linear regression. Results: CCS (53% male) of leukemia/lymphoma (59%), central nervous system tumors (6%), sarcomas (11.5%), embryonal tumors (22.5%), and other (1%) had a mean age at diagnosis 7.3 years (SD ±5.7). CCS and controls did not differ in current age (mean 34.1 ±9.2 vs. 33.5 years ±9.8), body mass index, smoking, mean systolic (124 mm Hg ±11.7 vs. 123 ±11.9) or diastolic blood pressure (73 ±9.5 vs. 71 ±9.5). Fasting low- (110 mg/dl ±31 vs. 102 ±30) and high-density (52 ±16 vs. 56 ±18) cholesterol levels differed between survivors and controls (p<0.01). Endothelial expression of VCAM-1 and PWV were statistically significantly increased in CCS; arterial elasticity was significantly reduced (table). Therapeutic exposures (anthracyclines and radiation) were not significantly associated with endothelial dysfunction. Conclusions: Childhood cancer survivors have greater endothelial dysfunction, a sign of atherosclerosis, and preventive measures should be investigated. [Table: see text]


2018 ◽  
Vol 42 (5) ◽  
pp. 533-539 ◽  
Author(s):  
Iliana C. Lega ◽  
Jason D. Pole ◽  
Peter C. Austin ◽  
Cindy Lau ◽  
Paul C. Nathan ◽  
...  

2020 ◽  
Author(s):  
Vincent Pluimakers ◽  
Marta Fiocco ◽  
Jenneke van Atteveld ◽  
Monique Hobbelink ◽  
Dorine Bresters ◽  
...  

BACKGROUND Potential late effects of treatment for childhood cancer include adiposity, insulin resistance, dyslipidemia and hypertension. These risk factors cluster together as metabolic syndrome (MetS) and increase the risk for development of diabetes mellitus and cardio- and cerebrovascular disease. Knowledge on risk factors, timely diagnosis and preventive strategies is of importance to prevent cardio- and cerebrovascular complications and improve quality of life. Currently, no studies in national cohorts on prevalence and determinants of MetS in childhood cancer survivors including biomarkers and genetic predisposition are available. OBJECTIVE The objectives of the Dutch LATER METS study are to assess 1) the prevalence and risk factors of MetS and its separate components, and 2) the potential value of additional biomarkers, in the national cohort of adult long-term survivors of childhood cancer. METHODS This is a cross-sectional study, based on recruitment of all survivors treated in the Netherlands between 1963 and 2002. MetS will be classified according to the definitions of the National Cholesterol Education Program (NCEP-ATP III) as well as the Joint Interim Statement (JIS), and compared to reference data. Dual-energy X-ray absorptiometry (DXA) scans were performed to assess body composition in more detail. The effect of patient characteristics, previous treatment, and genetic variation on the risk of MetS will be assessed. The diagnostic and predictive value of novel biomarkers will be tested. RESULTS Patient accrual started in 2016 and lasted until April 2020. A total of 2380 survivors has participated, in seven pediatric oncology hospitals. From July 2020, biomarker testing, SNP analysis and data analysis will be performed. CONCLUSIONS The Dutch LATER METS study will provide knowledge on clinical and genetic determinants of MetS, and the diagnostic value of biomarkers, in childhood cancer survivors. The results of this study will be used to optimize surveillance guidelines for MetS in survivors, based on enhanced risk stratification and screening strategies. This will improve diagnosis of MetS, and prevent complications. CLINICALTRIAL Registered at toetsingonline.nl, NL32117.018.10


2012 ◽  
Vol 30 (18_suppl) ◽  
pp. CRA9513-CRA9513 ◽  
Author(s):  
Chaya S. Moskowitz ◽  
Joanne F. Chou ◽  
Suzanne L. Wolden ◽  
Jonine L. Bernstein ◽  
Jyoti Malhotra ◽  
...  

CRA9513 Background: The risk of breast cancer (BC) by age 50 among women treated for childhood cancer with chest radiation therapy (RT) and how this risk compares with that of BRCA1 and BRCA2 (BRCA1/2) mutation carriers is unknown. Methods: We evaluated the risk of BC in a cohort of 1268 female 5-yr childhood cancer survivors treated with chest RT and estimated the cumulative incidence of BC non-parametrically treating death as a competing risk. The cumulative incidence of BC in BRCA1/2 mutation carriers was estimated with the kin-cohort method using data from 4570 female first-degree relatives of women diagnosed with unilateral BC (probands) participating in the WECARE Study. Absolute Excess Risks (AERs) were estimated using population-based data from the SEER program. Results: With a median follow-up of 26 yrs (range 5-39) for the CCSS cohort, 175 women were diagnosed with BC at a median age of 38 yrs (range 24-53) and a median latency of 23 yrs (range 7-38); the overall cumulative incidence of BC by age 50 was 24% (95% confidence interval [CI] 20-28%) and among Hodgkin lymphoma survivors was 30% (95% CI 25-35%). In comparison, among first-degree relatives of WECARE Study probands 324 were diagnosed with BC (median age at diagnosis, 55 yrs (range 26-90)). The estimated cumulative incidence by age 50 was 31% (95% CI 16-47%) and 10% (95% CI 2-23%) in carriers of BRCA1 and BRCA2 mutations, respectively. The population cumulative incidence of BC is 4% by age 50. Among the childhood cancer survivors, AERs for BCs diagnosed per 10,000 person-years of observation were respectively 34 (95% CI 18-52), 27 (95% CI 11-45), and 95 (95% CI 78-112) among women treated with 10-19 Gy (23%), 20-29 Gy (17%), and 30+ Gy (56%) of chest RT. Conclusions: Women treated for childhood cancer with chest RT have a substantial risk of BC comparable to BRCA1/2 mutation carriers and considerably greater than that of the general population. Women treated with 10-19 Gy RT had an increased excess risk warranting consideration of breast cancer surveillance strategies similar to the current recommendations for women treated with > 20 Gy.


2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 10057-10057
Author(s):  
Kirsten K. Ness ◽  
Robyn Partin, MS ◽  
Carrie R. Howell ◽  
Kevin R. Krull ◽  
Tara M. Brinkman ◽  
...  

10057 Background: Childhood cancer survivors are at risk for premature aging; over 8% (ages18-60 years) meet Fried Frailty Criteria (≥3 of low lean muscle mass, muscle weakness, slow walking speed, exhaustion, low energy expenditure). Longitudinal changes and new onset frailty has not been studied. Methods: Childhood cancer survivors (N = 1501, 51.5% male, 14.9% black, median age at diagnosis 7 [0-22] years), were evaluated clinically to ascertain frailty at baseline (median age 30 [18-45] years) and five years later. Risk factors for incident frailty and impact of baseline frailty on mortality were evaluated in proportional hazard models. Results: Frailty increased from 6.0% (95% CI 4.1-8.9) to 11.7% (95% CI 6.7-12.2) overall, and for all diagnoses (Table). Risk factors for new onset frailty among those not frail at baseline were amputation (HR 5.1, 95% CI 1.1-14.4), anthracyclines (HR 1.2, 95% CI 1.1-1.4 per 100 mg/m2), and carboplatin (HR 1.3, 95% CI 1.1-1.5 per 2000 mg/m2). Severe, disabling or life threatening chronic conditions (HR 1.2, 95% CI 1.1-1.4 per organ system) and inactivity (HR 2.0, 95% CI 1.2-3.2) also predicted new onset frailty. Sixty-nine participants died from baseline to follow-up. Accounting for age, sex and chronic conditions, baseline frailty was associated with a 2.9 (95% CI 1.6-5.2) increased hazard of death. Conclusions: Prevalent frailty nearly doubled in five years and was associated with increased risk for death. Given that previous treatment exposures cannot be altered, interventions to remediate chronic disease and promote activity may impact function and longevity for childhood cancer survivors. [Table: see text]


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