Gesundheitswesen 2017; 79(08/09): 656-804
DOI: 10.1055/s-0037-1606025
Poster
Georg Thieme Verlag KG Stuttgart · New York

Cytokine gene variants associated with persistent cancer related fatigue in breast cancer patients

T Kühl
1   University Medical Center Hamburg-Eppendorf/University Cancer Center Hamburg, Genetic Tumour Epidemiology, Hamburg
,
S Behrens
2   German Cancer Research Center (DKFZ), Cancer Epidemiology, Heidelberg
,
A Jung
2   German Cancer Research Center (DKFZ), Cancer Epidemiology, Heidelberg
,
K Thöne
3   University Medical Center Hamburg-Eppendorf/University Cancer Center Hamburg, Cancer Epidemiology/Clinical Cancer Registry, Hamburg
,
J Chang-Claude
1   University Medical Center Hamburg-Eppendorf/University Cancer Center Hamburg, Genetic Tumour Epidemiology, Hamburg
2   German Cancer Research Center (DKFZ), Cancer Epidemiology, Heidelberg
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Publikationsverlauf

Publikationsdatum:
01. September 2017 (online)

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Aim:

Cancer related fatigue (CRF), one of the most common side effects of cancer and its treatment, can persist for years after completion of treatment even in otherwise healthy survivors. Inflammation processes, both during and after treatment, have been linked to CRF. SNPs influencing cytokine gene expression could partly explain variability in CRF and be used to identify patients at high risk of developing CRF. This study aimed to examine cytokine SNPs previously associated to CRF and to explore further functional genetic variants.

Methods:

We used the prospective cohort of breast cancer patients aged 50 – 70 at recruitment in 2002 – 2005 to the German population-based MARIE study (N = 3,813), followed up in 2009 (FUP1) and 2014 (FUP2). The Fatigue Assessment Questionnaire (FAQ) assessed CRF on a 1 – 10 scale. Linear/logistic regression models adjusted for baseline CRF and other covariates were used to evaluate the per-allele association of 43 literature derived candidate SNPs with CRF.

Results:

A total of 1,364 patients fulfilled inclusion criteria (no missing CRF scores, recurrence, metastasis or second tumour) at FUP1 and 934 at FUP2. The TNF-SNP, rs3093662, was associated with 1.5 score increase per allele (p = 0.02) for CRF at FUP1. For FUP2, rs3093662 showed a positive association with CRF, albeit attenuated (p = 0.07), as well as rs4073 (IL-8) (p = 0.01) and rs2227306 (IL-8) (p = 0.03) whereas rs1800796 (IL-6) (p = 0.025) was negatively associated. Using a score of > 4 to define CRF and comparing patients with CRF at both FUPs to those with CRF at one or no time-point, rs3093662 (TNF-) was associated (per-allele OR = 1.2, p = 0.003) as well as rs4251961 (IL-1RN) (p = 0.03).

Conclusion:

In the to date largest study on cytokine SNPs and CRF, we found consistent associations between previously reported TNF-variant rs3093662 and persistent CRF. Further studies with large sample sizes are needed to replicate findings and identify further SNPs associated with CRF.