Cancer-Related Fatigue and Circulating Biomarkers in Breast Cancer Survivors

Author:

García-González David1ORCID,Romero-Elías María2,Álvarez-Bustos Alejandro3,Rosado-García Silvia4,Sánchez-López Antonio J.4,Cantos Blanca5,Maximiano Constanza5,Méndez Miriam5,Méndez-Otero Marta5,Cebolla Héctor6,García-Foncillas Jesús178,Ruiz-Casado Ana25

Affiliation:

1. School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain

2. Instituto de Investigación Sanitaria Puerta de Hierro-Segovia de Arana, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain

3. Biomedical Research Center Network for Frailty and Healthy Ageing (CIBERFES), Institute of Health Carlos III, Madrid, Spain

4. Biobank, Puerta de Hierro-Segovia de Arana Health Research Institute, Madrid, Spain

5. Department of Medical Oncology, IDIPHISA, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain

6. Spanish National Research Council (CSIC), Madrid, Spain

7. Translational Oncology Division, Oncohealth Institute, IIS-Fundación Jiménez Díaz-UAM, Madrid, Spain

8. Department of Medical Oncology, UAM, Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain

Abstract

Purpose Cancer-related fatigue (CRF) is the most common and disruptive symptom experienced by cancer survivors and because of its frequency and severity is especially worrisome in breast cancer survivors (BCS). Despite a great deal of research, the mechanisms underlying CRF have not been determined. The present study aims to describe associations between CRF in BCS and different blood biomarkers. Methods A descriptive and cross-sectional study was conducted. A set of biomarkers assessing inflammation were measured in BCS: C-reactive protein (CRP), neutrophil-lymphocyte ratio (NLR), IL-1β, IL-6, IL-8, IL-10, tumor necrosis factor (TNF); HPA axis dysfunction (cortisol), autonomic dysfunction (noradrenaline); oxidative stress (8-OH deoxyguanosine); insulin resistance markers (insulin, IGF-I, IGFBP3) and sexual hormones (estrogens, progesterone, testosterone). Results NLR ( p = .00) and cortisol ( p = .02) were positive and negatively associated with CRF, respectively. The rest of the blood markers were not associated with CRF. Conclusion Our results increase the evidence on pathophysiological mechanisms driving CRF in BCS. However, longitudinal studies are needed to explore the role of these factors as potential causal mechanisms.

Funder

Seom-Fontvella

Publisher

SAGE Publications

Subject

Research and Theory

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